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Muscarinic and GABA A receptors modulate acetylcholine release in feline basal forebrain
Author(s) -
Vazquez Jacqueline,
Baghdoyan Helen A.
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02451.x
Subject(s) - basal forebrain , bicuculline , muscarinic acetylcholine receptor , acetylcholine , gabaa receptor , substantia innominata , chemistry , endocrinology , cholinergic , medicine , neuroscience , cholinergic neuron , pharmacology , biology , receptor
Acetylcholine (ACh) release within the basal forebrain changes significantly as a function of sleep and wakefulness, hence identifying the neurochemical modulators of basal forebrain ACh release will contribute to a mechanistic understanding of sleep cycle regulation. This study tested the hypothesis that muscarinic and gamma aminobutyric acid A (GABA A ) receptors modulate basal forebrain ACh release. Cats were anaesthetized with halothane to hold arousal state constant and a microdialysis probe was aimed stereotaxically for the substantia innominata region of the basal forebrain. Four concentrations of the muscarinic antagonist scopolamine (0.1, 0.3, 1.0, and 10 n m ) and five concentrations of the GABA A antagonist bicuculline (3, 10, 30, 100, and 300 µ m ) were delivered by reverse dialysis from the same probes used to collect ACh. These results are based on 27 experiments in nine animals. Scopolamine and bicuculline each caused a concentration dependent enhancement of ACh release. Scopolamine increased ACh by 118% above control levels whereas bicuculline was more effective, causing a 287% increase in ACh release. Scopolamine was more potent (EC 50 = 0.16 n m ) than bicuculline (EC 50 ≥ 90 µ m ) for increasing ACh release. The results support the hypothesis that substantia innominata ACh release is modulated by muscarinic autoreceptors and inhibited by GABA A receptors. These findings are consistent with the interpretation that inhibition of basal forebrain cholinergic neurotransmission by GABA contributes to the generation of sleep.