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Nicotinic acetylcholine receptors (nAchRs) in supraoptic nucleus (SON) neurons: Potential role in regulation of food intake
Author(s) -
Song Zhilin
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.889.11
Subject(s) - acetylcholine , nicotine , endocrinology , nicotinic agonist , medicine , chemistry , muscarinic acetylcholine receptor , carbachol , nicotinic antagonist , acetylcholine receptor , hypothalamus , neuroscience , biology , receptor
Nicotine induces anorexia. nAchRs are expressed in SON of the hypothalamus, where oxytocin (OT) and vasopressin (VP) are synthesized. Nicotine stimulates release of VP as well as OT, an anorexic agent. Deficits in OT are associated with human obesity. Thus, nicotine may reduce food intake, in part, via modulation of OT neurons in SON. In our current studies, live‐cell calcium imaging was used to determine if acetylcholine (Ach) or nicotine altered intracellular calcium ([Ca ++ ] i )signaling in SON neurons. Hypothalamic explants that include SON were loaded with the calcium sensitive dye, Fura‐2AM. Changes in [Ca ++ ] i were monitored by changes in the 340/380 nm emission. A short application of Ach (5 mM) to the bath caused an increase in [Ca ++ ] i in a subset of SON neurons, in the presence or absence of PNU‐120596 (10 μM), a positive allosteric modulator of α7 nAchRs. Ca ++ response to Ach was reduced but still existed in the presence of atropine (10 μM) to block muscarinic AchRs. Nicotine (20–100 μM) also induced [Ca ++ ] i increase in a portion of SON neurons. These findings are consistent with activation of nAchRs in SON neurons. Future studies will further characterize the specific subtypes of nAchRs in SON and identify the peptidergic phenotype of responsive neurons. Supported by AHA 0735329N.