The DOI matches its Crossref record; 173 of the 173 references it cites were found in a registry or an index; 23 of the 116 sources its claims cite were checked for support.
It is not “either/or”: Activation and desensitization of nicotinic acetylcholine receptors both contribute to behaviors related to nicotine addiction and mood
Open accessAbstract
Nicotine can both activate and desensitize/inactivate nicotinic acetylcholine receptors (nAChRs). An ongoing controversy in the field is to what extent the behavioral effects of nicotine result from activation of nAChRs, and to what extent receptor desensitization is involved in these behavioral processes. Recent electrophysiological studies have shown that both nAChR activation and desensitization contribute to the effects of nicotine in the brain, and these experiments have provided cellular mechanisms that could underlie the contribution of both these processes to nicotine-mediated behaviors. For instance, desensitization of nAChRs may contribute to the salience of environmental cues associated with smoking behavior and activation and desensitization of nAChRs may contribute to both primary and conditioned drug reward. Similarly, studies of the antidepressant-like effects of nicotinic agents have revealed a balance between activation and desensitization of nAChRs. This review will examine the evidence for the contribution of these two very different consequences of nicotine administration to behaviors related to nicotine addiction, including processes related to drug reinforcement and affective modulation. We conclude that there are effects of nAChR activation and desensitization on drug reinforcement and affective behavior, and that both processes are important in the behavioral consequences of nicotine in tobacco smoking.
Overview
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Written from the paper’s full text.
TL;DR
This review argues that nicotine’s behavioral effects in addiction and mood cannot be explained by either nAChR activation or desensitization alone; both processes contribute, often simultaneously across receptor subtypes and brain regions. It synthesizes electrophysiological, pharmacological, genetic, imaging, and behavioral evidence to propose that activation and desensitization jointly shape nicotine reward, conditioned reinforcement, and antidepressant-like effects.
Key findings
- Both activation and desensitization of nicotinic acetylcholine receptors (nAChRs) contribute to nicotine-related behaviors, including primary reward, conditioned reinforcement, and affective modulation; the review concludes neither process alone is sufficient.
- β2* nAChRs, especially α4/β2* subtypes, are critical for primary reinforcing effects of nicotine: β2* antagonists block nicotine self-administration, and β2* null mice lack nicotine self-administration, DA-dependent locomotor activation, nicotine-enhanced NAc DA release, and nicotine-associated enhancement of conditioned reinforcement.
- Desensitization may enhance the salience of smoking-associated cues: low nicotine concentrations (20–80 nM) produced robust β2* desensitization without α7 desensitization, and desensitization of β2* nAChRs on GABA terminals in VTA can increase DA neuron activity and shift DA responses toward phasic firing.
- Antidepressant-like effects of nicotinic agents may reflect a balance between activation and desensitization: nicotine, nicotinic partial agonists, and nicotinic antagonists can all show antidepressant-like effects, with evidence implicating α4/β2* and α7* nAChRs.
- Human data cited include blood nicotine peaking at ∼50 ng/ml (300 nM) 5 minutes after one cigarette, chronic smoker levels of 10–50 ng/ml (60–300 nM), and PET β2* occupancy of ∼88% after one cigarette, corresponding to plasma levels linked to 50% desensitization of α4β2 nAChRs.
Methods
- Narrative review of published literature on nAChR activation and desensitization in nicotine addiction and mood, integrating electrophysiological, neurochemical, pharmacological, knockout mouse, imaging, and behavioral studies.
- Evidence discussed includes in vitro and brain-slice electrophysiology, cyclic voltammetry, microdialysis, PET/SPECT imaging in humans, self-administration and conditioned reinforcement paradigms in rodents, and forced swim/tail suspension/learned helplessness models.
- The review synthesizes findings across receptor subtypes (notably α7*, β2*, α4/β2*, α6/β2*) and brain regions including VTA, nucleus accumbens, hippocampus, and amygdala.
Limitations
- The paper states several unresolved issues: whether pre- and post-synaptic nAChR subtypes differ in desensitization susceptibility, whether nAChR upregulation increases functional activatable receptors or mainly desensitized receptors, and why α6/β2* upregulation findings are variable.
- The paper notes that the PET ligand may only reveal the highest-affinity subclass of nAChRs, likely desensitized receptors, so activatable nAChRs may not be measured; it also notes that the amygdala link is correlative and requires further causal testing.
- Evident from the text: this is a review, not a primary experimental study, so its conclusions depend on synthesis of heterogeneous animal, human, in vitro, and clinical findings; the paper also states there is no solid consensus on the neural substrates critical for mood disorders.
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Claims the paper makes
51 Own interpretation · 32 No full text of the sources · 10 Partly supported · 6 Supported · 6 Supported so far · 6 Not checked yet · 3 No basis given · 2 Sources not found · 1 Not supported · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In addition, electrophysiological studies show that steady states of nicotine that would be achieved in the bloodstream of a regular smoker can desensitize midbrain nAChRs with a time course of recovery that requires several minutes (Pidoplichko et al., 1997; Wooltorton et al., 2003).”
§ 2. Nicotine Reinforcement > 2.1 Introduction
What the sources say
- Not checked — no full text of the sourcecites Pidoplichko et al., 1997 source
- Partly supportedcites Wooltorton et al., 2003 sourceExperimental — accuracy not yet measured
The section on nicotine concentrations obtained from tobacco reports that smoker-relevant concentrations (20–80 nM) desensitized the slower nAChR current in VTA neurons. The discussion says recovery can be slow and variable, but our copy does not establish that recovery from this desensitization requires several minutes; it also notes that some receptor subtypes remain functional at these concentrations. Page numbers are unavailable in our copy. (LLM, conf=0.86)
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.
- Based: passes — The paper gives a reason why it holds.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“As noted in Section 1, it is clear that acute activation of nAChRs by nicotine can stimulate the firing of DA neurons (Grenhoff et al., 1986; Klink et al., 2001; Picciotto et al., 1998; Svensson et al., 1990).”
§ 2. Nicotine Reinforcement > 2.1 Introduction
What the sources say
- Not checked — no full text of the sourcecites Grenhoff et al., 1986 source
- Supportedcites Klink et al., 2001 source
The Physiological implications of nAChR diversity section (page unavailable) reports nicotine-elicited currents in DA neurons and says the functional receptors would affect “nicotine-elicited impulse flow.” The Diversity of nAChR currents section (page unavailable) also records currents elicited by brief nicotine application to DA neurons. Together, these support the qualified claim that acute nicotine activation can stimulate their firing, although the paper does not report a nicotine-induced change in firing rate. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites Picciotto et al., 1998 source
boosteddirect- 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.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“It appears that the increased surface expression of nAChRs following chronic nicotine can indeed result in increased activation of nAChRs (Vallejo et al., 2005; Wonnacott, 1990), although the discrepancy between studies suggests that there is a dynamic equilibrium between activation and desensitization of nAChRs following chronic nicotine exposure.”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.4 Upregulation of nAChRs following chronic nicotine exposure
What the sources say
- Partly supportedcites Vallejo et al., 2005 sourceExperimental — accuracy not yet measured
The Introduction reports increased receptor responses after long-term nicotine exposure, but explicitly concludes that upregulation is not caused by an increase in the number of surface receptors. The Discussion likewise describes a functional change in existing α4β2 receptors. Thus the increased activation is supported, but attributing it to increased surface expression is not. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites Wonnacott, 1990 source
hedgedconditional- 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.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Furthermore, when even lower nicotine concentrations (20-80 nM) were examined in an attempt to model the low levels experienced by chronic smokers over long time periods, robust β2* desensitization was observed without any α7 desensitization (Wooltorton et al., 2003).”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.4 Upregulation of nAChRs following chronic nicotine exposure
What the sources say
- Supportedcites Wooltorton et al., 2003 source
The section “Nicotine at the concentrations obtained from tobacco differentially desensitizes the nAChR subtypes” reports substantial desensitization of the mainly β2* slow current at both 20 and 80 nM. It reports no desensitization of the fast current at 20 nM; the same section says the putative α7* fast current was not significantly desensitized at 80–500 nM. The paper describes this as no significant α7* desensitization, rather than proving an absolute absence of any effect. (LLM, conf=0.91)
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.
- Based: passes — The paper gives a reason why it holds.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Despite the decreased response of AChRs to agonists in the desensitized state, desensitized nAChRs have a higher affinity for ACh and other ligands than those in the “activatable” state (Heidmann et al., 1983; Quick and Lester, 2002);”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.3 Desensitization of nAChRs
What the sources say
- Not checked — no full text of the sourcecites Heidmann et al., 1983 source
- Supportedcites Quick and Lester, 2002 source
In “Generalized Mechanistic Models of Desensitization” (page unavailable), the paper states that desensitized states generally have higher affinity for agonists and describes the activatable resting state as having low affinity for ACh. “Molecular Aspects of Desensitization” (page unavailable) also reports high-affinity binding of nicotine and some antagonists to desensitized states. (LLM, conf=0.93)
plaincorrelational- 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.
Every source the paper cites for this claim was checked and supports it.
In the paper
“the nicotinic partial agonist cytisine results in antidepressant-like effects in several behavioral paradigms in mice (Mineur et al., 2007).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.3 Smoking and depression
What the sources say
- Supportedcites Mineur et al., 2007 source
The Discussion reports antidepressant-like effects of acute cytisine in the tail suspension and forced swim tests, and of chronic cytisine in the novelty-suppressed feeding test. The paper identifies cytisine as a nicotinic partial agonist and the studied animals as mice. (LLM, conf=0.94)
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.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Animal models of depression-like behavior (e.g., forced swim, learned helplessness, tail suspension) are valid predictors of human depression and antidepressant efficacy.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Mecamylamine and the competitive nicotinic antagonist DhβE also have antidepressant-like properties in mice (Caldarone et al., 2004; Mineur et al., 2007; Rabenstein et al., 2006).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.3 Smoking and depression
What the sources say
- Not checked — no full text of the sourcecites Caldarone et al., 2004 source
- Partly supportedcites Mineur et al., 2007 sourceExperimental — accuracy not yet measured
The Results (page not provided) report significantly reduced immobility after mecamylamine treatment in both the tail suspension and forced swim tests, supporting its antidepressant-like effects in mice. The passages from this paper do not report antidepressant-like effects of DhβE; a search for its full chemical name found no such result. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites Rabenstein et al., 2006 source
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.
- Based: passes — The paper gives a reason why it holds.
- Rests on an assumption: Animal models of depression-like behavior (e.g., forced swim, learned helplessness, tail suspension) are valid predictors of human depression and antidepressant efficacy.
Every source the paper cites for this claim was checked and supports it.
In the paper
“Both mecamylamine and cytisine, in agreement with their antidepressant-like properties, decreased c-fos immunoreactivity in the basolateral amydgala, indicating a reduction of neuronal activity in this region (Mineur et al., 2007).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.7 Anatomical loci underlying nicotinic effects in depression
What the sources say
- Supportedcites Mineur et al., 2007 source
The Results report significantly reduced c-fos immunostaining in the basolateral amygdala after cytisine treatment, similar to the reduction observed with mecamylamine. The Discussion uses c-fos immunoreactivity as a measure of neuronal activation and interprets the finding as suggesting reduced activity in that region. The supplied passages have section labels but no page numbers. (LLM, conf=0.92)
hedgeddirect- 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.
- Rests on an assumption: Animal models of depression-like behavior (e.g., forced swim, learned helplessness, tail suspension) are valid predictors of human depression and antidepressant efficacy.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“bupropion, while having effects on monoamine transporters, has also been shown to be a non-competitive antagonist of nAChRs (Dwoskin et al., 2006).”
What the sources say
- Supportedcites Dwoskin et al., 2006 source
The Neurochemical Mechanisms Mediating the Pharmacological Effects of Bupropion section says that bupropion's inhibition of several nAChR subtypes is not overcome by increasing agonist concentrations, indicating a noncompetitive mechanism. The same section also describes its effects on dopamine and norepinephrine transporters. Page numbers are not provided in our copy. (LLM, conf=0.91)
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.
- Based: passes — The paper gives a reason why it holds.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“the α4/β2* subclass of nAChRs is necessary for the antidepressant-like effects of nicotinic antagonists as demonstrated in KO mice and using selective pharmacological agents (Gatto et al., 2004; Mineur et al., 2007; Rabenstein et al., 2006).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.6 Activation/desensitization of nAChR subtypes in depression-like behavior
What the sources say
- Not checked — no full text of the sourcecites Gatto et al., 2004 source
- Partly supportedcites Mineur et al., 2007 sourceExperimental — accuracy not yet measured
The Discussion reports that β2-subunit knockout mice do not show mecamylamine’s antidepressant-like effects, citing Rabenstein et al. (2006). It also says cytisine’s blockade of α4/β2* receptors may be critical to its effect. Those passages support a role for these receptors, but this paper does not demonstrate that the α4/β2* subclass is necessary for nicotinic antagonists’ antidepressant-like effects; its conclusion is hedged, and its knockout evidence is reported from another study. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites Rabenstein et al., 2006 source
boosteddirect- 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.
- Rests on an assumption: Animal models of depression-like behavior (e.g., forced swim, learned helplessness, tail suspension) are valid predictors of human depression and antidepressant efficacy.
- Rests on an assumption: nAChR subtypes and their functions are conserved between rodents and humans.
- It may state two separate claims as one. 33
- Probably not a substantial claim. 7
At least one cited source doesn’t support this claim or points to a different paper, and none confirmed it — see the verdicts below.
In the paper
“A number of studies in knockout (KO) mice lacking the β2 subunit of the nAChR have shown that both functional deletion in KO mice and nicotine administration in wild-type mice can lead to the same cellular or behavioral effects, suggesting that nicotine administration may normally desensitize β2* nAChRs in these paradigms and that desensitization then contributes to these cellular or behavioral”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.4 Upregulation of nAChRs following chronic nicotine exposure
What the sources say
- Not checked — no full text of the sourcecites Brunzell et al., 2006 source
- Not checked — no full text of the sourcecites Cohen et al., 2005 source
- Disputedcites Mechawar et al., 2004 sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 0 partially supported, 2 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Checked by a reasoning model — may be wrong.
hedgedconditional- 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 cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In a recent positron emission tomography (PET) imaging study, β2* occupancy was ∼ 88% percent after just 1 cigarette, with corresponding plasma levels that have been shown to lead to 50% desensitization of α4β2 nAChRs (Brody et al., 2006).”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.3 Desensitization of nAChRs
What the sources say
- Partly supportedcites Brody et al., 2006 sourceExperimental — accuracy not yet measured
The Results (Table 2; page unavailable) report 88% receptor occupancy 3.1 hours after one cigarette, with a corresponding venous plasma nicotine level of 3.8 ng/mL. The Comment (page unavailable) says a lower concentration, 0.87 ng/mL, is in the range associated with 50% desensitization; it does not establish that the level measured after one cigarette leads to exactly 50% desensitization. The PET study measured occupancy, not desensitization. (LLM, conf=0.85)
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“For instance, nicotine-mediated neurotransmitter release can occur after acute nicotine exposure that activates nAChRs and after chronic nicotine exposure that desensitizes nAChRs (Benwell and Balfour, 1992; Iyaniwura et al., 2001).”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.4 Upregulation of nAChRs following chronic nicotine exposure
What the sources say
- Partly supportedcites Benwell and Balfour, 1992 sourceExperimental — accuracy not yet measured
The Results and Discussion (pages not available in our copy) report increased nucleus accumbens dopamine after repeated nicotine treatment and infer dopamine release after acute treatment, although the acute increase in extracellular dopamine was not statistically significant without an uptake inhibitor. They do not establish that acute exposure activates nAChRs or that chronic exposure desensitizes them; those receptor mechanisms are not supported by this paper. (LLM, conf=0.86)
- Not checked — no full text of the sourcecites Iyaniwura et al., 2001 source
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“For instance, it has been suggested that maintained nAChR desensitization may be important for relieving nicotine withdrawal in human smokers (Brody et al., 2006) as is discussed below.”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.3 Desensitization of nAChRs
What the sources say
- Supportedcites Brody et al., 2006 source
The Conclusions state that smoking may alleviate withdrawal by maintaining nAChRs in a desensitized state. This directly supports the citing sentence’s hedged claim about human smokers. (LLM, conf=0.95)
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
- Rests on an assumption: The behavioral and neurochemical effects of nicotine in rodent models are relevant to human tobacco smoking and nicotine addiction.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“As mentioned earlier, repeated nicotine administration leads to increased release of dopamine that persists, and indeed shows a sensitized response (increased dopamine (DA) release in response to challenge with the same nicotine dose), despite any nAChR desensitization that is likely to have occurred (Benwell and Balfour, 1992; Iyaniwura et al., 2001).”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.4 Upregulation of nAChRs following chronic nicotine exposure
What the sources say
- Partly supportedcites Benwell and Balfour, 1992 sourceExperimental — accuracy not yet measured
The Results (‘The effect of acute and subchronic nicotine’; page unavailable) report elevated basal nucleus accumbens dopamine 27 hours after the last nicotine injection, and the Discussion reports an enhanced dopamine response to a nicotine challenge after pretreatment. The Discussion concludes that the dopamine system may become sensitized. Our copy does not establish that nAChRs had desensitized, so the ‘despite desensitization’ part is unsupported by this paper. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites Iyaniwura et al., 2001 source
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“More recent studies have shown that presynaptic effects of lower concentrations of nicotine that are blocked by nicotinic agents that are thought to be selective for α7* nAChRs persist in the continued presence of nicotine in rat (Mansvelder et al., 2002) and mouse (Wooltorton et al., 2003) brain slices, whereas presynaptic effects that are blocked with agents thought to be selective for β2* nAChR”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.3 Desensitization of nAChRs
What the sources say
- Not checked — no full text of the sourcecites Mansvelder et al., 2002 source
- Partly supportedcites Wooltorton et al., 2003 sourceExperimental — accuracy not yet measured
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
- Not checked — no full text of the sourcecites Mansvelder and McGehee, 2000 source
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Since sustained nicotine exposure shifts the balance toward glutamate-mediated excitation of DA neurons (Mansvelder et al., 2002; Wooltorton et al., 2003) the combination of increased drive on the cell bodies in the VTA and increased filtering in the striatum/nucleus accumbens suggests that chronic nicotine exposure would greatly increase response to environmental stimuli that increase DA neuron”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.4 Upregulation of nAChRs following chronic nicotine exposure
What the sources say
- Not checked — no full text of the sourcecites Mansvelder et al., 2002 source
- Supportedcites Wooltorton et al., 2003 source
The citation is attached to the premise that nicotine shifts the balance toward excitation of DA neurons, not to the citing authors’ subsequent prediction about burst and tonic firing. The paper’s discussion (indexed as “Donkelaar”; page unavailable) says nicotine desensitizes receptors on GABAergic afferents while receptors on glutamatergic afferents remain active and enhance excitation. (LLM, conf=0.89)
- Not checked — no full text of the sourcecites Rice and Cragg, 2004 source
hedgeddirect- 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 sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“The most striking connection between smoking and depression is the norepinephrine-dopamine reuptake inhibitor bupropion, which is prescribed as both an antidepressant and as an aid to smoking cessation (Dwoskin et al., 2006; Hayford et al., 1999).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.1 Introduction
What the sources say
- Supportedcites Dwoskin et al., 2006 source
The Clinical Studies section says bupropion was introduced as an antidepressant and later as a tobacco-use cessation product. The Introduction also describes it as an atypical antidepressant that inhibits dopamine and norepinephrine reuptake and has benefit as a tobacco-use cessation agent. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites Hayford et al., 1999 source
plain- 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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“this hypothesis suggests that the increased depressive symptoms observed in some patients following acute cessation from smoking might be explained by the fact that the clearance of nicotine following smoking cessation coupled with persistent nAChR upregulation (Staley et al., 2006) results in increased ability of ACh to activate these upregulated nAChRs.”
§ 3. Antidepressant Action of Nicotinic Agents > 3.3 Smoking and depression
What the sources say
- Supportedcites Staley et al., 2006 source
The citation is attached to persistent nAChR upregulation after nicotine clearance, not to the citing authors’ proposed explanation for depressive symptoms. The Results report elevated β2*-nAChR availability after seven days of withdrawal, when residual nicotine or metabolites were less likely to interfere with measurement; the Discussion describes increased receptor availability in recently abstinent smokers. (LLM, conf=0.90)
hedgedconditional- 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.
Probably not a substantial claim.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“cytisine, a nicotinic partial agonist that blocks α4/β2* nAChRs but activates α3/β4* and α7* nAChRs (Papke and Porter Papke, 2002; Picciotto et al., 1995)”
§ 3. Antidepressant Action of Nicotinic Agents > 3.6 Activation/desensitization of nAChR subtypes in depression-like behavior
What the sources say
- Partly supportedcites Papke and Porter Papke, 2002 sourceExperimental — accuracy not yet measured
The results section reports that cytisine activates human and rat α7 receptors, with lower efficacy in rat α7 receptors. The paper does not establish the claimed blockade of α4/β2* receptors or activation of α3/β4* receptors; its Introduction identifies GTS-21, not cytisine, as a partial agonist. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites Picciotto et al., 1995 source
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Partly supported
In the paper
“Nicotine can both activate and desensitize/inactivate nicotinic acetylcholine receptors (nAChRs).”
- Also stated in: § 1.2 Functional properties of nAChRs · plain
“A fundamental property of nAChRs is their susceptibility to desensitization and inactivation following, and indeed in some cases independent of, channel opening (Giniatullin et al., 2005).”
What the sources say
- Not checked — no full text of the sourcecites Giniatullin et al., 2005 source
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Also stated in: § 1.2 Functional properties of nAChRs · plain
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The β2* nAChRs are thought to have the highest affinity for nicotine and other agonists (Lippiello et al., 1987; McGehee and Role, 1995; Picciotto et al., 1995) while α7* nAChRs are thought to have a lower affinity for nicotine in vitro (Papke and Thinschmidt, 1998; Wonnacott, 1986).”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.2 Functional properties of nAChRs
What the sources say
hedgedcorrelational- 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.
- Based: passes — The paper gives a reason why it holds.
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
“Recent electrophysiological studies have shown that both nAChR activation and desensitization contribute to the effects of nicotine in the brain, and these experiments have provided cellular mechanisms that could underlie the contribution of both of these processes to nicotine-mediated behaviors.”
- Also stated in: § 1.1 Introduction · hedged
“Emerging evidence for electrophysiological consequences of both nAChR activation and desensitization has provided mechanisms that are consistent with the contribution of both of these processes to nicotine-mediated behaviors.”
boosteddirect- 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.
- Also stated in: § 1.1 Introduction · hedged
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
“We conclude that there are effects of nAChR activation and desensitization on drug reinforcement and affective behavior, and that both processes are important in the behavioral consequences of nicotine in tobacco smoking.”
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The behavioral and neurochemical effects of nicotine in rodent models are relevant to human tobacco smoking and nicotine addiction.
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
“Despite compelling evidence that chronic nicotine exposure, for example in human smokers, results in profound nAChR desensitization, examination of the different rates of activation and desensitization between α7 and β2* nAChRs suggests that not all nAChRs are desensitized under these conditions.”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.4 Upregulation of nAChRs following chronic nicotine exposure
hedged- 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.
- Rests on an assumption: The behavioral and neurochemical effects of nicotine in rodent models are relevant to human tobacco smoking and nicotine addiction.
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
“Thus, it appears that both chronic nicotine administration and early withdrawal are sufficient to drive nAChR up-regulation.”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.4 Upregulation of nAChRs following chronic nicotine exposure
hedgeddirect- 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.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The low level nicotine concentrations experienced by smokers over long periods are suggested to preferentially desensitize α4β2 nAChRs on GABAergic terminals and not α7 nAChRs on glutamatergic terminals in the VTA, thus shifting the presynaptic effects of nicotine from a mixed inhibition and excitation of DA neurons, toward the glutamatergic response to nicotine (Mansvelder et al., 2002; Mansvel”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.4 Upregulation of nAChRs following chronic nicotine exposure
What the sources say
hedgeddirect- 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.
None of the sources cited for this claim have been checked yet.
In the paper
“As mentioned earlier, at nicotine concentrations of 500 nM or higher, electrophysiological studies in combination with pharmacological agents to isolate individual nAChR-mediated currents have shown that α7* nAChR activation is characterized by fast currents that desensitize on a millisecond timescale while β2* nAChRs desensitize more slowly on a second timescale (Couturier et al., 1990a; Giniat”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.4 Upregulation of nAChRs following chronic nicotine exposure
What the sources say
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.
- Based: passes — The paper gives a reason why it holds.
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 likelihood that chronic nicotine exposure results in both peaks of activation and long-term desensitization of nAChRs suggests that functional responses associated with chronic nicotine exposure due to smoking are due, at least in part, to nAChR desensitization.”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.3 Desensitization of nAChRs
hedgeddirect- 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.
In the paper
“It should be noted, however, that this PET ligand may only reveal the highest affinity subclass of nAChRs, which are likely to be in the desensitized state (Changeux et al., 1984). Thus, nAChRs in the activatable state may not be measured using this technique.”
§ 1. Activation and Desensitization of Nicotinic Acetylcholine Receptors > 1.3 Desensitization of nAChRs
What the sources say
- Not checked — no full text of the sourcecites Changeux et al., 1984 source
hedgedconditional- 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.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Studies in β2* nAChR null mutant mice further show that β2* nAChRs are necessary for nicotine self-administration, DA-dependent locomotor activation, nicotine-associated enhancement of NAc DA release, and nicotine-associated enhancement of conditioned reinforcement (Brunzell et al., 2006; King et al., 2004; Marubio et al., 2003; Picciotto et al., 1998).”
§ 2. Nicotine Reinforcement > 2.2 nAChR subtypes that contribute to nicotine reward
What the sources say
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“the non-competitive, non-selective nAChR antagonist mecamylamine as well as the nicotine patch, decrease symptoms of depression in depressed non-smoking patients and patients with Tourette's syndrome (Dursun and Kutcher, 1999; Mihailescu and Drucker-Colin, 2000; Salin-Pascual et al., 1995; Salin-Pascual et al., 1996).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.3 Smoking and depression
What the sources say
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Following treatment with physostigmine, non-depressed subjects had heightened anxiety, aggression and irritability, whereas depressed patients exhibited prolonged and more severe symptoms (Janowsky et al., 1974) and a majority of bipolar patients exhibited signs of depression (Oppenheim et al., 1979).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.2 The cholinergic hypothesis of depression
What the sources say
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“genetic studies also emphasized that both can also have similar genetic susceptibility but that no causal connections exist between these two phenotypes (Kendler et al., 1993; McCaffery et al., 2003).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.3 Smoking and depression
What the sources say
plain- 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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“imaging studies have demonstrated that depressed patients have increased central concentrations of choline (the limiting precursor of ACh) and this is reversed after recovery (Charles et al., 1994).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.2 The cholinergic hypothesis of depression
What the sources say
- Not checked — no full text of the sourcecites Charles et al., 1994 source
boostedcorrelational- 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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The cholinergic-adrenergic theory of depression postulates that a fine balance exists between cholinergic and noradrenergic systems, and that over-activation of the cholinergic component would lead to depression (Janowsky et al., 1972).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.2 The cholinergic hypothesis of depression
What the sources say
- Not checked — no full text of the sourcecites Janowsky et al., 1972 source
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“it is believed that some depressed patients initiate smoking as an attempt to self medicate depressive symptoms with nicotine (Markou et al., 1998; Patton et al., 1998).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.3 Smoking and depression
What the sources say
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
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
“These data suggest that activation of β2*nAChRs on DA soma, and potentially activation of α7* nAChRs, may contribute to nicotine-associated elevations in cue responsivity.”
§ 2. Nicotine Reinforcement > 2.4 nAChR activation and desensitization contribute to primary and conditioned reward
hedgedconditional- 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.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“several classes of nicotinic agonists have antidepressant actions in both human studies and animal models (Ferguson et al., 2000; Gatto et al., 2004) but several nicotinic antagonists have shown to have potent antidepressant effects (Ferguson et al., 2000; Shytle et al., 2002).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.3 Smoking and depression
What the sources say
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“high doses of fluoxetine or other classes of antidepressants can increase quit rates, and these effects are reversed once the treatment is stopped (Hall et al., 1998; Hughes et al., 2000; Kotlyar et al., 2001).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.1 Introduction
What the sources say
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.
- Based: passes — The paper gives a reason why it holds.
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 section will review the evidence suggesting that nAChRs in both the activatable and the desensitized state might drive both primary and conditioned reward associated with tobacco smoking.”
§ 2. Nicotine Reinforcement > 2.1 Introduction
hedgedconditional- 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.
- Rests on an assumption: The behavioral and neurochemical effects of nicotine in rodent models are relevant to human tobacco smoking and nicotine addiction.
In the paper
“a subthreshold dose of the nicotinic antagonist mecamylamine combined with the tricyclic antidepressant amitriptyline results in antidepressant-like effects in mice, reinforcing the idea that blockade of nAChRs yields antidepressant-like effects (Caldarone et al., 2004)”
§ 3. Antidepressant Action of Nicotinic Agents > 3.5 Classical antidepressants can block nAChRs
What the sources say
- Not checked — no full text of the sourcecites Caldarone et al., 2004 source
hedgeddirect- 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.
- Rests on an assumption: Animal models of depression-like behavior (e.g., forced swim, learned helplessness, tail suspension) are valid predictors of human depression and antidepressant efficacy.
In the paper
“the tricyclic antidepressant amitriptyline has no effect in neurochemical and behavioral assays of antidepressant efficacy in KO mice lacking the β2 nAChR subunit, strongly suggesting that β2* nAChRs are involved in this antidepressant response (Caldarone et al., 2004).”
§ 3. Antidepressant Action of Nicotinic Agents > 3.5 Classical antidepressants can block nAChRs
What the sources say
- Not checked — no full text of the sourcecites Caldarone et al., 2004 source
boostedconditional- 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.
- Rests on an assumption: Animal models of depression-like behavior (e.g., forced swim, learned helplessness, tail suspension) are valid predictors of human depression and antidepressant efficacy.
- Rests on an assumption: nAChR subtypes and their functions are conserved between rodents and humans.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“Varenicline is a partial agonist of α4/β2* nAChRs (Coe et al., 2005), but also activates α7-type nAChRs (Mihalak et al., 2006).”
What the sources say
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.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“The observation that nicotine patch or mecamylamine can significantly improve mood in patients affected by Tourette's syndrome (Silver et al., 2001) supports the idea that this effect of the patch is likely to be a result of nAChR desensitization.”
What the sources say
- Not checked — no full text of the sourcecites Silver et al., 2001 source
hedgedconditional- 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.
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
“One potential reason for this possibility is that interference with cholinergic transmission ameliorates negative mood symptoms.”
hedgeddirect- 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: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
None of the sources cited for this claim have been checked yet.
In the paper
“neither patch (Jorenby et al., 1995) nor varenicline are reinforcing (Rollema et al., 2007).”
What the sources say
- Not matchedcites Jorenby et al., 1995
Couldn’t be matched to a paper in Crossref, so it can’t be checked.
- Not checked — no full text of the sourcecites Rollema et al., 2007 source
plain- 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.
- Not matched
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 may be a widespread mechanism underlying the effects of nAChRs on a number of different brain systems.”
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: fails — It may be too vague to check against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. It may be too vague to check against evidence. The paper’s conclusions may not depend on it.
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
“partial agonism or blockade of nAChRs may be helpful in decreasing cue-induced craving by decreasing the firing rate of VTA neurons, while maintaining the filtering effect on DA terminals that allows other salient reward signals to induce DA release in the NAc.”
hedgedconditional- 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: fails — The paper may give no reason why it holds.
Probably not a substantial claim. The paper may give no reason why it holds.
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
“In summary, both activation and desensitization appear to contribute to the primary rewarding properties of nicotine and to secondary conditioned reinforcement.”
hedgedconditional- 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.
The behavioral and neurochemical effects of nicotine in rodent models are relevant to human tobacco smoking and nicotine addiction.
“This review will examine the evidence for the contribution of these two very different consequences of nicotine administration to behaviors related to nicotine addiction, including processes related to drug reinforcement and affective modulation.”
The paper relies on this without support.
Animal models of depression-like behavior (e.g., forced swim, learned helplessness, tail suspension) are valid predictors of human depression and antidepressant efficacy.
“Animal studies have also shown that chronic nicotine administration can elicit antidepressant-like effects in rats both in the learned helplessness (Semba et al., 1998) and the forced swim (Djuric et al., 1999; Tizabi et al., 1999) paradigms.”
The paper relies on this without support.
nAChR subtypes and their functions are conserved between rodents and humans.
“the α4/β2* subclass of nAChRs is necessary for the antidepressant-like effects of nicotinic antagonists as demonstrated in KO mice and using selective pharmacological agents”
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
“This long-lasting level of nicotine ensures that high-affinity nAChRs recurrently bind and unbind nicotine throughout the day (Picciotto et al. 2008).”
From Nicotine Withdrawal (2015) · cites this paper as Picciotto et al. 2008
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Higher β2*-nAChR availability is thought to functionally reflect higher numbers of desensitized receptors13, 14.”
From β2-Nicotinic Acetylcholine Receptor Availability During Acute and Prolonged Abstinence From Tobacco Smoking (2009) · cites this paper as [14]
The cited source says what the claim attributes to it.
In the citing paper
“Because desensitized nAChR conformations have a higher affinity for agonist, nAChRs will increasingly adopt desensitized conformations in response to chronic nicotine exposure (Quick and Lester 2002; Picciotto et al. 2008).”
From Nicotine Withdrawal (2015) · cites this paper as Picciotto et al. 2008
In the citing paper
“Current studies indicate a network level balance between activation and desensitization is important in eliciting the behavioral effects of nicotinic compounds (for review, see Picciotto et al, 2008).”
From Divergent Functional Effects of Sazetidine-A and Varenicline During Nicotine Withdrawal (2013) · cites this paper as Picciotto et al, 2008
In the citing paper
“However, mechanisms underlying acute and chronic effects of nicotine and other nicotinic drugs in models of anxiety and depression are not well characterized (Picciotto et al., 2008).”
From Nicotinic Partial Agonists Varenicline and Sazetidine-A Have Differential Effects on Affective Behavior (2010) · cites this paper as Picciotto et al., 2008
In the citing paper
“Nicotine desensitizes nAChRs and renders them unresponsive and this phenomenon drives an increase in receptor levels as part of an attempt to maintain circuit-level homeostasis [87–89].”
From Mechanistic insights into nicotine withdrawal (2011) · cites this paper as [89]
In the citing paper
“This idea is consistent with an extensive literature suggesting that nicotine and other nAChR agonists induce their behavioral effects via this mechanism (Picciotto et al., 2008;Buccafusco et al., 2009;Bordia et al., 2010;Mineur and Picciotto, 2010;Grady et al., 2012).”
From Varenicline Is a Potent Partial Agonist at α6β2* Nicotinic Acetylcholine Receptors in Rat and Monkey Striatum (2012) · cites this paper as Picciotto et al., 2008
In the citing paper
“Moreover, it is well established that chronic administration of either nicotine or nAChR antagonists both result in nAChR up-regulation (Hulihan-Giblin et al., 1990a,b;Kuryatov et al., 2005;Picciotto et al., 2008;Buccafusco et al., 2009).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Picciotto et al., 2008
In the citing paper
“The molecular basis for these seemingly discrepant observations may relate to findings that nicotine initially activates and then subsequently desensitizes or inactivates nAChRs, with a consequent receptor block (Corringer et al., 2006;Picciotto et al., 2008;Buccafusco et al., 2009).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Picciotto et al., 2008
In the citing paper
“Desensitization most likely involves post-translational receptor changes including receptor phosphorylation (Corringer et al., 2006;Picciotto et al., 2008;Buccafusco et al., 2009).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Picciotto et al., 2008
In the citing paper
“Precedence for the idea that nAChR desensitization makes an important contribution to nicotine's functional effects is evident from previous work showing that nicotine and nAChR blockers may have comparable pharmacological/ physiological effects (Picciotto et al., 2008;Buccafusco et al., 2009).”
From Nicotinic receptor-mediated reduction in l-DOPA-induced dyskinesias may occur via desensitization (2010) · cites this paper as Picciotto et al., 2008
In the citing paper
“numerous studies suggest that decreasing activity of α4β2* nAChRs can improve symptoms of depression”
From Mood and anxiety regulation by nicotinic acetylcholine receptors: A potential pathway to modulate aggression and related behavioral states (2015) · cites this paper as Picciotto et al., 2008
In the citing paper
“These data suggest that a partial agonist, or a mix of agents with differing effects at heteromeric and homomeric nAChRs may be the most promising for developing nicotinic-based antidepressants”
From Mood and anxiety regulation by nicotinic acetylcholine receptors: A potential pathway to modulate aggression and related behavioral states (2015) · cites this paper as Picciotto et al., 2008
In the citing paper
“while the nicotinic antagonist mecamylamine can have antidepressant-like properties in mouse models (Picciotto et al., 2008; Picciotto et al., 2012), antidepressant effects of this drug are not observed in assays of rats (Tizabi et al., 2000)”
From Mood and anxiety regulation by nicotinic acetylcholine receptors: A potential pathway to modulate aggression and related behavioral states (2015) · cites this paper as Picciotto et al., 2008
In the citing paper
“These findings are consistent with the notion that reducing α4β2 nicotinic acetylcholine receptor activity either by antagonists or by partial agonists that can partially activate or desensitize acetylcholine receptors is associated with antidepressant-like properties.”
From Varenicline has antidepressant-like activity in the forced swim test and augments sertraline's effect (2009) · cites this paper as Picciotto et al., 2008
In the citing paper
“Neuronal nicotinic acetylcholine receptor antagonists and partial agonists may have utility in the treatment of depression, either alone or combined with antidepressants (Shytle et al, 2003; Picciotto et al, 2008).”
From Varenicline has antidepressant-like activity in the forced swim test and augments sertraline's effect (2009) · cites this paper as Picciotto et al, 2008
In the citing paper
“Partial agonists can modulate ACh signaling not only via their decreased efficacy at the receptor, but also via inactivating nicotinic acetylcholine receptors by desensitization (Hogg and Bertrand, 2007; Picciotto et al., 2008).”
From Varenicline has antidepressant-like activity in the forced swim test and augments sertraline's effect (2009) · cites this paper as Picciotto et al., 2008
Citations
Cites
The neural basis of drug craving: An incentive-sensitization theory of addiction
Robinson, T. (1993) · Brain Research Reviews · doi:10.1016/0165-0173(93)90013-p · Cited by 7,346
Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants
Santarelli, L., Saxe, M., Gross, C., Surget, A., Battaglia, F., Dulawa, S., Weisstaub, N., Lee, J., Duman, R., Arancio, O., et al. (2003) · Science · doi:10.1126/science.1083328 · Cited by 4,321
Chronic antidepressant treatment increases neurogenesis in adult rat hippocampus
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Metadata
- Authors
- PICCIOTTO, M., ADDY, N., MINEUR, Y., & BRUNZELL, D.
- Affiliations
- Yale University (US)
- Corresponding author
- PICCIOTTO, M
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2008-04
- Volume
- 84
- Issue
- 4
- Pages
- 329-342
- ISSN
- 0301-0082 (ISSN-L)
- PMC
- PMC2390914
- OpenAlex
- W2006670955
- Cited by
- 460
- References
- 173
- Citations by year
- 2026: 14 · 2025: 15 · 2024: 10 · 2023: 21 · 2022: 20 · 2021: 16 · 2020: 21 · 2019: 17 · 2018: 25 · 2017: 25 · 2016: 36 · 2015: 32 · 2014: 34 · 2013: 29 · 2012: 34
- FWCI
- 7.83
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Progress in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Alcohol Abuse and Alcoholism (P50AA015632)
- National Institute of Mental Health (R01MH077681)
- National Institute on Drug Abuse (DA14241, K02DA000436, DA 10455, R01DA014241, R29DA010455, R01DA010455, DA 00436, P50DA013334, R37DA014241)
- 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 › Neuroscience and Neuropharmacology Research
- Keywords
- nicotinic acetylcholine receptors, receptor desensitization, nicotine dependence, drug reinforcement, antidepressant-like effects, mood, smoking, emotional behavior
- MeSH terms
- Affect, Animals, Humans, Nicotine, Receptors, Nicotinic, Reward, Tobacco Use Disorder, Signal Transduction, Down-Regulation, Up-Regulation, Nicotinic Agonists
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