Abstract
Muscarinic cholinergic receptors (mAChRs) and nicotinic cholinergic receptors (nAChRs) regulating GABA release from striatal nerve endings were studied by monitoring release of previously accumulated [ 3H]GABA or endogenous GABA from superfused mouse striatal synaptosomes. Oxotremorine inhibited the release of [ 3H]GABA elicited by depolarization with 4-aminopyridine (4-AP), an effect antagonized by atropine. Agonists at nAChRs, including the α 4β 2 ∗ subunit-selective RJR2403, provoked the release of [ 3H]GABA as well as of the endogenous transmitter; these effects also were prevented by oxotremorine and pilocarpine suggesting coexpression of functional mAChRs and α 4β 2 ∗ nAChRs on GABAergic nerve endings. The inhibitory effects of oxotremorine on the release of [ 3H]GABA evoked by 4-AP or by RJR2403 were: (i) prevented by the M 2/M 4 mAChR antagonist himbacine; (ii) insensitive to the M2 antagonist AFDX116; (iii) blocked by the selective M 4 mAChR antagonists MT3, thus indicating the involvement of receptors of the M 4 subtype. In conclusion, in the corpus striatum, acetylcholine released from cholinergic interneurons can activate α 4β 2 ∗ nAChRs mediating release of GABA; this evoked release can be negatively modulated by M 4 mAChRs coexpressed on the same GABAergic terminals.
Published Version
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