The DOI matches its Crossref record; 300 of the 305 references it cites were found in a registry or an index; none of the 310 sources its claims cite is checked for support yet.
Reward, Addiction, Withdrawal to Nicotine
Open accessAbstract
Nicotine is the principal addictive component that drives continued tobacco use despite users' knowledge of the harmful consequences. The initiation of addiction involves the mesocorticolimbic dopamine system, which contributes to the processing of rewarding sensory stimuli during the overall shaping of successful behaviors. Acting mainly through nicotinic receptors containing the α4 and β2 subunits, often in combination with the α6 subunit, nicotine increases the firing rate and the phasic bursts by midbrain dopamine neurons. Neuroadaptations arise during chronic exposure to nicotine, producing an altered brain condition that requires the continued presence of nicotine to be maintained. When nicotine is removed, a withdrawal syndrome develops. The expression of somatic withdrawal symptoms depends mainly on the α5, α2, and β4 (and likely α3) nicotinic subunits involving the epithalamic habenular complex and its targets. Thus, nicotine taps into diverse neural systems and an array of nicotinic acetylcholine receptor (nAChR) subtypes to influence reward, addiction, and withdrawal.
Overview
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Written from the paper’s full text.
TL;DR
Nicotine drives reward and addiction mainly by acting on β2-containing nAChRs in the mesocorticolimbic dopamine system, increasing midbrain dopamine neuron firing and phasic bursts. Withdrawal depends on distinct nAChR subunits—especially α5, α2, and β4—in the habenulo-interpeduncular axis, so reward, addiction, and withdrawal are mediated by partially separate neural circuits.
Key findings
- Nicotine increases dopamine neuron firing and phasic burst activity, with tonic firing roughly 4 Hz and phasic bursts roughly 20–80 Hz; β2* nAChRs, often with α4 and/or α6, are essential for nicotine reinforcement and dopamine release.
- In mice lacking β2, nicotine does not induce phasic bursts, dopamine release, or self-administration; re-expression of β2 in the VTA, but not SNc, reinstates self-administration, and either α4 or α6 re-expression also reinstates it.
- Somatic withdrawal signs depend on α5, α2, and β4 nAChR subunits in the medial habenula/interpeduncular nucleus (MHb/IPN); mecamylamine injected into Hb/IPN precipitates withdrawal, whereas injection into VTA, hippocampus, or cortex does not.
- Withdrawal is associated with decreased extracellular dopamine in the NAc and increased dopamine output in the PFC; symptoms appear within a few hours and include irritability, anxiety, anger, difficulty concentrating, sleep disturbance, increased appetite, and weight gain.
Methods
- Narrative review synthesizing published literature on nicotinic acetylcholine receptors, mesocorticolimbic dopamine circuitry, nicotine reward, neuroadaptations, and withdrawal.
- Draws on animal models (especially mouse knockout and re-expression studies, rat electrophysiology, microdialysis, fast-scan cyclic voltammetry) and human genetic/imaging findings.
- Main analysis is qualitative integration of cited studies rather than a systematic review, meta-analysis, or new primary data.
Limitations
- Not stated in the paper: the review does not include a formal limitations section.
- Evident from the text: it is a narrative review without described systematic search criteria, inclusion/exclusion rules, or quantitative synthesis.
- Evident from the text: some conclusions are explicitly speculative, such as the proposed interpretation of SNP rs16969968 in CHRNA5 and its possible link to smoking behavior and addiction risk.
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Claims the paper makes
151 Not checked yet · 17 Own interpretation · 2 No basis given
None of the sources cited for this claim have been checked yet.
In the paper
“The epithalamic habenular complex and its targets appear to be critical for the withdrawal syndrome.”
§ Reward, Addiction, Withdrawal to Nicotine > INTRODUCTION AND SUMMARY
What the sources say
- Not checked yetcites Salas et al. 2004b
- Not checked yetcites Salas et al. 2009
hedgedconditional- Asserted: passes — The authors put it forward as true.
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In the paper
“Self-stimulation of the medial forebrain bundle facilitates DA release (Garris et al. 1999, Gratton et al. 1988, Phillips et al. 1989), and DA receptor antagonists or DA neuron lesions inhibit brain self-stimulation (Fouriezos & Wise 1976, Lippa et al. 1973, Stellar & Corbett 1989).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Garris et al. 1999
- Not checked yetcites Gratton et al. 1988
- Not checked yetcites Phillips et al. 1989
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In the paper
“The effectiveness or value of rewards can be estimated by measuring the effort a subject expends on behaviors that achieve the rewarded goal (Hodos 1961, Schultz 2006).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Hodos 1961
- Not checked yetcites Schultz 2006
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The withdrawal syndrome is not mediated exactly by the same mechanisms or by the same neural circuits that initiate addiction or dependency.”
§ Reward, Addiction, Withdrawal to Nicotine > INTRODUCTION AND SUMMARY
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In the paper
“The DA efferents originating from the midbrain VTA and particularly targeting the PFC and NAc became recognized as paramount neural structures shaping reward-related behavior (Schultz et al. 1997; Wise 2004, 2009; Wise & Rompre 1989).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Schultz et al. 1997
- Not checked yetcites Wise 2004
- Not checked yetcites Wise & Rompre 1989
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In the paper
“as exemplified by lesions in the PPT reducing nicotine self-administration (Lanca et al. 2000).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Lanca et al. 2000
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In addition, the PPT/LDT cholinergic afferents have important endogenous influences over DA neurons by acting via nAChRs (Maskos 2008, 2010).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Maskos 2008 source
- Not checked yetcites Maskos 2010
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“nicotine is the main addictive component (Benowitz 2009, Dani et al. 2009, Dani & Heinemann 1996, Mansvelder & McGehee 2002).”
§ Reward, Addiction, Withdrawal to Nicotine > INTRODUCTION AND SUMMARY
What the sources say
- Not checked yetcites Benowitz 2009
- Not checked yetcites Dani et al. 2009
- Not checked yetcites Dani & Heinemann 1996
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In the paper
“Therefore, reward mechanisms are observed across species, from insects to primates (Hodos 1961, Lau et al. 2006, McClure et al. 2007, Qin & Wheeler 2007, Wise 2006).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Hodos 1961
- Not checked yetcites Lau et al. 2006
- Not checked yetcites McClure et al. 2007
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Likewise, this DA system plays a critical role in the acquisition of behaviors that are inappropriately reinforced by psychostimulant drugs, including nicotine (Balfour 2004, Corrigall 1999, Dani et al. 2009, Dani & Heinemann 1996, Di Chiara 2000, Mansvelder & McGehee 2002).”
§ Reward, Addiction, Withdrawal to Nicotine > INTRODUCTION AND SUMMARY
What the sources say
- Not checked yetcites Balfour 2004
- Not checked yetcites Corrigall 1999
- Not checked yetcites Dani et al. 2009
plaindirect- Asserted: passes — The authors put it forward as true.
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- It may state two separate claims as one. 60
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In the paper
“After chronic use of nicotine, removal of nicotine produces a withdrawal syndrome that can be relieved by nicotine replacement therapy (Dani et al. 2009, Dani & Heinemann 1996, De Biasi & Salas 2008, Di Chiara 2000, Mansvelder & McGehee 2002, Stolerman & Shoaib 1991).”
§ Reward, Addiction, Withdrawal to Nicotine > INTRODUCTION AND SUMMARY
What the sources say
- Not checked yetcites Dani et al. 2009
- Not checked yetcites Dani & Heinemann 1996
- Not checked yetcites De Biasi & Salas 2008
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Self-stimulation of the medial forebrain bundle facilitates DA release (Garris et al. 1999, Gratton et al. 1988, Phillips et al. 1989), and DA receptor antagonists or DA neuron lesions inhibit brain self-stimulation (Fouriezos & Wise 1976, Lippa et al. 1973, Stellar & Corbett 1989).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Fouriezos & Wise 1976
- Not checked yetcites Lippa et al. 1973
- Not checked yetcites Stellar & Corbett 1989
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
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In the paper
“Acting mainly via midbrain nAChRs composed of the β2 subunit in combination with the α4 and/or α6 subunits, nicotine increases the firing rate and phasic burst activity of midbrain DA neurons and elevates DA in the PFC, NAc, and other targets (Imperato et al. 1986, Grenhoff et al. 1986, Mameli-Engvall et al. 2006, Pons et al. 2008, Zhang et al. 2009b).”
§ Reward, Addiction, Withdrawal to Nicotine > INTRODUCTION AND SUMMARY
What the sources say
- Not checked yetcites Imperato et al. 1986
- Not checked yetcites Grenhoff et al. 1986
- Not checked yetcites Mameli-Engvall et al. 2006
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Rewarding stimuli promote learning of goal-directed behaviors, generate positive emotions, and subsequently stimulate repetition of those learned behaviors (Schultz 2010, Thorndike 1911).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Schultz 2010
- Not checked yetcites Thorndike 1911
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In particular, the mesocorticolimbic dopamine (DA) system plays an important role in self-stimulation and in processing environmental reward.”
§ Reward, Addiction, Withdrawal to Nicotine > INTRODUCTION AND SUMMARY
What the sources say
- Not checked yetcites Olds 1958
- Not checked yetcites Olds & Milner 1954
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Early investigations showed that the midbrain dopamine (DA) systems have an important role in the response to salient stimuli and to brain self-stimulation (Phillips & Olds 1969; Fibiger 1978, Wise 1978).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Phillips & Olds 1969
- Not checked yetcites Fibiger 1978
- Not checked yetcites Wise 1978
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The medial habenula (MHb) and one of its primary targets, the interpeduncular nucleus (IPN), richly express β4 and α5 nAChR subunits (and α2 only in the rodent IPN), which are necessary for the neuroadaptations that lead to somatic withdrawal symptoms during nicotine abstinence (Salas et al. 2004b, 2009).”
§ Reward, Addiction, Withdrawal to Nicotine > INTRODUCTION AND SUMMARY
What the sources say
- Not checked yetcites Salas et al. 2004b
- Not checked yetcites Salas et al. 2009
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The PPT/LDT cholinergic afferents boost glutamate afferent transmission via presynaptic nAChRs (Pidoplichko et al. 2004, Schilstrom et al. 2000) and provide some excitatory drive to GABA projection neurons and interneurons, mainly via β2-containing (β2*) nAChRs (Mansvelder et al. 2002, Pidoplichko et al. 2004, Pons et al. 2008).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Pidoplichko et al. 2004
- Not checked yetcites Schilstrom et al. 2000
- Not checked yetcites Mansvelder et al. 2002
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Although only ~2% of the striatal neurons are cholinergic, they have extremely dense axonal arbors that provide denser cholinergic innervation than is seen anywhere else in the brain (Butcher & Woolf 1984, Zhou et al. 2001, 2002).”
§ Reward, Addiction, Withdrawal to Nicotine > DOWNSTREAM FROM DOPAMINE NEURON PHASIC BURSTS
What the sources say
- Not checked yetcites Butcher & Woolf 1984
- Not checked yetcites Zhou et al. 2001
- Not checked yetcites Zhou et al. 2002
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Addictive drugs (including nicotine) increase the basal DA concentration in the NAc shell as measured by microdialysis, but that background increase is smaller or not detected in the dorsolateral striatum (Di Chiara 1999, Pidoplichko et al. 2004, Pontieri et al. 1996, Zhang et al. 2009b).”
§ Reward, Addiction, Withdrawal to Nicotine > DOWNSTREAM FROM DOPAMINE NEURON PHASIC BURSTS
What the sources say
- Not checked yetcites Di Chiara 1999
- Not checked yetcites Pidoplichko et al. 2004
- Not checked yetcites Pontieri et al. 1996
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Nicotine, at the concentration obtained from tobacco, induces phasic bursts from VTA/SNc DA neurons (Figure 1b) that innervate much of the dorsal to ventral extent of the striatum (Grenhoff et al. 1986, Pidoplichko et al. 1997, Schilstrom et al. 2003, Zhang et al. 2009b), suggesting that the DA signal should be comparable throughout the striatum.”
§ Reward, Addiction, Withdrawal to Nicotine > DOWNSTREAM FROM DOPAMINE NEURON PHASIC BURSTS
What the sources say
- Not checked yetcites Grenhoff et al. 1986
- Not checked yetcites Pidoplichko et al. 1997
- Not checked yetcites Schilstrom et al. 2003
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“For example, phasic burst firing is induced by unpredicted reward or unanticipated cues that have been conditioned to a known reward (Schultz 2007b, Schultz et al. 1997).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Schultz 2007b
- Not checked yetcites Schultz et al. 1997
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Tonic firing is at a relatively low frequency (roughly 4 Hz) that generally consists of individual action potentials. Phasic firing is usually at a higher average frequency, and it includes high-frequency burst discharges (roughly 20–80 Hz) (Grace et al. 2007; Grace & Bunney 1983, 1984; Hyland et al. 2002; Robinson et al. 2004).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Grace et al. 2007
- Not checked yetcites Grace & Bunney 1983
- Not checked yetcites Hyland et al. 2002
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In the paper
“Nicotine self-administration is reinstated by re-expression of the β2 subunit in the VTA but not in the neighboring SNc (Avale et al. 2008), confirming the specific role of the VTA in reward.”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Avale et al. 2008
boosteddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Thus, β2* nAChRs in combinations with both α4 and α6 subunits are important for the reinforcing properties of nicotine, and the α4 and α6 subunits cannot completely substitute for each other even though they are abundantly expressed in VTA neurons (Champtiaux et al. 2003, Salminen et al. 2007).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Champtiaux et al. 2003
- Not checked yetcites Salminen et al. 2007
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Interestingly, local re-expression of α7 in the VTA did not reinstate self-administration in α7 −/− mice (Pons et al. 2008), consistent with the pharmacological evidence indicating that the α7 subunit does not influence chronic nicotine self-administration in trained rats (Grottick & Higgins 2000) nor nicotine-induced conditioned place preference (Stolerman et al. 2004, Walters et al. 2006).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Grottick & Higgins 2000
- Not checked yetcites Stolerman et al. 2004
- Not checked yetcites Walters et al. 2006
hedged- Asserted: passes — The authors put it forward as true.
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In the paper
“Nicotinic receptors are expressed on DA neuron fibers and terminals, and the activity of those nAChRs, particularly containing the β2, α4, and α6 subunits (Pons et al. 2008), is highly regulated by ongoing striatal cholinergic interneuron discharges and dense acetylcholine esterase activity (Zhou et al. 2001, 2003).”
§ Reward, Addiction, Withdrawal to Nicotine > DOWNSTREAM FROM DOPAMINE NEURON PHASIC BURSTS
What the sources say
- Not checked yetcites Pons et al. 2008
- Not checked yetcites Zhou et al. 2001
- Not checked yetcites Zhou et al. 2003
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Those DA projection target areas are involved in reinforcement (ventral striatum), learning and declarative memory (hippocampus), emotional memory (amygdala), and habit formation (dorsal striatum), as well as executive functions and working memory (PFC and orbitofrontal cortex) (Schultz W. 2007b, Laviolette 2007, Seamans & Yang 2004).”
§ Reward, Addiction, Withdrawal to Nicotine > DOWNSTREAM FROM DOPAMINE NEURON PHASIC BURSTS
What the sources say
- Not checked yetcites Schultz W. 2007b
- Not checked yetcites Laviolette 2007
- Not checked yetcites Seamans & Yang 2004
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Disrupting those bursts impairs conditioned behavioral responses, diminishes the ability to learn cues about reward and salience, and disrupts the overall processing of reward (Schultz 2007b).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Schultz 2007b
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Nicotine self-administration is also reinstated by the re-expression of either the α4 or the α6 nAChR subunit, consistent with the expression of α4β2 and α4α6β2 nAChRs in the VTA (Pons et al. 2008).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Pons et al. 2008
plaindirect- Asserted: passes — The authors put it forward as true.
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A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Phasic burst firing by DA neurons and the consequent downstream phasic DA signals are vital for processing reward-related information and, thus, are important for the initial phase of addiction.”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Nicotine directly activates DA neurons via those and other nAChR subtypes (Pidoplichko et al. 1997), and nicotine modifies the firing modes and firing frequency of DA neurons through excitatory and inhibitory inputs and synaptic plasticity (Mameli-Engvall et al. 2006; Schilstrom et al. 2000, 2003; Zhang et al. 2009b).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Pidoplichko et al. 1997
- Not checked yetcites Mameli-Engvall et al. 2006
- Not checked yetcites Schilstrom et al. 2000
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In mice lacking the β2 nAChR subunit (β2 −/−), nicotine does not induce phasic bursts by DA neurons (Mameli-Engvall et al. 2006), nicotine does not induce DA release, and nicotine does not support self-administration (Picciotto et al. 1998).”
§ Reward, Addiction, Withdrawal to Nicotine > REWARD AND INITIATION OF ADDICTION
What the sources say
- Not checked yetcites Mameli-Engvall et al. 2006
- Not checked yetcites Picciotto et al. 1998
plain- Asserted: passes — The authors put it forward as true.
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The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Measured in vivo from the VTA, nicotine administration to a rat causes (some) DA neurons to fire at a higher rate and to fire more and longer bursts (Figure 1).”
§ Reward, Addiction, Withdrawal to Nicotine > DOWNSTREAM FROM DOPAMINE NEURON PHASIC BURSTS
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The details of the DA signaling change in both anatomical areas, but as judged by the area under the curves (Figure 3a,b), the data suggest that the background DA concentration would increase in the NAc shell and not the dorsal striatum (Zhang et al. 2009b).”
§ Reward, Addiction, Withdrawal to Nicotine > DOWNSTREAM FROM DOPAMINE NEURON PHASIC BURSTS
What the sources say
- Not checked yetcites Zhang et al. 2009b
hedged- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“However, when nicotine is added to striatal brain slices, a significant proportion of presynaptic and axonal nAChRs is desensitized. As a consequence, low-frequency, tonic DA release is inhibited (Rice & Cragg 2004, Zhang & Sulzer 2004, Zhou et al. 2001), but phasic DA release is regulated differently, such that phasic bursts induce large DA signals (Cragg 2003; Rice & Cragg 2004; Zhang et al. 200”
§ Reward, Addiction, Withdrawal to Nicotine > DOWNSTREAM FROM DOPAMINE NEURON PHASIC BURSTS
What the sources say
- Not checked yetcites Rice & Cragg 2004
- Not checked yetcites Zhang & Sulzer 2004
- Not checked yetcites Zhou et al. 2001
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In the NAc shell, phasic burst discharges produce a greater increase in DA release than in the dorsal striatum, where the DA release from a single-pulse stimulus is comparable to the release from a phasic-burst stimulus.”
§ Reward, Addiction, Withdrawal to Nicotine > DOWNSTREAM FROM DOPAMINE NEURON PHASIC BURSTS
What the sources say
- Not checked yetcites Zhang et al. 2009a
- Not checked yetcites Zhang et al. 2009b
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Reward omission induces phasic inhibition of VTA neurons (Schultz 2007a,b), and aversive stimuli excite ventral (Brischoux et al. 2009) and inhibit dorsal (Ungless et al. 2004) VTA neurons.”
§ Reward, Addiction, Withdrawal to Nicotine > AVERSIVE SENSORY SIGNALING IN THE MESOCORTICOLIMBIC SYSTEM
What the sources say
- Not checked yetcites Brischoux et al. 2009
- Not checked yetcites Ungless et al. 2004
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“DA axon terminals in the dorsolateral striatum and NAc shell respond differently to incoming action potentials, consistent with phasic bursts inducing a greater increase of DA release in the NAc shell (Cragg 2003; Rice & Cragg 2004; Zhang et al. 2009a,b; Zhang & Sulzer 2004), which has a more important role in mediating the rewarding properties of nicotine that drive the early phases of addiction.”
§ Reward, Addiction, Withdrawal to Nicotine > DOWNSTREAM FROM DOPAMINE NEURON PHASIC BURSTS
What the sources say
- Not checked yetcites Cragg 2003
- Not checked yetcites Rice & Cragg 2004
- Not checked yetcites Zhang et al. 2009a
hedgeddirect- Asserted: passes — The authors put it forward as true.
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In the paper
“As in the LHb, RMTg neurons are phasically activated by aversive stimuli and inhibited by natural rewards such as food or reward-predictive stimuli, and conversely, RMTg neurons are stimulated by aversive stimuli (Jhou et al. 2009b).”
§ Reward, Addiction, Withdrawal to Nicotine > AVERSIVE SENSORY SIGNALING IN THE MESOCORTICOLIMBIC SYSTEM
What the sources say
- Not checked yetcites Jhou et al. 2009b
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Owing to afferents mediating sensory input, NAc neurons decrease their firing to appetitive stimuli and increase their firing to aversive stimuli (Roitman et al. 2005).”
§ Reward, Addiction, Withdrawal to Nicotine > AVERSIVE SENSORY SIGNALING IN THE MESOCORTICOLIMBIC SYSTEM
What the sources say
- Not checked yetcites Roitman et al. 2005
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Nicotine exposure also increases high-affinity DA D2 receptors in the NAc (Novak et al. 2010), an effect, also produced by cocaine, that causes DA hypersensitivity (Briand et al. 2008, Grigoriadis & Seeman 1986).”
§ Reward, Addiction, Withdrawal to Nicotine > NICOTINE-INDUCED NEUROADAPTATIONS
What the sources say
- Not checked yetcites Novak et al. 2010
- Not checked yetcites Briand et al. 2008
- Not checked yetcites Grigoriadis & Seeman 1986
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“In the NAc of rats, intraoral sucrose (i.e., rewarding) infusion increased DA levels, whereas quinine (i.e., aversive) infusion decreased DA levels (Roitman et al. 2008).”
§ Reward, Addiction, Withdrawal to Nicotine > AVERSIVE SENSORY SIGNALING IN THE MESOCORTICOLIMBIC SYSTEM
What the sources say
- Not checked yetcites Roitman et al. 2008
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Nicotinic receptor upregulation differs among the diverse subtypes, varies among brain regions for the same nAChR subtype, and depends on the contingency of nicotine administration (Gaimarri et al. 2007, Marks et al. 1983, McCallum et al. 2006, Metaxas et al. 2010, Nguyen et al. 2004, Pauly et al. 1996, Schwartz & Kellar 1983).”
§ Reward, Addiction, Withdrawal to Nicotine > NICOTINE-INDUCED NEUROADAPTATIONS
What the sources say
- Not checked yetcites Gaimarri et al. 2007
- Not checked yetcites Marks et al. 1983 source
- Not checked yetcites McCallum et al. 2006
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“Because nicotine is not hydrolyzed by acetylcholine esterase, as ACh is, nicotine’s long-lasting presence favors excessive nAChR desensitization. The homeostatic response to desensitized (turned-off) receptors is upregulation (Dani & Heinemann 1996, Fenster et al. 1999, Picciotto et al. 2008).”
§ Reward, Addiction, Withdrawal to Nicotine > NICOTINE-INDUCED NEUROADAPTATIONS
What the sources say
- Not checked yetcites Dani & Heinemann 1996
- Not checked yetcites Fenster et al. 1999
- Not checked yetcites Picciotto et al. 2008
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“The RMTg sends GABAergic projections to the VTA and SNc and inhibits DA cells (Ikemoto 2010, Jhou et al. 2009a).”
§ Reward, Addiction, Withdrawal to Nicotine > AVERSIVE SENSORY SIGNALING IN THE MESOCORTICOLIMBIC SYSTEM
What the sources say
- Not checked yetcites Ikemoto 2010
- Not checked yetcites Jhou et al. 2009a
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“The IPN, in turn, sends projections to the serotonergic raphé nuclei and to the dopaminergic VTA (Groenewegen et al. 1986, Klemm 2004, Montone et al. 1988).”
§ Reward, Addiction, Withdrawal to Nicotine > AVERSIVE SENSORY SIGNALING IN THE MESOCORTICOLIMBIC SYSTEM
What the sources say
- Not checked yetcites Groenewegen et al. 1986
- Not checked yetcites Klemm 2004
- Not checked yetcites Montone et al. 1988
plaincorrelational- Asserted: passes — The authors put it forward as true.
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In the paper
“The emergence of negative affective symptoms such as dysphoria, anxiety, and irritability (Koob & Le Moal 2001) and, to a lesser extent, the somatic manifestations of withdrawal, signal dependency and underlie drug-seeking behavior (Koob & Le Moal 2005, Koob & Volkow 2009).”
§ Reward, Addiction, Withdrawal to Nicotine > BEHAVIORAL MANIFESTATIONS OF NICOTINE WITHDRAWAL
What the sources say
- Not checked yetcites Koob & Le Moal 2005
- Not checked yetcites Koob & Volkow 2009
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Other quantifiable manifestations include reduced heart rates, altered neurohormonal profiles, disrupted electroencephalographic theta power, and perturbations of learned behaviors (Buchhalter et al. 2008, Koob & Le Moal 2005).”
§ Reward, Addiction, Withdrawal to Nicotine > BEHAVIORAL MANIFESTATIONS OF NICOTINE WITHDRAWAL
What the sources say
- Not checked yetcites Buchhalter et al. 2008
- Not checked yetcites Koob & Le Moal 2005
plain- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Powerful cravings also accompany withdrawal, and they may be precipitated by drug-reinforced memories, such as the sight of a cigarette and the place associated with smoking (Dalley & Everitt 2009, Dani & Montague 2007, Shiffman et al. 2002, Smolka et al. 2005, Volkow et al. 2002).”
§ Reward, Addiction, Withdrawal to Nicotine > BEHAVIORAL MANIFESTATIONS OF NICOTINE WITHDRAWAL
What the sources say
- Not checked yetcites Dalley & Everitt 2009
- Not checked yetcites Dani & Montague 2007
- Not checked yetcites Shiffman et al. 2002
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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In the paper
“Nicotine cessation increases the levels of prodynorphin mRNA in NAc dynorphinergic neurons, possibly as a compensatory mechanism to increased dynorphinergic tone (Isola et al. 2008).”
§ Reward, Addiction, Withdrawal to Nicotine > BEHAVIORAL MANIFESTATIONS OF NICOTINE WITHDRAWAL
What the sources say
- Not checked yetcites Isola et al. 2008
hedgeddirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
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In the paper
“In particular, dynorphins decrease and enkephalins increase the release of DA (Devine et al. 1993; Di Chiara & Imperato 1988; Longoni et al. 1991; Pentney & Gratton 1991; Spanagel et al. 1990a,b, 1992).”
§ Reward, Addiction, Withdrawal to Nicotine > NICOTINE-INDUCED NEUROADAPTATIONS
What the sources say
- Not checked yetcites Devine et al. 1993 source
- Not checked yetcites Di Chiara & Imperato 1988
- Not checked yetcites Longoni et al. 1991
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“The overall neuroadaptations contribute to the mechanisms that maintain nicotine consumption, including mechanisms underlying associative learning (Tang & Dani, 2009), and they also participate in the nicotine-withdrawal syndrome (De Biasi & Salas 2008, Hadjiconstantinou & Neff 2010).”
§ Reward, Addiction, Withdrawal to Nicotine > NICOTINE-INDUCED NEUROADAPTATIONS
What the sources say
- Not checked yetcites Tang & Dani, 2009
- Not checked yetcites De Biasi & Salas 2008
- Not checked yetcites Hadjiconstantinou & Neff 2010
plaindirect- Asserted: passes — The authors put it forward as true.
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None of the sources cited for this claim have been checked yet.
In the paper
“The endogenous opioid system influences positive and negative motivational and affective states (Steiner & Gerfen 1998) and participates in the behavioral effects of several addictive drugs, including nicotine (Berrendero et al. 2005, Hadjiconstantinou & Neff 2010, Trigo et al. 2009).”
§ Reward, Addiction, Withdrawal to Nicotine > NICOTINE-INDUCED NEUROADAPTATIONS
What the sources say
- Not checked yetcites Steiner & Gerfen 1998
- Not checked yetcites Berrendero et al. 2005
- Not checked yetcites Hadjiconstantinou & Neff 2010
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This phenomenon is similar to the anxiety reported by humans experiencing nicotine abstinence and suggests that the sensitivity to anxiety influences the degree of withdrawal signs.”
§ Reward, Addiction, Withdrawal to Nicotine > BEHAVIORAL MANIFESTATIONS OF NICOTINE WITHDRAWAL
hedgedconditional- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“During withdrawal, the NAc displays a DA deficit, whereas the PFC has an increase in DA output (Carboni et al. 2000).”
§ Reward, Addiction, Withdrawal to Nicotine > MOLECULAR MECHANISMS OF WITHDRAWAL
What the sources say
- Not checked yetcites Carboni et al. 2000
plaincorrelational- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Withdrawal reflects the abrupt disruption of the equilibrium maintained in the presence of nicotine, and withdrawal triggers new neuroadaptations that counteract the negative state.”
§ Reward, Addiction, Withdrawal to Nicotine > MOLECULAR MECHANISMS OF WITHDRAWAL
plaindirect- Asserted: passes — The authors put it forward as true.
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In the paper
“Mecamylamine, which has a slightly higher affinity for α3β4* nAChRs than for β2* receptors, is the best antagonist at precipitating nicotine withdrawal (Damaj et al. 2003).”
§ Reward, Addiction, Withdrawal to Nicotine > BEHAVIORAL MANIFESTATIONS OF NICOTINE WITHDRAWAL
What the sources say
- Not checked yetcites Damaj et al. 2003
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Nicotine abstinence is accompanied by increased DA uptake into synaptosomes and elevated DA transporters (DATs) in the SNc/VTA (Hadjiconstantinou & Neff 2010, Rahman et al. 2004).”
§ Reward, Addiction, Withdrawal to Nicotine > MOLECULAR MECHANISMS OF WITHDRAWAL
What the sources say
- Not checked yetcites Hadjiconstantinou & Neff 2010
- Not checked yetcites Rahman et al. 2004
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Anhedonia, conditioned place aversion, anxiety-related behavior, and conditioned fear are four major affective manifestations of nicotine withdrawal.”
§ Reward, Addiction, Withdrawal to Nicotine > BEHAVIORAL MANIFESTATIONS OF NICOTINE WITHDRAWAL
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Because enhanced DA transmission in the PFC occurs during stressful and aversive stimuli and is implicated in anxiety”
§ Reward, Addiction, Withdrawal to Nicotine > MOLECULAR MECHANISMS OF WITHDRAWAL
What the sources say
- Not checked yetcites Bradberry et al. 1991
- Not checked yetcites Broersen et al. 2000
- Not checked yetcites Inglis & Moghaddam 1999
plaincorrelational- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Buproprion may aid smoking cessation, in part, by normalizing NAc DA levels, and those DA levels may in turn attenuate anhedonia and somatic withdrawal signs (Cryan et al. 2003, Paterson & Markou 2007).”
§ Reward, Addiction, Withdrawal to Nicotine > MOLECULAR MECHANISMS OF WITHDRAWAL
What the sources say
- Not checked yetcites Cryan et al. 2003
- Not checked yetcites Paterson & Markou 2007
hedgedconditional- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
- Rests on an assumption: Bupropion inhibits nAChRs and is mainly a norepinephrine/dopamine reuptake blocker.
In the paper
“as nicotine withdrawal produces deficits in contextual fear conditioning and affects the acquisition of learned responses (Portugal et al. 2008).”
§ Reward, Addiction, Withdrawal to Nicotine > BEHAVIORAL MANIFESTATIONS OF NICOTINE WITHDRAWAL
What the sources say
- Not checked yetcites Portugal et al. 2008
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Both spontaneous (Epping-Jordan et al. 1998, Harrison et al. 2001) and mecamylamine-precipitated (Watkins et al. 2000) nicotine withdrawal induce increases in self-stimulation thresholds.”
§ Reward, Addiction, Withdrawal to Nicotine > BEHAVIORAL MANIFESTATIONS OF NICOTINE WITHDRAWAL
What the sources say
- Not checked yetcites Epping-Jordan et al. 1998
- Not checked yetcites Harrison et al. 2001
- Not checked yetcites Watkins et al. 2000 source
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
In the paper
“Absence of β4 abolishes the somatic signs of withdrawal precipitated by systemic injection of mecamylamine (Salas et al. 2004b) and prevents withdrawal-induced hyperalgesia (Salas et al. 2004b).”
§ Reward, Addiction, Withdrawal to Nicotine > DISTINCT NICOTINIC RECEPTOR SUBTYPES MEDIATE WITHDRAWAL
What the sources say
- Not checked yetcites Salas et al. 2004b
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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None of the sources cited for this claim have been checked yet.
In the paper
“Third, a derivative of the alkaloid ibogaine, 18-methoxycoronaridine (18-MC) (Vastag 2005), is a potent antagonist of β4* nAChRs (Glick et al. 2002) with significant antiaddictive properties (Maisonneuve & Glick 2003).”
§ Reward, Addiction, Withdrawal to Nicotine > DISTINCT NICOTINIC RECEPTOR SUBTYPES MEDIATE WITHDRAWAL
What the sources say
- Not checked yetcites Glick et al. 2002
- Not checked yetcites Maisonneuve & Glick 2003
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The primary circuits underlying this exquisitely regulated dosing are mainly the mesocorticolimbic DA system and the epithalamic habenular circuits: One supports the rising arm, the other the falling arm of the inverted U dose-response curve.”
§ Reward, Addiction, Withdrawal to Nicotine > DISTINCT NICOTINIC RECEPTOR SUBTYPES MEDIATE WITHDRAWAL
plaindirect- Asserted: passes — The authors put it forward as true.
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It may state two separate claims as one.
- Rests on an assumption: Smokers regulate puffing and inhalation depth to achieve the most desirable nicotine dose at the top of the inverted U dose-response curve.
In the paper
“In animal models, 18-MC reduced self-administration of nicotine, morphine, cocaine, and methamphetamine; reduced oral intake of alcohol and nicotine; and decreased signs of opioid withdrawal (Maisonneuve & Glick 2003).”
§ Reward, Addiction, Withdrawal to Nicotine > DISTINCT NICOTINIC RECEPTOR SUBTYPES MEDIATE WITHDRAWAL
What the sources say
- Not checked yetcites Maisonneuve & Glick 2003
plaindirect- Asserted: passes — The authors put it forward as true.
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- Load-bearing: passes — The paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Attenuation of nicotine-induced seizure is also present in mice heterozygous for the α3 subunit, which is found in the same gene cluster that contains α5 and β4 (Boulter et al. 1990, Salas et al. 2004a).”
§ Reward, Addiction, Withdrawal to Nicotine > DISTINCT NICOTINIC RECEPTOR SUBTYPES MEDIATE WITHDRAWAL
What the sources say
- Not checked yetcites Boulter et al. 1990 source
- Not checked yetcites Salas et al. 2004a
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
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It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Recent findings on the influence of gene variants in the CHRNA5-CHRNA3-CHRNB4 gene cluster on nicotine addiction (Bierut et al. 2008, Thorgeirsson et al. 2008) show that a single nucleotide polymorphism (SNP) within CHRNA5, rs16969968, seems to correlate with nicotine dependency risk, heavy smoking, and the pleasurable sensation produced by a cigarette (Berrettini et al. 2008, Bierut et al. 2008,”
§ Reward, Addiction, Withdrawal to Nicotine > DISTINCT NICOTINIC RECEPTOR SUBTYPES MEDIATE WITHDRAWAL
What the sources say
- Not checked yetcites Berrettini et al. 2008
- Not checked yetcites Bierut et al. 2008
- Not checked yetcites Saccone et al. 2007
hedgedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The paper relies on this without support.
No mRNA encoding nAChR subunits can be detected in the lateral habenula by in situ hybridization.
“and no mRNA encoding for nAChR subunits can be detected in the LHb by in situ hybridization techniques.”
The paper relies on this without support.
Smokers regulate puffing and inhalation depth to achieve the most desirable nicotine dose at the top of the inverted U dose-response curve.
“Smokers finely control nicotine intake by regulating how they puff on a cigarette and how deeply they inhale. In that way, they achieve the most desirable nicotine dose, at the top of the inverted U dose-response curve.”
The paper relies on this without support.
Bupropion inhibits nAChRs and is mainly a norepinephrine/dopamine reuptake blocker.
“Although buproprion inhibits nAChRs, it is mainly a norepinephrine/DA re-uptake blocker.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Therefore, during the withdrawal period, phasic DA neuron activity of the kind induced by nicotine (9, 30) re-exposure induces DA signals that may make smokers in the withdrawal period more vulnerable to the reinforcing influence of nicotine (2).”
From Withdrawal from Chronic Nicotine Exposure Alters Dopamine Signaling Dynamics in the Nucleus Accumbens (2012) · cites this paper as [2]
Experimental — accuracy not yet measuredIn the citing paper
“The role of the DAergic system (in particular the mesocorticolimbic pathway) in drug addiction derives from DA’s ability to modulate many of the limbic and cortical sites involved in goal-directed behavior (Fig. 1) [18, 28–31].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [18]
In the citing paper
“Studies conducted in recent years have identified the LHb as a source of anti-reward signals that plays an important role in determining the reward-related activity of DA neurons [18, 30, 68–70].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [18]
In the citing paper
“Nicotine follows an inverted U-shaped dose-response curve [18, 60], and smokers titrate their nicotine intake to experience the rewarding while avoiding the aversive effects produced by high nicotine doses [61–64].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [18]
In the citing paper
“as well as the habenulo-interpeduncular pathway, which has been implicated in the addictive effects of smoking (Dani and Bertrand, 2007;De Biasi and Dani, 2011).”
From Varenicline Is a Potent Partial Agonist at α6β2* Nicotinic Acetylcholine Receptors in Rat and Monkey Striatum (2012) · cites this paper as De Biasi and Dani, 2011
In the citing paper
“Another critical site of action would be the mesolimbic dopamine system, which is a major contributor to reward function and addiction”
From Varenicline Is a Potent Partial Agonist at α6β2* Nicotinic Acetylcholine Receptors in Rat and Monkey Striatum (2012) · cites this paper as De Biasi and Dani, 2011
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Rated minor: it would not touch a result — a value no result rests on, a p-value that stays on the same side of the significance level, or a conflict that is clerical, resolved elsewhere in the paper, or outside its own findings.
In the paper
§ Reward, Addiction, Withdrawal to Nicotine > DISTINCT NICOTINIC RECEPTOR SUBTYPES MEDIATE WITHDRAWAL
“Because the nAChR subunits comprised in the CHRNA5-CHRNA3-CHRNB4 reduce the aversive effects of nicotine and drive its consumption”
§ Reward, Addiction, Withdrawal to Nicotine > DISTINCT NICOTINIC RECEPTOR SUBTYPES MEDIATE WITHDRAWAL
“people with SNP rs16969968 smoke more and become addicted at a younger age because they lack sufficient functional α5* nAChRs. The presence of fewer aversive effects (even at higher nicotine doses) during the initial contact with the drug would promote the hedonic drive”
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“…are directly related to its addictive properties, including reinforcing effects and withdrawal symptoms (reviewed in Dani and Bertrand, 2007; De Biasi and Dani, 2011). nAChR expressed in the mesocorticolimbic pathway, one of the main reinforcement circuits of the brain, where they modulate DA…”
BackgroundShao, X. M., Xu, B., Liang, J., Xie, X., Zhu, Y., & Feldman, J. L. (2012) · Nicotine & Tobacco Research · doi:10.1093/ntr/nts261 · Cited by 34
“…at 32%, 56%, or 68% in multiple trials. this rapid arterial peak/decline concentration pattern stimulates brain nicotinic acetylcholine receptors, activating the dopaminergic reward system that plays an important role in initiation of addiction (De Biasi & Dani, 2011; Henningfield & Keenan, 1993).”
BackgroundRoche, D. J. O., Ray, L. A., Yardley, M. M., & King, A. C. (2016) · Current Addiction Reports · doi:10.1007/s40429-016-0081-3 · Cited by 39
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“For example, using knockout (KO) mouse technology, previous reports have concluded that the α 2, α 3, α 5, α 7, and β 4 subunits modulate physical signs, whereas α 6 and β 2 modulate affective states produced by nicotine withdrawal (DeBiasi and Dani, 2011; Jackson et al., 2008; Salas et al., 2009).”
Mesolimbic Dopamine and Habenulo-Interpeduncular Pathways in Nicotine Withdrawal
Dani, J. A., & De Biasi, M. (2013) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a012138 · Cited by 34
Self-citationNeurobiological and Neurophysiological Mechanisms Underlying Nicotine Seeking and Smoking Relapse
Schmidt, H. D., Rupprecht, L. E., & Addy, N. (2018) · Complex Psychiatry · doi:10.1159/000494799 · Cited by 33
Crucial Role of Dopamine D2 Receptor Signaling in Nicotine-Induced Conditioned Place Preference
Wilar, G., Shinoda, Y., Sasaoka, T., & Fukunaga, K. (2019) · Molecular Neurobiology · doi:10.1007/s12035-019-1635-x · Cited by 34
Brain Region Specific Single-Molecule Fluorescence Imaging
Fu, X., Moonschi, F. H., Fox-Loe, A. M., Snell, A. A., Hopkins, D. M., Avelar, A. J., Henderson, B. J., Pauly, J. R., & Richards, C. I. (2019) · Analytical Chemistry · doi:10.1021/acs.analchem.9b02133 · Cited by 25
Ngolab, J., Liu, L., Zhao-Shea, R., Gao, G., Gardner, P. D., & Tapper, A. R. (2015) · Journal of Neuroscience · doi:10.1523/jneurosci.4453-14.2015 · Cited by 35
“…by activating neurons within the ventral tegmental area (VTA) of the mesocorticolimbic reward circuitry, ultimately driving the release of dopamine (DA) within the nucleus accumbens (NAc), a phenomenon widely associated with the rewarding or reinforcing value of nicotine (De Biasi and Dani, 2011).”
BackgroundJackson, A. B., Bağdaş, D., Muldoon, P. P., Lichtman, A. H., Carroll, F. I., Greenwald, M. K., Miles, M. F., & Damaj, M. I. (2017) · Neuropharmacology · doi:10.1016/j.neuropharm.2017.03.005 · Cited by 33
“Somatic signs have shown to contribute less to nicotine-seeking behavior than affective signs (De Biasi and Dani, 2011; Epping-Jordan et al., 1998); thus, the modest reduction of somatic signs by fenofibrate may not predict its efficacy as a smoking cessation aid.”
Prevalence and predictors of fatigue after aneurysmal subarachnoid hemorrhage
Western, E., Sorteberg, A. G., Brunborg, C., & Nordenmark, T. H. (2020) · Acta Neurochirurgica · doi:10.1007/s00701-020-04538-9 · Cited by 32
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Domi, E., Caputi, F. F., Romualdi, P., Domi, A., Scuppa, G., Candeletti, S., Atkins, A. L., Heilig, M. A., Demopulos, G. A., Gaitanaris, G., et al. (2019) · Journal of Neuroscience · doi:10.1523/jneurosci.1922-19.2019 · Cited by 32
“Our results demonstrate the implication of neuronal PPAR in nicotine withdrawal and suggest that PPAR agonism may represent a promising treatment to aid smoking cessation. neuronal circuits that control reward, motivation, and habit processes (De Biasi and Dani, 2011).”
BackgroundN-acetylcysteine decreased nicotine reward-like properties and withdrawal in mice
Bowers, M. S., Jackson, A. B., Maldoon, P. P., & Damaj, M. I. (2015) · Psychopharmacology · doi:10.1007/s00213-015-4179-4 · Cited by 31
“…withdrawal signs are mediated by both central and peripheral nicotinic receptors, while anhedonia and aversion are mediated solely through central nicotinic receptor populations such as the nucleus accumbens (NAc) and habenulo-interpeduncular system (Watkins et al. 2000; De Biasi and Dani 2011).”
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“Tobacco-related products are a major cause of preventable deaths [48].”
BackgroundThe modulatory role of nicotine on cognitive and non-cognitive functions
Zarrindast, M., & Khakpai, F. (2018) · Brain Research · doi:10.1016/j.brainres.2018.12.002 · Cited by 34
Transdermal Nicotine Treatment and Progression of Early Parkinson’s Disease
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“Heteromeric α4β2 nAChRs, the predominant high-affinity binding sites for nicotine in the central nervous system, are well known to mediate the reinforcing, rewarding and dependence-inducing properties of nicotine (De Biasi and Dani, 2011) and its anti-nociceptive actions (Hurst et al., 2013).”
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Altered amygdala function in nicotine addiction: Insights from human neuroimaging studies
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“Along with the progress of recent research, emerging evidence suggests that neuronal nAChRs in the mesocorticolimbic–dopamine system mediate both the rewarding effects of nicotine and the development of NA [1].”
BackgroundInfluentialPerez, X. A., Khroyan, T. V., McIntosh, J. M., & Quik, M. (2014) · Pharmacology Research & Perspectives · doi:10.1002/prp2.105 · Cited by 30
“Multiple studies have shown that a mechanism through which nicotine regulates neuronal function is via nAChR desensitization (Buisson and Bertrand 2002; Benowitz 2010; De Biasi and Dani 2011).”
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Cholinergic Receptors and Addiction
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Thomas D. Geracioti, Jr. (2013) · Pain Physician · doi:10.36076/ppj.2013/16/e25 · Cited by 25
BDNF and nicotine dependence: associations and potential mechanisms
Huang, Z., Wu, D., Qu, X., Li, M., Zou, J., & Tan, S. (2020) · Reviews in the Neurosciences · doi:10.1515/revneuro-2020-0044 · Cited by 25
“D1R and D2R activation stimulated phosphorylation of MEK and the upstream activity of ERK1/ 2 for influencing the phosphorylation of CREB (De Biasi and Dani 2011; Inoue et al. 2007), which is crucial for the reinforcing effect of nicotine (Wilar et al. 2019).”
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Fowler, C. D., & Kenny, P. J. (2011) · Human Genetics · doi:10.1007/s00439-011-1129-z · Cited by 30
Placzek, A. N., Molfese, D. L., Khatiwada, S., Prisco, G. V. D., Huang, W., Sidrauski, C., Krnjević, K., Amos, C. L., Ray, R. S., Dani, J. A., et al. (2016) · eLife · doi:10.7554/elife.12056 · Cited by 27
“Nicotine modifies dopamine (DA) signaling in key regions of the brain’s reward system (Jasinska et al., 2014; De Biasi and Dani, 2011).”
BackgroundSelf-citationAlcohol and nicotine interactions: pre-clinical models of dependence
Tarren, J. R., & Bartlett, S. E. (2016) · The American Journal of Drug and Alcohol Abuse · doi:10.1080/00952990.2016.1197232 · Cited by 26
Carboni, L., Romoli, B., Bate, S. T., Romualdi, P., & Zoli, M. (2018) · Drug and Alcohol Dependence · doi:10.1016/j.drugalcdep.2018.04.027 · Cited by 25
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Voxelwise meta-analysis of gray matter anomalies in chronic cigarette smokers
Zhong, J., Shi, H., Shen, Y., Dai, Z., Zhu, Y., Ma, H., & Sheng, L. (2016) · Behavioural Brain Research · doi:10.1016/j.bbr.2016.05.016 · Cited by 26
Bueno-Júnior, L. S., Simon, N. W., Wegener, M. A., & Moghaddam, B. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2017.15 · Cited by 24
“Extensive work continues to inform us about mechanisms underlying nicotine’s reinforcing properties (De Biasi and Dani, 2011; Markou, 2008), but less is known about mechanisms that subserve nicotine’s cognitive-enhancing effects.”
Mantey, D. S., Harrell, M. B., Case, K. R., Crook, B., Kelder, S. H., & Perry, C. L. (2017) · Drug and Alcohol Dependence · doi:10.1016/j.drugalcdep.2016.12.010 · Cited by 27
“Experimentation is a first step towards established use, partially due to nicotinestimulating regions of the brain associated with pleasure and reward (De Biasi and Dani, 2011), as well as other factors associated with long-term tobacco use, such as social reinforcement (Benowitz, 2010).”
BackgroundFlannery, J. S., Riedel, M. C., Poudel, R., Laird, A. R., Ross, T. J., Salmeron, B. J., Stein, E. A., & Sutherland, M. T. (2019) · Science Advances · doi:10.1126/sciadv.aax2084 · Cited by 26
“Nicotine stimulates midbrain DA neurons projecting primarily to striatal and prefrontal brain regions through agonist effects on nicotinic acetylcholine receptors (nAChRs) [5-7].”
Cole, R. D., Poole, R. L., Guzman, D. M., Gould, T. J., & Parikh, V. (2014) · Psychopharmacology · doi:10.1007/s00213-014-3754-4 · Cited by 25
“…sustained activation and desensitization states of multiple nAChRs, most likely α4β2 and α7 nAChRs, and functional coordination between nAChR subtypes may contribute to the behavioral effects of chronic nicotine (Besson et al. 2007; Picciotto et al. 2008; Changeux 2010; De Biasi and Dani 2011).”
Mikellides, G., Michael, P., Psalta, L., Stefani, A., Schuhmann, T., & Sack, A. T. (2022) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2022.892075 · Cited by 25
Petruzziello, F., Falasca, S., Andrén, P. E., Rainer, G., & Zhang, X. (2013) · Molecular & Cellular Proteomics · doi:10.1074/mcp.m112.024828 · Cited by 25
“Nicotine is the main psychoactive ingredient of tobacco (1).”
BackgroundFischell, S. A., Ross, T. J., Deng, Z., Salmeron, B. J., & Stein, E. A. (2020) · Biological Psychiatry Cognitive Neuroscience and Neuroimaging · doi:10.1016/j.bpsc.2019.12.020 · Cited by 26
“Withdrawalrelated reduced plasticity may be secondary to nicotinic acetylcholine receptor (nAChR) desensitization with chronic smoking (93–95), necessitating acute nicotine to restore synaptic calcium dynamics (96,97), although this is speculative as the current data cannot Aronson Fischell et al.”
BackgroundMorud, J., Strandberg, J., Andrén, A., Ericson, M., Söderpalm, B., & Adermark, L. (2017) · Neuropharmacology · doi:10.1016/j.neuropharm.2017.10.002 · Cited by 24
“This is an open access article u subregions, e.g. in the nucleus accumbens (nAc) (De Biasi and Dani, 2011; Pontieri et al., 1996; Schilstrom et al., 2000; Zhou et al., 2001).”
BackgroundNicotine Inhibits Memory CTL Programming
Sun, Z., Smyth, K., Garcia, K. Y., Mattson, E., Li, L., & Xiao, Z. (2013) · PLoS ONE · doi:10.1371/journal.pone.0068183 · Cited by 22
“Nicotine shares nicotinic acetylcholine receptors (nAChRs) with the neurotransmitter acetylcholine [1,3,28,29].”
BackgroundNicotine Receptor Subtype-Specific Effects on Auditory Evoked Oscillations and Potentials
Featherstone, R. E., Phillips, J. M., Thieu, T., Ehrlichman, R. S., Halene, T. B., Leiser, S. C., Christian, E. P., Johnson, E., Lerman, C. E., & Siegel, S. J. (2012) · PLoS ONE · doi:10.1371/journal.pone.0039775 · Cited by 21
“rewarding and addicting effects of nicotine [45] and is expressed in brain regions that are likely important for the P50 response, such as the medial habenula.”
BackgroundLeach, P. T., Cordero, K. A., & Gould, T. J. (2013) · Behavioral Neuroscience · doi:10.1037/a0031913 · Cited by 23
Thompson, M. F., Poirier, G. L., Dávila‐García, M. I., Huang, W., Tam, K., Robidoux, M., Dubuke, M. L., Shaffer, S. A., Colón-Pérez, L. M., Febo, M., et al. (2017) · Journal of Psychopharmacology · doi:10.1177/0269881117719265 · Cited by 23
“Nicotine increases the firing rate of dopamine neurons in the striatum, as well as nucleus accumbens (Bahk et al., 2002; De Biasi and Dani, 2011; Rasmussen and Czachura, 1995).”
BackgroundRecent findings in the pharmacology of inhaled nicotine: Preclinical and clinical in vivo studies
Jackson, A. B., Grobman, B., & Krishnan‐Sarin, S. (2020) · Neuropharmacology · doi:10.1016/j.neuropharm.2020.108218 · Cited by 21
Vicario, C. M., Komeilipoor, N., Cesari, P., Rafal, R. D., & Nitsche, M. A. (2014) · Journal of Psychiatry and Neuroscience · doi:10.1503/jpn.130086 · Cited by 24
“For example, placebo is able to affect reward system regions, such as the cingulate cortex, the insula and the ventral striatum,(35) which are also activated by nicotine consumption.(15) The tongue MEP normalization following placebo makes it improbable that this pattern is caused by nicotine.”
Naha, N., Gandhi, D., Ak, G., & Prakash, J. R. (2017) · Human & Experimental Toxicology · doi:10.1177/0960327117698543 · Cited by 22
Sun, K., Xiao, L., Wu, Y., Zuo, D., Zhang, C., Liu, S., He, Z., Rong, S., Wang, F., & Sun, T. (2020) · Life Sciences · doi:10.1016/j.lfs.2020.117655 · Cited by 21
Fennell, A. M., Pitts, E. G., Sexton, L. L., & Ferris, M. J. (2020) · Scientific Reports · doi:10.1038/s41598-019-56884-z · Cited by 24
Zhu, M., Sanchez, M. E., Douglass, E. A., Jahad, J. V., Hanback, T., Lee, T. N. G., Esther, C. R., Cole, M., Roberts, A. J., & Herman, M. A. (2021) · eNeuro · doi:10.1523/eneuro.0189-21.2021 · Cited by 19
“…of repeated electronic nicotine vapor exposure on CeA neuron activity Previous research has shown that repeated exposure to nicotine can cause differential changes in synaptic transmission and/or neuronal activity in a number of brain regions (De Biasi and Dani, 2011; Picciotto and Mineur, 2014).”
BackgroundBitter taste and nicotine preference: evidence for sex differences in rats
Nesil, T., Kanıt, L., & Pöğün, Ş. (2014) · The American Journal of Drug and Alcohol Abuse · doi:10.3109/00952990.2014.990091 · Cited by 19
“nicotine addiction because especially younger people with these SNPs do not experience the aversive effects of nicotine when they initiate smoking (62).”
BackgroundGovind, A. P., Vallejo, Y. F., Stolz, J. R., Yan, J.-Z., Swanson, G. T., & Green, W. N. (2017) · eLife · doi:10.7554/elife.25651 · Cited by 17
“Nicotine upregulation of nAChRs is linked to different processes in nicotine addiction, including sensitization (Govind et al., 2009; Vezina et al., 2007) and withdrawal (De Biasi et al., 2011) and is the only effect of nicotine on nAChRs that lasts longer than a few minutes.”
BackgroundChemosensory Contributions of E-Cigarette Additives on Nicotine Use
Johnson, N. L., Patten, T., Ma, M., Biasi, M. D., & Wesson, D. W. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.893587 · Cited by 19
Self-citationSmoking increases the risk of delirium for older inpatients: a prospective population-based study
Hessler, J. B., Brönner, M., Etgen, T., Gotzler, O., Förstl, H., Poppert, H., Sander, D., & Bickel, H. (2015) · General Hospital Psychiatry · doi:10.1016/j.genhosppsych.2015.03.009 · Cited by 19
“Nicotine is thought to exert its neuroregulatory effects mainly by binding to nicotinic acetylcholine receptors (nAChR), which, in turn, affect other neurotransmitters such as dopamine, glutamate, γ-aminobutyric acid, serotonin and opioid peptides throughout the brain [33–36].”
Backgroundde la Peña, J. B., Ahsan, H. M., Botanas, C. J., dela Peña, I. J., Woo, T., Kim, H. J., & Cheong, J. H. (2016) · International Journal of Developmental Neuroscience · doi:10.1016/j.ijdevneu.2016.09.007 · Cited by 19
“…estlessness, or irritability (Faraday et al., 2001; Varvel et al., 2007). estlessness and irritability are common affective properties of moking withdrawal (De Biasi and Dani, 2011; Hughes, 1992). ike anxiety, these affective symptoms can promote drug-seeking ehavior and may lead to relapse.”
BackgroundResultMolecular, Neuronal, and Behavioral Effects of Ethanol and Nicotine Interactions
Klenowski, P. M., & Tapper, A. R. (2018) · Handbook of experimental pharmacology · doi:10.1007/164_2017_89 · Cited by 15
Self-Administration of Cotinine in Wistar Rats: Comparisons to Nicotine
Ding, Z., Gao, Y., Sentir, A. M., & Tan, X. (2020) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.120.000367 · Cited by 16
“It activates nicotinic acetylcholine receptors (nAChRs) to produce its effects (De Biasi and Dani, 2011).”
BackgroundAdolescent alcohol exposure decreased sensitivity to nicotine in adult Wistar rats
Boutros, N., Semenova, S., & Markou, A. (2015) · Addiction Biology · doi:10.1111/adb.12263 · Cited by 18
“The reinforcing, motivational and discriminative effects of nicotine are mediated by nicotinic acetylcholine receptors (nAChRs) that contain the α4β2 subunit (Stolerman et al. 1997; Zaniewska et al. 2006; Smith et al. 2007; De Biasi & Dani 2011).”
BackgroundExpression of cloned α6* nicotinic acetylcholine receptors
Wang, J., Kuryatov, A., & Lindstrom, J. M. (2014) · Neuropharmacology · doi:10.1016/j.neuropharm.2014.10.009 · Cited by 21
Passlick, S., Thapaliya, E. R., Chen, Z., Richers, M. T., & Ellis‐Davies, G. C. R. (2018) · The Journal of Physiology · doi:10.1113/jp276615 · Cited by 18
UBXN2A regulates nicotinic receptor degradation by modulating the E3 ligase activity of CHIP
Teng, Y., Rezvani, K. S., & Biasi, M. D. (2015) · Biochemical Pharmacology · doi:10.1016/j.bcp.2015.08.084 · Cited by 18
“Neuronal nAChRs are homo- or hetero-pentameric ligand-gated ion channels composed of α and β or α only-subunits [3].”
BackgroundSelf-citationGao, Y., Peng, S., Wen, Q., Zheng, C., Lin, J., Tan, Y., Ma, Y., Luo, Y., Xue, Y.-X., Wu, P., et al. (2014) · International Journal of Neuropsychopharmacology · doi:10.1017/s1461145714000650 · Cited by 18
“…abundant evidence indicates that nicotinic acetylcholine receptors (nAChR) are densely distributed in the mesocorticolimbic dopamine system (De Biasi and Dani, 2011) and functional nAChRs expressed on pyramidal cells (somatodendritic α7), GABAergic interneurons (α7, α4β2, and α3β4), and…”
BackgroundMutschler, J., Abbruzzese, E., von der Goltz, C., Dinter, C., Mobascher, A., Thiele, H., Diaz-Lacava, A., Dahmen, N., Gallinat, J., Majic, T., et al. (2012) · European Addiction Research · doi:10.1159/000338276 · Cited by 17
Gözen, O., Nesil, T., Kanıt, L., Koylu, E. O., & Pöğün, Ş. (2016) · The American Journal of Drug and Alcohol Abuse · doi:10.1080/00952990.2016.1198799 · Cited by 17
“De Biasi and Dani (60) propose that people with SNPs that reduce the function of the α5 sub-”
BackgroundInfluentialRepeated nicotine vapor inhalation induces behavioral sensitization in male and female C57BL/6 mice
Honeycutt, S. C., Garrett, P. I., Barraza, A. G., Maloy, A. N., & Hillhouse, T. M. (2020) · Behavioural Pharmacology · doi:10.1097/fbp.0000000000000562 · Cited by 16
Sobriety and Satiety: Is NAD+ the Answer?
Braidy, N., Villalva, M. D., & van Eeden, S. (2020) · Antioxidants · doi:10.3390/antiox9050425 · Cited by 17
Mathuru, A. S. (2017) · Seminars in Cell and Developmental Biology · doi:10.1016/j.semcdb.2017.09.030 · Cited by 19
Waeiss, R. A., Knight, C. P., Carvajal, G. B., Bell, R. L., Engleman, E. A., McBride, W. J., Hauser, S. R., & Rodd, Z. A. (2019) · Behavioural Brain Research · doi:10.1016/j.bbr.2019.112190 · Cited by 16
Keeley, R. J., Hsu, L., Brynildsen, J. K., Lu, H., Yang, Y., & Stein, E. A. (2020) · Neuropsychopharmacology · doi:10.1038/s41386-020-0635-x · Cited by 17
Wang, J., Kuryatov, A., Jin, Z., Norleans, J., Kamenecka, T. M., Kenny, P. J., & Lindstrom, J. M. (2015) · Journal of Biological Chemistry · doi:10.1074/jbc.m115.676551 · Cited by 15
Varani, A. P., Moutinho, L. M., & Balerio, G. N. (2014) · Synapse · doi:10.1002/syn.21763 · Cited by 16
Wageman, C. R., Marks, M. J., & Grady, S. R. (2013) · Nicotine & Tobacco Research · doi:10.1093/ntr/ntt146 · Cited by 16
“These receptors are desensitized by chronic exposure to nicotine (Barik & Wonnacott, 2009; De Biasi & Dani, 2011).”
BackgroundNicotine‐induced molecular alterations are modulated by GABAB receptor activity
Varani, A. P., Pedrón, V. T., Aon, A. J., Höcht, C., Acosta, G. B., Bettler, B., & Balerio, G. N. (2017) · Addiction Biology · doi:10.1111/adb.12506 · Cited by 16
“NIC stimulates nAChRs located on dopaminergic, glutamatergic and GABAergic neurons of the VTA, causing the release of DA in the Acb that is responsible for the NIC-induced rewarding properties (Paterson 2009; De Biasi & Dani 2011; Polosa & Benowitz 2011).”
BackgroundSimmons, S. J., & Gould, T. J. (2014) · Journal of Clinical Pharmacy and Therapeutics · doi:10.1111/jcpt.12171 · Cited by 18
Neuroanatomical circuitry mediating the sensory impact of nicotine in the central nervous system
Dehkordi, O., Rose, J. E., Asadi, S., Manaye, K. F., Millis, R. M., & Jayam‐Trouth, A. (2014) · Journal of Neuroscience Research · doi:10.1002/jnr.23477 · Cited by 17
“…the CNS and on the mesocorticolimbic pathways, which include dopaminergic neurons of the ventral tegmental area (VTA) and its projections to the nucleus accumbens (Acb) and the medial prefrontal cortex (MPFC; Schultz et al., 1997; Wise, 2009; Schultz, 2010; Ikemoto, 2010; De Biasi and Dani, 2011).”
BackgroundJiang, J. W., Li, X., Hu, A., Zhou, G., Gao, Y.-H., Xu, C., Wu, X., & Wang, H. (2025) · Frontiers in Neuroscience · doi:10.3389/fnins.2025.1670883 · Cited by 24
“This process is completely abolished in β 2 subunit knockout mice, confirming its role as the molecular basis of rewarding eects (Maskos et al., 2005; Picciotto et al., 1998; Tolu et al., 2013; Dani and Bertrand, 2007; De Biasi and Dani, 2011; Mao et al., 2011; Pidoplichko et al., 1997).”
Carboni, L., Ponzoni, L., Braida, D., Sala, M., Gotti, C., & Zoli, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22020599 · Cited by 15
“A first step in this process is the observed up-regulation of nicotinic receptors, which modulates the activity of a plethora of other neurotransmitters and neuromodulators, thus influencing the mesocorticolimbic pathway as well as a widespread network of other circuits [5,7,8].”
BackgroundInfluentialZhu, X.-P., Wang, S., Kaas, Q., Yu, J.-P., Wu, Y., Harvey, P., Zhangsun, D.-T., Craik, D., & Luo, S.-L. (2023) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.2c01786 · Cited by 14
Gao, R., Schneider, A. M., Mulloy, S., & Lee, A. M. (2023) · European Journal of Neuroscience · doi:10.1111/ejn.16109 · Cited by 12
“…expressed in the brain and are involved in drug reward responses, attention, memory, affective behaviours, pain processing and inflammation (De Biasi & Dani, 2011; Galvin et al., 2020; Hurst et al., 2013; Picciotto et al., 2008). nAChRs are penta-meric ligand-gated cation channels that are…”
Tobacco habits in nocturnal frontal lobe epilepsy
Naldi, I., Bisulli, F., Vignatelli, L., Licchetta, L., Pittau, F., Vito, L. D., Mostacci, B., Menghi, V., Provini, F., Montagna, P., et al. (2012) · Epilepsy & Behavior · doi:10.1016/j.yebeh.2012.10.014 · Cited by 14
“This substance initiates addiction by directly involving the neural circuitry that normally reinforces reward-seeking behaviors [22].”
Translational Research on Nicotine Dependence
Falcone, M., Lee, B., Lerman, C. E., & Blendy, J. A. (2015) · Current topics in behavioral neurosciences · doi:10.1007/7854_2015_5005 · Cited by 15
Dong, Y., Dani, J. A., & Blakely, R. (2013) · Biochemical Pharmacology · doi:10.1016/j.bcp.2013.07.019 · Cited by 14
“With respect to addiction, central ACh receptors contribute to both the alerting and reinforcing effects of nicotine, the latter action funneling into the mesoaccumbal dopamine (DA) system to mimic, and when abused, commandeer DA signaling that is engaged normally recognize the novelty and saliency of stimuli [14,15].”
BackgroundSelf-citationActivation of trace amine‐associated receptor 1 attenuates nicotine withdrawal‐related effects
Wu, R., Liu, J., Johnson, B., Huang, Y., Zhang, Y., & Li, J. (2021) · Addiction Biology · doi:10.1111/adb.13075 · Cited by 14
Jeon, D.-W., Shim, J.-C., Kong, B.-G., Moon, J., Seo, Y.-S., Kim, S.-J., Oh, M., & Jung, D.-U. (2016) · Schizophrenia Research · doi:10.1016/j.schres.2016.08.016 · Cited by 14
“In the midbrain, nAChRs comprising the β2 nAChR subunit in combination with α4 and/or α6 subunits are essential for nicotine-induced reinforcement and the DA signal (De Biasi and Dani, 2011).”
BackgroundLuo, J., Bian, L.-H., Yao, Z., Wang, X., Li, Q., Guo, J., & Shi, J. (2021) · Neuroscience Letters · doi:10.1016/j.neulet.2021.136152 · Cited by 15
Filchakova, O., & McIntosh, J. M. (2013) · PLoS ONE · doi:10.1371/journal.pone.0064655 · Cited by 15
“addiction [10], [11] and schizophrenia [12], [13].”
Ondachi, P. W., Castro, A. H., Bartkowiak, J., Luetje, C. W., Damaj, M. I., Mascarella, S. W., Navarro, H. A., & Carroll, F. I. (2014) · Journal of Medicinal Chemistry · doi:10.1021/jm401602p · Cited by 14
Secondary Ammonium Agonists Make Dual Cation-π Interactions in α4β2 Nicotinic Receptors
Post, M. R., Tender, G. S., Lester, H. A., & Dougherty, D. A. (2017) · eNeuro · doi:10.1523/eneuro.0032-17.2017 · Cited by 14
“For example, the 4 2-containing subtypes are expressed throughout the brain and are most associated with several aspects of nicotine addiction (De Biasi and Dani, 2011).”
BackgroundMirtazapine attenuates nicotine-seeking behavior in rats
Barbosa-Méndez, S., & Salazar‐Juárez, A. (2018) · Journal of Psychopharmacology · doi:10.1177/0269881118764991 · Cited by 14
Matera, C., Pucci, L., Fiorentini, C., Fucile, S., Missale, C., Grazioso, G., Clementi, F., Zoli, M., Amici, M. D., Gotti, C., et al. (2015) · European Journal of Medicinal Chemistry · doi:10.1016/j.ejmech.2015.06.039 · Cited by 13
Neuroscience of nicotine for addiction medicine
D’Souza, M. S. (2015) · Progress in brain research · doi:10.1016/bs.pbr.2015.07.008 · Cited by 13
Fernandes, T. P., Butler, P. D., Rodrigues, S. J., Silva, G. M., Anchieta, M. V., Souto, J. J. S., Gomes, G. H., de Almeida, N. L. P., & dos Santos, N. A. (2020) · Journal of Addictive Diseases · doi:10.1080/10550887.2020.1805093 · Cited by 13
Metadata
- Authors
- De Biasi, M., & Dani, J. A.
- Affiliations
- Baylor College of Medicine (US)
- ORCID
- Dani, John A.
- Venue
- Annual Review of Neuroscience
- Publisher
- Annual Reviews
- Published
- 2011-07-21
- Volume
- 34
- Issue
- 1
- Pages
- 105-130
- ISSN
- 0147-006X (ISSN-L)
- 1545-4126
- PMC
- PMC3137256
- OpenAlex
- W2165425515
- Semantic Scholar
- c6462f78d05c8073c59243cb5544623aa43f3c33
- Cited by
- 366
- References
- 305
- Citations by year
- 2026: 12 · 2025: 17 · 2024: 20 · 2023: 13 · 2022: 13 · 2021: 14 · 2020: 32 · 2019: 23 · 2018: 22 · 2017: 36 · 2016: 28 · 2015: 29 · 2014: 42 · 2013: 27 · 2012: 33
- FWCI
- 3.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annual Review of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Cancer Research Institute
- Cancer Prevention and Research Institute of Texas
- National Institutes of Health
- National Institute on Drug Abuse (R21DA029157, DA09411, DA017173, R01DA017173, R01DA009411, DA029157)
- National Cancer Institute (U19CA148127)
- National Institute of Neurological Disorders and Stroke (NS 21229, R37NS021229, R01NS021229)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Smoking Behavior and Cessation
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- nicotine, nicotine dependence, nicotine withdrawal, reward, mesocorticolimbic dopamine system, nicotinic acetylcholine receptors, nicotinic receptor subunits, dopaminergic neurons, neural adaptation, habenula, tobacco use
- MeSH terms
- Animals, Cerebral Cortex, Dopamine, Humans, Limbic System, Neuronal Plasticity, Neurons, Nicotine, Receptors, Nicotinic, Reward, Substance Withdrawal Syndrome, Behavior, Addictive
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