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Activation of muscarinic receptors stimulates GABA release in the rat globus pallidus
Author(s) -
Kayadjanian Nathalie,
Menétrey Annie,
Besson MarieJo
Publication year - 1997
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(199706)26:2<131::aid-syn4>3.0.co;2-9
Subject(s) - carbachol , pirenzepine , muscarinic acetylcholine receptor , chemistry , endocrinology , medicine , globus pallidus , muscarine , cnqx , methoctramine , biology , receptor , glutamate receptor , ampa receptor , biochemistry , basal ganglia , central nervous system
The effect of carbachol on the spontaneous release of 3 H‐GABA was investigated on rat globus pallidus (GP) slices. Carbachol dose‐dependently enhanced the release of 3 H‐GABA. The carbachol (5 × 10 −4 M) induced 3 H‐GABA release is mediated by muscarinic receptors since atropine (10 −6 M), pirenzepine (10 −6 M) and AF‐DX384MS (10 −6 M) abolished the effect. An indirect carbachol effect mediated by dopaminergic and glutamatergic afferents was ruled out since the effect was not blocked by either D1 (SCH23390 10 −6 ) and D2 (sulpiride 10 −5 M) receptor antagonists or by ionotropic glutamate receptor antagonists (CNQX 10 −6 M and 10 −5 M, MK801 10 −6 M). A direct effect is further evidenced by the persistence of the carbachol effect in the presence of tetrodotoxin (5 × 10 −7 M). Surprisingly the carbachol effect was not abolished by lowering the Ca 2+ concentration of the superfusion medium or by increasing concomitantly the Mg 2+ concentration. The involvement of a GABA transporter can partially explain this latter result, as nipecotic acid (10 −3 M) blocked the effect by only 50%. Carbachol stimulated the accumulation of 3 H‐phosphoinositides in pallidal slices, an effect that was antagonized by atropine (10 −6 M), pirenzepine (10 −6 M), and AF‐DX384MS (10 −6 M). These results suggest that the activation of muscarinic receptors localized on striatopallidal terminals stimulates the release of GABA in the globus pallidus through inositol phosphate hydrolysis. Synapse 26:131–139, 1997. © 1997 Wiley‐Liss, Inc.