Chronic oral nicotine increases brain [3H]epibatidine binding and responsiveness to antidepressant drugs, but not nicotine, in the mouse forced swim test

Andreasen, Jesper T.; Nielsen, Elsebet Ø.; Redrobe, John P.

doi:10.1007/s00213-009-1560-1

Cited by 20 publications

(16 citation statements)

References 66 publications

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“…For example, KO mice that lack the β2 subunit of nAChRs show decreased amount of baseline immobility in both the FST and tail-suspension test, indication of reduced depression-like phenotype, compared to wild-type animals (Caldarone et al, 2004). Furthermore, it has also been shown that mecamylamine, a nonselective nAChR antagonist, has similar antidepressant-like effects in the FST and tail-suspension test in wild-type but not in β2 KO animals (Andreasen, Nielsen, & Redrobe, 2009; Caldarone et al, 2004; Rabenstein, Caldarone, & Picciotto, 2006). Also consistent with the modulatory role of β2-containing high-affinity nAChRs in the depression-like behavior, an α4β2 selective high-affinity nAChR antagonist, DHβE, has been found to decrease immobility in the FST and tail-suspension test (Andreasen, Olsen, Wiborg, & Redrobe, 2009; Rabenstein et al, 2006).…”

Section: Effects Of Nicotine Dependence Withdrawal and Nachr Regmentioning

confidence: 99%

“…Apart from the β2-containing nAChRs, there is also evidence showing that α7 subtype of nAChRs may also play a modulatory role in the depression-like behavior in animals. For example, Andreasen, Olsen, et al (2009) found that MLA (α7-nAChR selective antagonist) also reduced immobility in the FST, while another study found that mecamylamine had antidepressant effects in the FST for wild-type but not on α7-nAChR KO mice. In addition to the β2 and α7 nAChRs, α5 may also be involved in the modulation of depressive-like behavior.…”

Section: Effects Of Nicotine Dependence Withdrawal and Nachr Regmentioning

confidence: 99%

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Nicotine Addiction and Psychiatric Disorders

Kutlu

Parikh

Gould

2015

International Review of Neurobiology

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Even though smoking rates have long been on the decline, nicotine addiction still affects 20% of the US population today. Moreover, nicotine dependence shows high comorbidity with many mental illnesses including, but are not limited to, attention deficit hyperactivity disorder, anxiety disorders, and depression. The reason for the high rates of smoking in patients with mental illnesses may relate to attempts to self-medicate with nicotine. While nicotine may alleviate the symptoms of mental disorders, nicotine abstinence has been shown to worsen the symptoms of these disorders. In this chapter, we review the studies from animal and human research examining the bidirectional relationship between nicotine and attention deficit hyperactivity disorder, anxiety disorders, and depression as well as studies examining the roles of specific subunits of nicotinic acetylcholine receptors (nAChRs) in the interaction between nicotine and these mental illnesses. The results of these studies suggest that activation, desensitization, and upregulation of nAChRs modulate the effects of nicotine on mental illnesses.

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Section: Effects Of Nicotine Dependence Withdrawal and Nachr Regmentioning

confidence: 99%

Section: Effects Of Nicotine Dependence Withdrawal and Nachr Regmentioning

confidence: 99%

Nicotine Addiction and Psychiatric Disorders

Kutlu

Parikh

Gould

2015

International Review of Neurobiology

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“…These studies have also shown that mice lacking high-affinity nAChRs are insensitive to the tricyclic antidepressant amitriptyline, suggesting that alterations of nicotinic signaling can play a role in the response to classical antidepressants. Interestingly, chronic nicotine administration, which increases the number of high-affinity (α4/β2) nAChRs results in increased response to classical antidepressants 43.…”

Section: Signaling Through Cholinergic Receptors Modulates Affective mentioning

confidence: 99%

Nicotine receptors and depression: revisiting and revising the cholinergic hypothesis

Mineur¹,

Picciotto²

2010

Trends in Pharmacological Sciences

233

150

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There is a well-established connection between smoking and depression, with depressed individuals over-represented among smokers and ex-smokers often experiencing increased depressive symptoms immediately after quitting. Nicotine in tobacco binds, activates and desensitizes nicotinic acetylcholine receptors (nAChRs), but it is not known whether activation or desensitization is more important for nicotine’s effects on depressive symptoms. In this article, we review the hypothesis that blockade rather than activation of neuronal nAChRs might be important for the effects of nicotinic agents on depressive symptoms based on clinical and preclinical studies of nicotinic drugs. The endogenous neurotransmitter for nAChRs is acetylcholine, and the effects of nicotine on depression-like behaviors support the idea that dysregulation of the cholinergic system might contribute to the etiology of major depressive disorder. Thus, pharmacological agents that limit acetylcholine signaling through neuronal nAChRs might be promising for the development of novel antidepressant medications.

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“…Acute and subacute duloxetine treatment decreased the immobility time in the FST in most studies [52,[56][57][58][59][60]. However, when a lower dose was used no such decrease in immobility time was observed after acute duloxetine administration, yet antidepressant-like effects were observed when duloxetine was co-administered with a 5-HT 1A antagonist (WAY100,635) [17].…”

Section: Behavioral Studiesmentioning

confidence: 99%