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2005 SESSIONS-Complete.Qxd SRNT ◆ Symposia INTERACTIONS OF ANTIDEPRESSANTS WITH SYM1A NICOTINIC ACETYLCHOLINE RECEPTORS Ronald J. Lukas*, Lincoln H. Wilkins, Jr., John D. Fryer Nicotinic acetylcholine receptors (nAChR) play a variety of roles in the central nervous system, including modulation of sensation, attention, cognition, and emo- tion, and are found in relevant brain centers. Several lines of evidence, including human clinical and animal behavioral studies, suggest roles for nAChR in depres- sion. Conversely, clinical or subclinical mood disorders may predispose individuals to nicotine use and dependence, which may reflect self-medication to alleviate mood imbalance or other psychiatric indications. Work by us and others indicates that chronic nicotine exposure induces long-lasting inactivation of various nAChR subtypes. This persistent inactivation may contribute to nicotine dependence and some of the mood modulating effects of chronic tobacco use. We have defined interactions of antidepressants with diverse, human nAChR subtypes naturally or heterologously expressed by human cell lines. The atypical antidepressant and smoking cessation aid, bupropion (Wellbutrin, Zyban), a variety of selective sero- tonin reuptake inhibitors, and even some antipsychotic agents, act acutely as non- competitive inhibitors of human nAChR function at clinically-relevant doses. SYMPOSIA Among the more sensitive nAChR subtypes are alpha3* and alpha4* nAChRs. nAChR subtype selectivity of action is evident and is sensitive to metabolism of these agents, as exemplified by comparisons between effects of bupropion and its (2S,3S)hydroxymetabolites. Functional inhibitory potency also is increased and persists after chronic exposure to some of these ligands, such as fluoxetine. Collectively, with caveats about the pharmacokinetics of antidepressants and acknowledgement of their pharmacodynamic actions at other targets, these pre- clinical studies support the notion that nAChRs participate in control of mood and emotion and in actions of antidepressants. These findings have implications for rational design of antidepressant and nicotinic drugs and for scientifically sound strategies to facilitate smoking cessation. Supported by the Arizona Disease Control Research Commission (97301, 1-353, 5007), Barrow Neurological Foundation, and National Institutes of Health (NS40417, DA015389). CORRESPONDING AUTHOR: Ronald J. Lukas, Ph.D., Division of Neurobiology, Barrow Neurological Institute, 350 West Thomas Road, Phoenix, AZ 85013, USA; email: [email protected]. NICOTINIC RECEPTOR ANTAGONISM BY NICOTINIC ACETYLCHOLINE RECEPTORS ARE SYM1 ANTIDEPRESSANTS: PARSING THE LINK SYM1B IMPORTANT FOR ANTIDEPRESSANT BETWEEN SMOKING AND DEPRESSION RESPONSE IN MOUSE MODELS OF DEPRESSION Chair: Marina R. Picciotto; Presenters: Ronald J. Lukas, Marina R. Picciotto, R. Douglas Shytle, Tony P. George; Discussant: Tony P. George Marina R. Picciotto*, Rebecca L. Rabenstein, Barbara J. Caldarone Many studies have demonstrated a high co-morbidity between cigarette smok- To explore the relationship between nAChRs and depression we used male ing and depression. Depressed patients also have more difficulty quitting smoking, C57BL/6J mice to determine the effect of the nicotinic antagonist mecamylamine while nicotine can improve mood in depressed patients, suggesting that smokers in the tail suspension and forced swim animal models of depression. may be using nicotine as self-medication to relieve depressive symptoms. In this Mecamylamine (1 mg/kg) or saline was administered by i.p. injection thirty minutes panel, we will explore the idea that inactivating nicotinic acetylcholine receptors prior to the onset of testing and resulted in a decrease in immobility in the tail sus- (nAChRs), using nicotinic antagonists, genetic manipulation, smoking or classical pension task, while only the nicotine pre-treated animals showed a decrease in antidepressants, is a mechanism involved in antidepressant action. Dr. Ron Lukas depression-like behavior. We also used a mouse genetic model to determine will present evidence at the molecular level that a wide range of antidepressants whether the behavioral effects of antidepressants may be mediated, in part, act as non-competitive antagonists of nAChRs. Dr. Marina Picciotto will show work through actions on nAChRs. Knockout mice lacking the beta2 subunit of the from animal studies demonstrating that mecamylamine, a nicotinic antagonist, can nAChR (beta2KO) were administered the tricyclic antidepressant amitriptyline mimic the effects of classical antidepressants in behavioral models of depression- (AMI) in their drinking water (200ug/ml in 2% saccharin) and control mice received like behavior, and that amitriptyline, a tricyclic antidepressant is ineffective in mice 2% saccharin. Following antidepressant treatment, mice were tested in the learned lacking high-affinity nAChRs. Dr. Doug Shytle will discuss findings that mecamy- helplessness, forced swim and tail suspension models of depression. Wild type lamine (Inversine) can relieve anxiety and mood instability in adolescents. Finally, mice showed robust antidepressant-like effects of AMI in all 3 models. In contrast, Dr. Tony George will present results from a placebo-controlled clinical trial using beta2KO mice treated with AMI were not different from saccharin-treated beta2KO mecamylamine to augment SSRI antidepressants in treatment-resistant patients. mice in any of the 3 models. The effects of antidepressant treatment were also Taken together, these studies provide further evidence that some smokers may use seen at the cellular level such that AMI increased adult neurogenesis in wild type nicotine to self-treat depressive symptoms. Understanding the mechanism under- but not beta2KO mice. These data support the idea that nicotinic receptor block- lying these effects of nicotinic agents may lead to more effective treatments for ade has antidepressant-like effects and that administration of nicotinic receptor smoking cessation in this subpopulation of smokers. antagonists or antidepressant might aid in smoking cessation particularly in NA-Symposium. depressed subjects. In addition, these data demonstrate that beta2KO mice are insensitive to the tricyclic antidepressant AMI, suggesting that some of the thera- CORRESPONDING AUTHOR: Marina R. Picciotto, Yale University, 34 Park peutic effects of antidepressants may be mediated through actions at high affinity Street–3rd Floor Research, New Haven, CT 06508, USA; email: marina.picciotto@ nAChRs. Yale.edu. This work was supported by grants DA13334, DA10455, DA00436 and NARSAD. CORRESPONDING AUTHOR: Marina R. Picciotto, Yale University, 34 Park Street–3rd Floor Research, New Haven, CT 06508, USA; email: marina.picciotto@ Yale.edu. 1 SRNT ◆ Symposia POTENTIAL ANTIDEPRESSANT PROPERTIES ADOLESCENT SMOKERS AND SMOKING SYM1C OF NICOTINIC RECEPTOR ANTAGONIST, SYM2 CESSATION STUDIES: ISSUES IN ELIGIBILITY, MECAMYLAMINE (INVERSINE(r)) IN CHILDREN ENROLLMENT, RECRUITMENT AND RETENTION AND ADOLESCENTS Cathy L. Backinger*, Ph.D., M.P.H., National Cancer Institute, Scott McIntosh, R. Douglas Shytle*, Archie A. Silver, and Paul R. Sanberg Ph.D., University of Rochester, Paul W. McDonald, Ph.D., University of Waterloo, Eric T. Moolchan, M.D., National Institute on Drug Abuse A growing body of evidence suggests that many established antidepressants inhibit nicotinic acetylcholine receptors at physiologically relevant concentrations With less than 100 smoking cessation studies conducted with adolescents, this and that this common pharmacological property may contribute to these drugs’ symposium will explore the challenges of recruiting, enrolling, and retaining ado- overall mechanism of action. Evidence will be presented suggesting the hyper- lescents into smoking cessation studies. A review of the published smoking cessa- cholinergic neurotransmission, which is associated with depressed mood states, tion studies will be presented examining youngest age at enrollment, number of may be mediated through excessive neuronal nicotinic receptor activation and that cigarettes smoked, intervention site, means of recruitment, sample size, and length the therapeutic actions of many antidepressants may be, in part, mediated through of follow-up in relation to percent recruited into the study, percent retained at first inhibition of these receptors. In support of this hypothesis, clinical observations as session, and percent retained at follow-up. Results from a second meta-analysis of well as supporting evidence from a recent controlled trial suggests that mecamy- 48 recruitment campaigns conducted in Canada in the United States will provide lamine (Inversine(r)), a nicotinic receptor antagonist, is well tolerated in doses up evidence on what type of messages, channels, sources, program and participant to 7.5 mg/day and may be useful for reducing sudden mood changes and symp- characteristics influence participation rates the most. toms of depression in children and adolescents with mood disorders. These pre- NA-Symposium. liminary controlled findings support our anecdotal observations that mecamylamine has antidepressant and mood stabilizing effects in patients with mood disorders CORRESPONDING AUTHOR: Cathy Backinger, Ph.D., M.P.H., Tobacco Control and has formed the impetus for a series of clinical studies to further investigate the Research Branch, National Cancer Institute, 6130 Executive Blvd., Rockville, MD therapeutic potential of mecamylamine for the treatment of affective disorders. 20852, USA;
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