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Local GABAergic modulation of acetylcholine release from the cortex of freely moving rats
Author(s) -
Giorgetti Marco,
Bacciottini Lucia,
Giovannini Maria Grazia,
Colivicchi Maria Alessandra,
Goldfarb Joseph,
Blandina Patrizio
Publication year - 2000
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.1460-9568.2000.00079.x
Subject(s) - gabaergic , acetylcholine , neuroscience , modulation (music) , chemistry , cortex (anatomy) , psychology , biology , physics , pharmacology , inhibitory postsynaptic potential , acoustics
Cortical perfusion with GABA agonists and antagonists modulates the spontaneous release of cortical acetylcholine and GABA in freely moving rats. Twenty‐four hours after implantation of a dialysis fibre, cerebral cortex spontaneously released acetylcholine (3.8 ± 0.2 pmol/10 min) and GABA (6.6 ± 0.4 pmol/10 min) at a stable rate. Local administration of GABA (1 or 5 m m ) or the GABA A agonist muscimol (25 or 50 μ m ) had no effect on the spontaneous release of acetylcholine. However, bicuculline (1–25 μ m ), a GABA A antagonist, added to the dialysis perfusate, elicited a concentration‐dependent increase of acetylcholine release to approximately double that of control. This effect of bicuculline (25 μ m ) was completely prevented by coperfusion with muscimol (50 μ m ). Local administration of the GABA B receptor agonist baclofen (10 or 50 μ m ) elicited a concentration‐dependent increase in spontaneous acetylcholine release with a maximal increase of about 60%. Intracortical administration of baclofen also decreased the spontaneous release of GABA. The GABA B receptor antagonist CGP 35348 (1 m m ), administered alone for 20 min through the dialysis fibre, was without effect on spontaneous acetylcholine release; however, it completely blocked both the baclofen‐induced increase in acetylcholine release and the decrease in GABA release. These results suggest that cortically released GABA exerts a tonic influence on cholinergic activity.