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This Article Full Text Full Text (PDF) All Versions of this Article: 90/3/1662    most recent 01165.2002v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via ISI Web of Science (10) Citing Articles via Google Scholar Google Scholar Articles by Nakamura, M. Articles by Akaike, N. Search for Related Content PubMed PubMed Citation Articles by Nakamura, M. Articles by Akaike, N.

Possible Roles of Kainate Receptors on GABAergic Nerve Terminals Projecting to Rat Substantia Nigra Dopaminergic Neurons

¹ Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Kyushu University, Fukuoka 812-8582, Japan; ² Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan; ³ Cellular and System Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan; ⁴ Research Division for Life Sciences, Kumamoto Health Science University, Kumamoto 861-5533, Japan

Submitted 26 December 2002; accepted in final form 30 May 2003

GABAergic afferent inputs are thought to play an important role in the control of the firing pattern of substantia nigra pars compacta (SNc) dopaminergic neurons. We report here the actions of presynaptic kainite (KA) receptors in GABAergic transmission of rat SNc dopaminergic neurons. In mechanically dissociated rat SNc dopaminergic neurons attached with native presynaptic nerve terminals, GABAergic miniature inhibitory postsynaptic currents (mIPSCs) were recorded by use of conventional whole cell patch recording mode. In the voltage-clamp condition, KA (3 µM) significantly increased GABAergic mIPSC frequency without affecting the current amplitude. This facilitatory effect of KA was not affected in the presence of 20 µM GYKI52466, a selective AMPA receptor antagonist, but was completely inhibited in the presence of 20 µM CNQX, an AMPA/KA receptor antagonist. Presynaptic KA receptors on GABAergic terminals were mainly permeable to Na⁺ but impermeable to Ca²⁺ because KA-induced facilitation of mIPSC frequency was completely suppressed in either Na⁺-free or Ca²⁺-free external solutions, and in the presence of 200 µM Cd²⁺, a general voltage-dependent Ca²⁺ channel blocker. In the slice preparation, KA increased GABAergic spontaneous mIPSC frequency, but significantly suppressed evoked IPSC (eIPSC) amplitude. However, this inhibitory action on eIPSCs was reversed by 10 µM CGP55845, a selective GABA_B receptor antagonist, implicating the possible involvement of GABA_B autoreceptors in KA-induced modulation of GABAergic transmission. Thus presynaptic KA receptors on GABAergic nerve terminals synapsing onto SNc neurons may play functional roles contributing the fine control of neuronal excitability and firing pattern of SNc.