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Nicotine increases stress‐induced serotonin release by stimulating nicotinic acetylcholine receptor in rat striatum
Author(s) -
Takahashi Hiroshi,
Takada Yumiko,
Nagai Nobuo,
Urano Tetsumei,
Takada Akikazu
Publication year - 1998
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(199803)28:3<212::aid-syn4>3.0.co;2-d
Subject(s) - striatum , nicotine , mecamylamine , nicotinic agonist , chemistry , acetylcholine , microdialysis , serotonin , pharmacology , 5 ht receptor , endocrinology , medicine , dopamine , receptor , biochemistry
We used a microdialysis technique to analyze the effects of footshock stress on the release of serotonin (5‐hydroxytryptamine: 5‐HT) in the striatum or prefrontal cortex (PFC) in rats that were pretreated with nicotine. Neither nicotine administration alone nor stress application alone changed 5‐HT release. During stress application, however, both chronic nicotine administration and local infusion of nicotine to the striatum significantly increased 5‐HT release in the striatum, though not in the PFC. These increases in 5‐HT release were eradicated by a local infusion of mecamylamine. Release of 5‐HT increased in the striatum during stress application when nicotine was injected to the striatum, while nicotinic injection to the dorsal raphe nucleus did not increase 5‐HT release in the striatum. The present study demonstrates that nicotine induced a release of 5‐HT upon stress application by stimulating presynaptic nicotinic receptors in the striatum. Synapse 28:212–219, 1998. © 1998 Wiley‐Liss, Inc.

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