Reward, Addiction, Withdrawal to Nicotine

In the paper

“The epithalamic habenular complex and its targets appear to be critical for the withdrawal syndrome.”

What the sources say

• Not checked yetcites Salas et al. 2004b
• Not checked yetcites Salas et al. 2009

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).”

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

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).”

What the sources say

• Not checked yetcites Hodos 1961
• Not checked yetcites Schultz 2006

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.”

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).”

What the sources say

• Not checked yetcites Schultz et al. 1997
• Not checked yetcites Wise 2004
• Not checked yetcites Wise & Rompre 1989

In the paper

“as exemplified by lesions in the PPT reducing nicotine self-administration (Lanca et al. 2000).”

What the sources say

• Not checked yetcites Lanca et al. 2000

In the paper

“In addition, the PPT/LDT cholinergic afferents have important endogenous influences over DA neurons by acting via nAChRs (Maskos 2008, 2010).”

What the sources say

• Not checked yetcites Maskos 2008 source
• Not checked yetcites Maskos 2010

In the paper

“nicotine is the main addictive component (Benowitz 2009, Dani et al. 2009, Dani & Heinemann 1996, Mansvelder & McGehee 2002).”

What the sources say

• Not checked yetcites Benowitz 2009
• Not checked yetcites Dani et al. 2009
• Not checked yetcites Dani & Heinemann 1996

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).”

What the sources say

• Not checked yetcites Hodos 1961
• Not checked yetcites Lau et al. 2006
• Not checked yetcites McClure et al. 2007

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).”

What the sources say

• Not checked yetcites Balfour 2004
• Not checked yetcites Corrigall 1999
• Not checked yetcites Dani et al. 2009

In the paper

“Recent research shows that nicotine-induced reward, addiction, and withdrawal involve a wide range of nAChR subtypes expressed in diverse neural systems.”

In the paper

“This influence of the PPT/LDT arises, at least in part, because these areas contribute to the phasic burst firing of DA neurons (Floresco et al. 2003, Lodge & Grace 2006).”

What the sources say

• Not checked yetcites Floresco et al. 2003
• Not checked yetcites Lodge & Grace 2006

In the paper

“Nicotine initiates addiction by impinging directly on neural circuitry that normally reinforces behaviors that lead to rewarding goals.”

What the sources say

• Not checked yetcites Balfour 2004
• Not checked yetcites Corrigall 1999
• Not checked yetcites Dani et al. 2009

In the paper

“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 (Drenan et al. 2010, Mameli-Engvall et al. 2006, Picciotto et al. 1998, Pons et al. 2008, Tapper et al. 2004).”

What the sources say

• Not checked yetcites Drenan et al. 2010
• Not checked yetcites Mameli-Engvall et al. 2006
• Not checked yetcites Picciotto et al. 1998

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).”

What the sources say

• Not checked yetcites Pons et al. 2008

In the paper

“For instance, the α7 nAChRs seem to fine-tune nicotine-induced DA neuron firing only after β2* nAChRs have been activated (Mameli-Engvall et al. 2006).”

What the sources say

• Not checked yetcites Mameli-Engvall et al. 2006

In the paper

“While increasing the firing of DA neurons, nicotine potently increases the number and length of phasic bursts that mediate the processing of reward (Figure 1) (Grenhoff et al. 1986, Mameli-Engvall et al. 2006, Zhang et al. 2009b).”

What the sources say

• Not checked yetcites Grenhoff et al. 1986
• Not checked yetcites Mameli-Engvall et al. 2006
• Not checked yetcites Zhang et al. 2009b

In the paper

“The phasic burst firing induced by nicotine causes greater extracellular DA release compared with tonic, single-spike firing (Floresco et al. 2003, Gonon 1988, Grace 1991, Zhang et al. 2009b).”

What the sources say

• Not checked yetcites Floresco et al. 2003
• Not checked yetcites Gonon 1988
• Not checked yetcites Grace 1991

In the paper

“This increase in basal or background DA measured by microdialysis in the NAc shell is considered indicative of a drug’s addictive influence.”

In the paper

“However, nicotinic and other local striatal mechanisms regulate the frequency dependence of DA release (Cragg 2003, Rice & Cragg 2004, Zhang et al. 2009a, Zhang & Sulzer 2004, Zhou et al. 2001).”

What the sources say

• Not checked yetcites Cragg 2003
• Not checked yetcites Rice & Cragg 2004
• Not checked yetcites Zhang et al. 2009a

In the paper

“Aside from effects on the peripheral nervous system, this dose-response relationship arises from nicotine acting on a heterogeneous population of nAChR subtypes in different neuronal circuits that mediate rewarding and aversive effects.”

In the paper

“Despite these potent effects of nicotine in the striatum, it is the nAChRs and nicotinic mechanisms within and impinging on the midbrain DA centers that are required for the addictive drive of nicotine (Mameli-Engvall et al. 2006, Maskos et al. 2005, Pons et al. 2008).”

What the sources say

• Not checked yetcites Mameli-Engvall et al. 2006
• Not checked yetcites Maskos et al. 2005
• Not checked yetcites Pons et al. 2008

In the paper

“Presynaptic or axonal nAChRs enhance DA release evoked at low firing frequencies (Zhou et al. 2001).”

What the sources say

• Not checked yetcites Zhou et al. 2001

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.”

What the sources say

• Not checked yetcites Schultz 2007a
• Not checked yetcites Schultz 2007b

In the paper

“Nicotine in both humans and animals follows an inverted U-shaped dose-response curve, with aversive effects coming into play at higher nicotine concentrations (Ashton et al. 1980, Fattore et al. 2002, Herskovic et al. 1986, Paterson et al. 2003).”

What the sources say

• Not checked yetcites Ashton et al. 1980
• Not checked yetcites Fattore et al. 2002
• Not checked yetcites Herskovic et al. 1986

In the paper

“The dense striatal acetylcholine esterase rapidly hydrolyzes the released ACh, preventing the appearance of long-lasting ACh signals that would strongly desensitize the high-affinity subtypes of nAChRs (Dani et al. 2000, Grady et al. 1994, Wooltorton et al. 2003).”

What the sources say

• Not checked yetcites Dani et al. 2000
• Not checked yetcites Grady et al. 1994
• Not checked yetcites Wooltorton et al. 2003

In the paper

“With identical DA neuron bursting, nicotine increases the average DA release more in the NAc shell than in the dorsal striatum (Figure 3c).”

What the sources say

• Not checked yetcites Zhang et al. 2009b

In the paper

“The background firing rate of striatal cholinergic neurons is ~6 Hz, providing ongoing acetylcholine (ACh) release via direct synaptic transmission and volume transmission (Dani & Bertrand 2007, de Rover et al. 2002, Koos & Tepper 2002, Wilson 2004).”

What the sources say

• Not checked yetcites Dani & Bertrand 2007
• Not checked yetcites de Rover et al. 2002
• Not checked yetcites Koos & Tepper 2002

In the paper

“Synaptic plasticity within the midbrain and onto DA neurons is an important early step in the nicotine addiction process (Dani et al. 2001, Mansvelder et al. 2002, Mansvelder & McGehee 2000, Pidoplichko et al. 2004).”

What the sources say

• Not checked yetcites Dani et al. 2001
• Not checked yetcites Mansvelder et al. 2002
• Not checked yetcites Mansvelder & McGehee 2000

In the paper

“These results arise, in part, because the probability of DA release to a single-action potential is greater in the dorsal striatum than the NAc shell (Zhang et al. 2009a,b; Zhang & Sulzer 2004).”

What the sources say

• Not checked yetcites Zhang et al. 2009a
• Not checked yetcites Zhang et al. 2009b
• Not checked yetcites Zhang & Sulzer 2004

In the paper

“The frequency dependence and nicotinic modulation of DA release differ in the dorsolateral striatum and NAc shell (Chergui et al. 1994; Cragg 2003; Cragg et al. 2002; Zhang et al. 2009a,b).”

What the sources say

• Not checked yetcites Chergui et al. 1994
• Not checked yetcites Cragg 2003
• Not checked yetcites Cragg et al. 2002

In the paper

“Direct measures of DA release using fast-scan cyclic voltammetry indicate that the transfer function relating DA neuron activity and DA release differs in those (and likely other) locations (Figure 2) (Cragg 2003, Rice & Cragg 2004, Zhang et al. 2009a, Zhang & Sulzer 2004, Zhou et al. 2001).”

What the sources say

• Not checked yetcites Cragg 2003
• Not checked yetcites Rice & Cragg 2004
• Not checked yetcites Zhang et al. 2009a

In the paper

“Although investigators originally postulated that the DA released from the VTA mediates only the hedonic or pleasurable effects of natural reinforcers and drugs in the NAc, evidence indicates that DA can signal events of opposite hedonic valence based on novelty or salience.”

What the sources say

• Not checked yetcites Schultz 2007a
• Not checked yetcites Schultz 2007b
• Not checked yetcites Brischoux et al. 2009

In the paper

“Smokers titrate their nicotine intake to experience the rewarding while avoiding the aversive actions (Benowitz 2001, Benowitz & Jacob 1985, Dani et al. 2009, Hutchison & Riley 2008, Kassel et al. 2007, Simpson & Riley 2005, Wise et al. 1976).”

What the sources say

• Not checked yetcites Benowitz 2001
• Not checked yetcites Benowitz & Jacob 1985
• Not checked yetcites Dani et al. 2009

In the paper

“Because physiological doses of nicotine commonly stimulate DA neurons (Grenhoff et al. 1986, Mameli-Engvall et al. 2006, Pidoplichko et al. 1997, Zhang et al. 2009b), nicotine-induced RMTg activity may contribute to the inverted U-shaped dose-response curve.”

What the sources say

• Not checked yetcites Grenhoff et al. 1986
• Not checked yetcites Mameli-Engvall et al. 2006
• Not checked yetcites Pidoplichko et al. 1997

In the paper

“Nicotine-induced synaptic plasticity increases the α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid/N-methyl-D-aspartate current ratio of glutamate receptors (GluRs) at locations mediating drug-associated memory (Dani et al. 2001, Kauer & Malenka 2007, Tang & Dani 2009), including at DA neurons (Gao et al. 2010, Placzek et al. 2009, Saal et al. 2003).”

What the sources say

• Not checked yetcites Dani et al. 2001
• Not checked yetcites Kauer & Malenka 2007
• Not checked yetcites Tang & Dani 2009

In the paper

“Nicotine increases the RMTg neuron activity (Lecca et al. 2010).”

What the sources say

• Not checked yetcites Lecca et al. 2010

In the paper

“An aversive sensory input administered to monkeys elicits LHb activity that indirectly inhibits DA neurons (Hikosaka et al. 2008; Ikemoto 2010; Matsumoto & Hikosaka 2007, 2009).”

What the sources say

• Not checked yetcites Hikosaka et al. 2008
• Not checked yetcites Ikemoto 2010
• Not checked yetcites Matsumoto & Hikosaka 2007

In the paper

“A human decision-making error that causes a negative sensory feedback or the absence of an expected sensory reward produces strong activity within the habenular complex (Salas et al. 2010, Shepard et al. 2006, Ullsperger & von Cramon 2003).”

What the sources say

• Not checked yetcites Salas et al. 2010
• Not checked yetcites Shepard et al. 2006
• Not checked yetcites Ullsperger & von Cramon 2003

In the paper

“Aversive, negative sensory input is processed by the habenular complex, an epithalamic structure involved in fear, anxiety, depression, and stress (Geisler et al. 2008, Ikemoto 2010, Winter et al. 2010).”

What the sources say

• Not checked yetcites Geisler et al. 2008
• Not checked yetcites Ikemoto 2010
• Not checked yetcites Winter et al. 2010

In the paper

“Furthermore, a transient inhibition of some DA neurons can be detected before the longer-lasting, nicotine-induced excitation (Erhardt et al. 2002).”

What the sources say

• Not checked yetcites Erhardt et al. 2002

In the paper

“The addiction process produces cellular adaptations that influence widely distributed neural circuits, particularly including the mesocorticolimbic system (Koob & Le Moal 2001).”

What the sources say

• Not checked yetcites Koob & Le Moal 2001

In the paper

“Furthermore, electrical stimulation of the LHb inhibits most DA neurons (Christoph et al. 1986, Ji & Shepard 2007, Matsumoto & Hikosaka 2007).”

What the sources say

• Not checked yetcites Christoph et al. 1986
• Not checked yetcites Ji & Shepard 2007
• Not checked yetcites Matsumoto & Hikosaka 2007

In the paper

“Although projections have been identified from the MHb to the LHb (Kim & Chang 2005), the MHb sends most of its projections to the IPN (Klemm 2004).”

What the sources say

• Not checked yetcites Klemm 2004

In the paper

“Recent studies suggest that the LHb, rather than projecting directly to the VTA, exerts its effects through the stimulation of neurons in the newly characterized rostromedial tegmental nucleus (RMTg), a region at the tail of the VTA (Perrotti et al. 2005).”

What the sources say

• Not checked yetcites Perrotti et al. 2005

In the paper

“In contrast, habenular lesions increase DA turnover in the NAc and PFC, reflecting an activation of the dopaminergic system (Lisoprawski et al. 1980, Nishikawa et al. 1986).”

What the sources say

• Not checked yetcites Lisoprawski et al. 1980
• Not checked yetcites Nishikawa et al. 1986

In the paper

“Acting via distinct anatomical distributions and cellular locations of nAChR subtypes, nicotine produces neuroadaptations through its influence over intracellular pathways (Wonnacott et al. 2005).”

What the sources say

• Not checked yetcites Wonnacott et al. 2005

In the paper

“One of the most direct and important neuroadaptations induced by chronic nicotine use is the subtype-specific upregulation of nAChRs (Buisson & Bertrand 2001; Changeux et al. 1984; Dani & Heinemann 1996; Flores et al. 1997; Mansvelder et al. 2002; Marks et al. 1983, 1992; Perry et al. 1999; Rezvani et al. 2007, 2009; Rowell & Wonnacott 1990; Schwartz & Kellar 1983).”

What the sources say

• Not checked yetcites Buisson & Bertrand 2001
• Not checked yetcites Changeux et al. 1984
• Not checked yetcites Dani & Heinemann 1996

In the paper

“Therefore, the MHb, at least, influences monoaminergic transmission via its connections to the IPN.”

In the paper

“The firing patterns of glutamatergic LHb neurons negatively correlate with the firing patterns of DA neurons.”

What the sources say

• Not checked yetcites Hikosaka et al. 2008
• Not checked yetcites Matsumoto & Hikosaka 2007

In the paper

“Drug taking is then maintained through negative reinforcement mechanisms.”

In the paper

“Withdrawal is also associated with dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and the stress-response system (Koob 2008).”

What the sources say

• Not checked yetcites Koob 2008

In the paper

“The endogenous opioid system, dynorphin in particular, engages (Hadjiconstantinou & Neff 2010).”

What the sources say

• Not checked yetcites Hadjiconstantinou & Neff 2010

In the paper

“Nicotine withdrawal is a collection of somatic and affective symptoms that is observed within a few hours after discontinuation of nicotine intake (De Biasi & Salas 2008).”

What the sources say

• Not checked yetcites De Biasi & Salas 2008

In the paper

“Chronic nicotine exposure also has indirect effects on motivational systems by altering synthesis and release of opioid peptides in a time-dependent and peptide-specific fashion (Berrendero et al. 2010).”

What the sources say

• Not checked yetcites Berrendero et al. 2010

In the paper

“The negative emotional state produced by the combination of withdrawal symptoms causes enough distress to become a deterrent to abstinence and a drive to relapse (Bruijnzeel & Gold 2005, Koob & Le Moal 2005, West et al. 1989).”

What the sources say

• Not checked yetcites Bruijnzeel & Gold 2005
• Not checked yetcites Koob & Le Moal 2005
• Not checked yetcites West et al. 1989

In the paper

“More generally, nAChRs affect the release of virtually every major neurotransmitter (Alkondon et al. 1997, Dani & Bertrand 2007, Hadjiconstantinou & Neff 2010, Kenny 2010, McGehee et al. 1995, Gray et al. 1996, Role & Berg 1996).”

What the sources say

• Not checked yetcites Alkondon et al. 1997 source
• Not checked yetcites Dani & Bertrand 2007
• Not checked yetcites Hadjiconstantinou & Neff 2010

In the paper

“During nicotine withdrawal, corticotropin-releasing factor receptor CRF1 influences anxiety and brain reward functions (Bruijnzeel et al. 2009, George et al. 2007).”

What the sources say

• Not checked yetcites Bruijnzeel et al. 2009
• Not checked yetcites George et al. 2007

In the paper

“Acute withdrawal from many drugs elevates corticosterone and corticotropin-releasing factor (CRF) (Koob 2008, Koob & Kreek 2007).”

What the sources say

• Not checked yetcites Koob 2008
• Not checked yetcites Koob & Kreek 2007

In the paper

“The most prominent withdrawal symptoms are irritability, anxiety, anger, difficulty concentrating, sleep disturbance, increased appetite, and weight gain (APA 2000, Hogle et al. 2010, Hughes 2007).”

What the sources say

• Not checked yetcites APA 2000
• Not checked yetcites Hogle et al. 2010
• Not checked yetcites Hughes 2007

In the paper

“Therefore, neuroadaptations arising from chronic nicotine exposure may cause widespread alterations in brain neurotransmission.”

In the paper

“Withdrawal symptoms can be assessed in animals chronically exposed to nicotine by the sudden discontinuation of nicotine treatment or administration of nAChR antagonists (De Biasi & Salas 2008).”

What the sources say

• Not checked yetcites De Biasi & Salas 2008

In the paper

“Beyond the well-studied events of synaptic plasticity, chronic nicotine exposure leads to further remodeling of synapses, producing changes in scaffolding proteins, such as PSD95 and Shank (Hwang & Li 2006, Rezvani et al. 2007).”

What the sources say

• Not checked yetcites Hwang & Li 2006
• Not checked yetcites Rezvani et al. 2007

In the paper

“When access to nicotine is not available, these homeostatic neuroadaptations are no longer appropriate, which contributes to the withdrawal syndrome (Koob & Volkow 2009).”

What the sources say

• Not checked yetcites Koob & Volkow 2009

In the paper

“Consequently, the concept that only certain brain areas narrowly and rigidly mediate reward, aversion, and addiction to nicotine is becoming obsolete.”

In the paper

“In addition, DA controls the synthesis of striatal dynorphin and enkephalin by affecting mRNA levels (Angulo & McEwen 1994, Hadjiconstantinou & Neff 2010).”

What the sources say

• Not checked yetcites Angulo & McEwen 1994
• Not checked yetcites Hadjiconstantinou & Neff 2010

In the paper

“These changes derive, at least in part, from nicotine-induced changes in protein turnover and from partial inhibition of proteasomal function (Rezvani et al. 2007).”

What the sources say

• Not checked yetcites Rezvani et al. 2007

In the paper

“As the brain adapts to chronic nicotine exposure, a new homeostatic condition is achieved by the brain’s circuitry that requires the presence of nicotine to be maintained.”

What the sources say

• Not checked yetcites Koob & Volkow 2009

In the paper

“The symptoms reflect the imbalance in brain neurochemistry created by the absence of nicotine in the addicted brain.”

In the paper

“The conditioned fear paradigm can be used to measure the cognitive symptoms of withdrawal (Davis et al. 2005)”

What the sources say

• Not checked yetcites Davis et al. 2005

In the paper

“A previously neutral environment becomes aversive because of the association of the place with the negative affective state of withdrawal (Suzuki et al. 1996).”

What the sources say

• Not checked yetcites Suzuki et al. 1996

In the paper

“Jumping, which is not normally observed, also appears in mice undergoing nicotine withdrawal (Damaj et al. 2003, De Biasi & Salas 2008, Isola et al. 1999).”

What the sources say

• Not checked yetcites Damaj et al. 2003
• Not checked yetcites De Biasi & Salas 2008
• Not checked yetcites Isola et al. 1999

In the paper

“In the conditioned place-aversion paradigm, the animal learns to avoid the compartment in which nicotine withdrawal is experienced (Jackson et al. 2009, Kenny & Markou 2001).”

What the sources say

• Not checked yetcites Jackson et al. 2009
• Not checked yetcites Kenny & Markou 2001

In the paper

“These properties may contribute to the more severe withdrawal symptoms commonly experienced by those suffering from depression or anxiety disorders (Dani & Harris 2005, Pomerleau et al. 2005).”

What the sources say

• Not checked yetcites Dani & Harris 2005
• Not checked yetcites Pomerleau et al. 2005

In the paper

“Increased brain-stimulation reward thresholds reflect a decreased sensitivity to the rewarding effect of the electrical stimulation.”

In the paper

“the elevated PFC DA during nicotine withdrawal may contribute to the aversive manifestations (Bradberry et al. 1991, Broersen et al. 2000, Inglis & Moghaddam 1999, Kawasaki et al. 2001, Thierry et al. 1976).”

What the sources say

• Not checked yetcites Bradberry et al. 1991
• Not checked yetcites Broersen et al. 2000
• Not checked yetcites Inglis & Moghaddam 1999

In the paper

“Anhedonia is quantifiable in animals as an increase in stimulus threshold needed to induce intracranial electrical self-stimulation to reward pathways (Paterson & Markou 2007).”

What the sources say

• Not checked yetcites Paterson & Markou 2007

In the paper

“Spontaneous or mecamylamine-precipitated nicotine withdrawal is associated with a decrease in extracellular DA levels in the NAc (Carboni et al. 2000, Gaddnas et al. 2002, Hildebrand et al. 1998, Rada et al. 2001, Rahman et al. 2004).”

What the sources say

• Not checked yetcites Carboni et al. 2000
• Not checked yetcites Gaddnas et al. 2002
• Not checked yetcites Hildebrand et al. 1998

In the paper

“This phenomenon is also observed during ethanol, morphine, cocaine, and amphetamine withdrawal (Rossetti et al. 1992, Weiss et al. 1992) and is a trigger of the withdrawal syndrome.”

What the sources say

• Not checked yetcites Rossetti et al. 1992
• Not checked yetcites Weiss et al. 1992

In the paper

“Mice and rats undergoing nicotine withdrawal show increased anxiety-like behavior in the elevated plus maze (Damaj et al. 2003, Irvine et al. 2001).”

What the sources say

• Not checked yetcites Damaj et al. 2003
• Not checked yetcites Irvine et al. 2001

In the paper

“In rats, somatic signs of physical dependency include teeth-chattering, chewing, gasps, palpebral ptosis, tremors, shakes, and yawns (Malin et al. 1992).”

What the sources say

• Not checked yetcites Malin et al. 1992

In the paper

“The decrease in extracellular DA concentrations reflects changes in both DA release and reuptake (Duchemin et al. 2009).”

What the sources say

• Not checked yetcites Duchemin et al. 2009

In the paper

“Similar symptoms are observed in mice, including shaking, grooming, and scratching, which become repetitive and long lived.”

What the sources say

• Not checked yetcites Damaj et al. 2003
• Not checked yetcites De Biasi & Salas 2008
• Not checked yetcites Isola et al. 1999

In the paper

“Changes in DA release and uptake are short lived and normalize within 48 h after nicotine cessation (Hadjiconstantinou & Neff 2010).”

What the sources say

• Not checked yetcites Hadjiconstantinou & Neff 2010

In the paper

“DAT upregulation and decreased DA overflow may contribute to withdrawal symptoms because those DA signaling changes temporally coincide with the emergence of somatic and affective signs of withdrawal (Hadjiconstantinou & Neff 2010).”

What the sources say

• Not checked yetcites Hadjiconstantinou & Neff 2010

In the paper

“Like humans, rodents manifest both somatic and nonsomatic signs of withdrawal (Malin & Goyarzu 2009).”

What the sources say

• Not checked yetcites Malin & Goyarzu 2009

In the paper

“Besides DA, other neurotransmitters, such as serotonin and norepinephrine, known to mediate the manifestations of withdrawal from other drugs may play a role (Bruijnzeel et al. 2010, Fletcher et al. 2008, Semenova & Markou 2010, Slotkin & Seidler 2007).”

What the sources say

• Not checked yetcites Bruijnzeel et al. 2010
• Not checked yetcites Fletcher et al. 2008
• Not checked yetcites Semenova & Markou 2010

In the paper

“Another nonsomatic manifestation of nicotine withdrawal is increased anxiety-like behavior in the elevated plus maze (Pellow et al. 1985).”

What the sources say

• Not checked yetcites Pellow et al. 1985

In the paper

“The data suggest the existence of reward and withdrawal circuits with partially overlapping functions.”

In the paper

“Second, most stimulant drugs of abuse cause axonal degeneration in the LHb and the fasciculus retroflexus”

What the sources say

• Not checked yetcites Ellison 2002
• Not checked yetcites Ellison et al. 1996

In the paper

“This phenotype is in sharp contrast with that of β2 −/− mice, which display normal somatic signs of withdrawal (Besson et al. 2006, Salas et al. 2004b).”

What the sources say

• Not checked yetcites Besson et al. 2006
• Not checked yetcites Salas et al. 2004b

In the paper

“Physical signs of dependency are also absent in α5 −/− mice in which nicotine withdrawal occurs either spontaneously or upon nicotine cessation or is precipitated by mecamylamine injection (Salas et al. 2009).”

What the sources say

• Not checked yetcites Salas et al. 2009

In the paper

“This result suggests that α5-containing nAChRs in the MHb are key to controlling the amounts of nicotine self-administered (Fowler et al. 2011).”

What the sources say

• Not checked yetcites Fowler et al. 2011

In the paper

“The same mice manifested decreased hyperalgesia upon spontaneous nicotine withdrawal (Grabus et al. 2005).”

What the sources say

• Not checked yetcites Grabus et al. 2005

In the paper

“The α7 subunit also plays some role in mecamylamine-precipitated somatic signs of withdrawal as α7 −/− mice showed an intermediate withdrawal phenotype (Salas et al. 2007).”

What the sources say

• Not checked yetcites Salas et al. 2007

In the paper

“In the mouse, the α5, α2, and β4 nAChR subunits are expressed at high levels in either MHb and/or IPN (De Biasi & Salas 2008, Grady et al. 2009)”

What the sources say

• Not checked yetcites De Biasi & Salas 2008
• Not checked yetcites Grady et al. 2009

In the paper

“establishing the MHb and IPN as mediators of somatic withdrawal from nicotine.”

What the sources say

• Not checked yetcites Salas et al. 2009

In the paper

“This nonsynonymous SNP, located in the second intracellular loop of the α5 subunit, leads to a reduction in receptor function (Bierut et al. 2008).”

What the sources say

• Not checked yetcites Bierut et al. 2008

In the paper

“The use of mouse models has clarified the specific brain area that mediates physical dependency.”

In the paper

“Salas et al. (2003a, 2004a) observed that mice null for the α5 and β4 nAChR subunits are less sensitive to the acute effects of nicotine measured as hypolocomotion in the open field arena and nicotine-induced seizure activity.”

What the sources say

• Not checked yetcites Salas et al. 2003a
• Not checked yetcites Salas et al. 2004a

In the paper

“and nicotine causes degeneration of neurons in the portion of the fasciculus retroflexus that connects the MHb to the IPN (Ellison 2002, Ellison et al. 1996).”

What the sources say

• Not checked yetcites Ellison 2002
• Not checked yetcites Ellison et al. 1996

In the paper

“First, electrical stimulation of the MHb and the fasciculus retroflexus produces rewarding effects (Sutherland & Nakajima 1981).”

What the sources say

• Not checked yetcites Sutherland & Nakajima 1981

In the paper

“in contrast with β2 −/− mice, which show normal anxiety-like responses (Maskos et al. 2005).”

What the sources say

• Not checked yetcites Maskos et al. 2005