作者: M. Tanabe
DOI: 10.1523/JNEUROSCI.4642-05.2006
关键词: Neurotransmission 、 Efaroxan 、 Idazoxan 、 Internal medicine 、 Chemistry 、 Moxonidine 、 Receptor 、 Cyclase activity 、 Pharmacology 、 Imidazoline receptor 、 Endocrinology 、 Medium spiny neuron
摘要: Imidazoline receptors are expressed widely in the CNS. In present study, whole-cell patch-clamp recordings were made from medium spiny neurons dorsal striatum slices rat brain, and roles of I1-imidazoline modulation synaptic transmission studied. Moxonidine, an receptor agonist, decreased GABAA receptor-mediated IPSCs a concentration-dependent manner. However, glutamate-mediated EPSCs hardly affected. The depression by moxonidine was antagonized either idazoxan or efaroxan, which both imidazoline antagonists containing moiety. contrast, yohimbine [SKF86466][1] (6-chloro-2,3,4,5-tetrahydro-3-methyl-1 H -3-benzazepine), α2-adrenergic with no affinity for receptors, did not affect moxonidine-induced inhibition IPSCs. Moxonidine increased paired-pulse ratio reduced frequency miniature without affecting their amplitude, indicating that this agent inhibits via presynaptic mechanisms. Moreover, sulfhydryl alkylating N -ethylmaleimide (NEM) significantly Thus, activation decreases GABA-mediated striatum, NEM-sensitive proteins such as Gi/o-type G-proteins play essential role. adenylate cyclase activator forskolin partly opposed IPSC elicited subsequently applied moxonidine. Furthermore, protein kinase C (PKC) phorbol 12,13-dibutyrate attenuated PKC inhibitor chelerythrine potentiated These results suggest involves intracellular activity is influenced static striatum. [1]: /lookup/external-ref?link_type=GENPEPT&access_num=SKF86466&atom=%2Fjneuro%2F26%2F6%2F1795.atom