Regulation by nicotine of its own receptors

Lukas, Ronald J.; Ke, Lu; Bencherif, Merouane; Eisenhour, Cynthia M.

doi:10.1002/(sici)1098-2299(199607/08)38:3/4<136::aid-ddr2>3.0.co;2-n

Cited by 39 publications

(25 citation statements)

References 31 publications

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“…102,103 We have previously proposed that the therapeutic effect of transdermal nicotine as an adjunct to neuroleptic treatment of Tourette's disorder 104 may involve nAChR inactivation resulting from a prolonged continuous exposure to nicotine. 105 In vitro studies with nicotine 71 and preliminary positive clinical observations with mecamylamine in the clinical treatment of TD patients, further support the receptor inactivation hypothesis. 106 Mecamylamine was originally used as a ganglionic blocker to treat hypertension with doses ranging from 25 to 90 mg day −1 .…”

Section: Preliminary Clinical Findings With Mecamylaminementioning

confidence: 65%

“…64,71 A reversible (within minutes) loss of nAChR function induced after seconds-minutes of agonist exposure is termed 'desensitization.' More prolonged exposure to agonist can lead to more slowly reversible phases of loss of nAChR responsiveness termed 'persistent inactivation,' at least for some nAChR subtypes.…”

Section: Nicotinic Acetylcholine Receptors and Their Distributionmentioning

confidence: 99%

“…64,72 Long exposures to low concentrations of agonist will favor deeper levels of desensitization, and this situation is often the case for smokers, who maintain low concentrations of nicotine throughout the day. 71,[73][74][75] With this in mind, it has been proposed that nicotine's predominant effect on many nAChR subtypes over time (its time-averaged effect) is that of an antagonist. 76 However, some nAChR subtypes are more resistant to desensitization than others, and there is some evidence that certain receptor subtypes become more sensitive to repeated agonist exposure.…”

Section: Nicotinic Acetylcholine Receptors and Their Distributionmentioning

confidence: 99%

“…81,82 Nicotinic receptor ␣3, ␣6 and ␤3 subunits are enriched in midbrain nuclei associated with behavioral reinforcement. 71,[73][74][75] …”

Section: Nicotinic Acetylcholine Receptors and Their Distributionmentioning

confidence: 99%

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Nicotinic acetylcholine receptors as targets for antidepressants

et al. 2002

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While the monoamine deficiency hypothesis of depression is still most commonly used to explain the actions of antidepressant drugs, a growing body of evidence has accumulated that is not adequately explained by the hypothesis. This article draws attention to contributions from another apparently common pharmacological property of antidepressant medications-the inhibition of nicotinic acetylcholine receptors (nAChR). Evidence is presented suggesting the hypercholinergic neurotransmission, which is associated with depressed mood states, may be mediated through excessive neuronal nicotinic receptor activation and that the therapeutic actions of many antidepressants may be, in part, mediated through inhibition of these receptors. In support of this hypothesis, preliminary evidence is presented suggesting that the potent, centrally acting nAChR antagonist, mecamylamine, which is devoid of monoamine reuptake inhibition, may reduce symptoms of depression and mood instability in patients with comorbid depression and bipolar disorder. If this hypothesis is supported by further preclinical and clinical research, nicotinic acetylcholine receptor antagonists may represent a novel class of therapeutic agents for treating mood disorders.

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Section: Preliminary Clinical Findings With Mecamylaminementioning

confidence: 65%

Section: Nicotinic Acetylcholine Receptors and Their Distributionmentioning

confidence: 99%

Section: Nicotinic Acetylcholine Receptors and Their Distributionmentioning

confidence: 99%

“…81,82 Nicotinic receptor ␣3, ␣6 and ␤3 subunits are enriched in midbrain nuclei associated with behavioral reinforcement. 71,[73][74][75] …”

Section: Nicotinic Acetylcholine Receptors and Their Distributionmentioning

confidence: 99%

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Nicotinic acetylcholine receptors as targets for antidepressants

et al. 2002

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“…Among various regions of the central nervous system, the ␣ 3 , ␣ 4 , ␤ 2 , and ␤ 4 subunits of nnAChRs are unequally distributed in the different layers of the cerebral cortex (60), and several investigations have reported that the up-regulation of the receptors is due to the increased numbers of ␣ 4 /␤ 2 , ␣ 3 /␤ 4 , and ␣ 7 nnAChR subunits in neurons and nonneuronal expression systems (13,17,61). In addition to these data, nnAChRs composed with ␣ 4 /␤ 2 are adequately activated by nicotine at concentrations less than 10 - 100 nM (13) and also have been reported to show up-regulation after long term nicotine treatment (13)(14)(15)18).…”

Section: Camentioning

confidence: 99%