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NMDA‐induced acetylcholine release in mouse striatum: role of NO synthase isoforms
Author(s) -
Buchholzer MarieLuise,
Klein Jochen
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2002.01132.x
Subject(s) - acetylcholine , cholinergic , nmda receptor , striatum , glutamatergic , stimulation , glutamate receptor , neuroscience , nitric oxide synthase , chemistry , neurochemical , endocrinology , medicine , biology , nitric oxide , dopamine , receptor , biochemistry
Striatal cholinergic interneurons are stimulated by glutamatergic inputs from thalamus and cortex via NMDA receptors. The present microdialysis study was designed to characterize the role of nitric oxide (NO) in this process and to identify the NO synthase (NOS) isoform responsible for this effect. For this purpose, we studied the effects of NMDA and 3‐morpholino sydnonimine (SIN‐1) perfusions on the release of acetylcholine (ACh) in mouse striatum. In wild‐type C57/Bl6 mice, perfusion of NMDA (100 µ m ) induced a two‐fold stimulation of ACh release. This effect was attenuated in mice lacking endothelial NOS but was completely absent in mice lacking neuronal NOS. Local perfusion of SIN‐1 (300 µ m ), an NO donor, increased ACh release by more than two‐fold in all three mouse lines. We conclude that NO synthesized by neuronal NOS provides a nitrergic link in the glutamatergic stimulation of striatal cholinergic interneurons.