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This Article Full Text Full Text (PDF) All Versions of this Article: 560/2/469    most recent jphysiol.2004.067017v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Katsurabayashi, S. Articles by Ito, Y. Search for Related Content PubMed PubMed Citation Articles by Katsurabayashi, S. Articles by Ito, Y.

¹ Cellular and System Physiology
² Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
³ Department of Physiology, Kurume University School of Medicine, Fukuoka Japan
⁴ Research Division for Life Sciences, Kumamoto Health Science University, Kumamoto, Japan

Corelease of glycine and GABA from the single synaptic terminal (synaptic bouton) is well accepted in immature rat spinal cord and brainstem. However, it raises the question of how glycine and GABA are accumulated in the same synaptic vesicles and coreleased. To address this issue, spontaneous miniature inhibitory postsynaptic currents (mIPSCs) and focally evoked IPSCs (eIPSCs) mediated via a single synapse were recorded from synaptic bouton preparations of the rat immature sacral dorsal commissural nucleus (SDCN) neurones by whole-cell patch recording. Focal stimulation of a single synaptic bouton revealed that three different quantal releases occur from a single synaptic bouton: i.e. pure glycine, pure GABA, and mixed. Prolonged treatment with bafilomycin A1, a vacuolar-type H⁺/ATPase inhibitor, to the SDCN neurone greatly suppressed frequency and amplitude of the mIPSCs. During washing out of bafilomycin A1, complete recovery in the amplitude of glycinergic mIPSCs was observed, while that of GABAergic and mixed mIPSCs was incomplete. These observations indicate that three types of vesicles coexist in single synaptic terminals, and that refilling of glycine into the synaptic vesicle predominantes over GABA after pretreatment with bafilomycin A1 in immature rats. This could be explained by the decrease in the cytosolic concentration of GABA, or by the presence of subtypes of vesicular inhibitory amino acid transporter in the synaptic vesicle membrane.

(Received 23 April 2004; accepted after revision 11 August 2004; first published online 19 August 2004)
Corresponding author N. Akaike: Research Division for Life Sciences, Kumamoto Health Science University, Kumamoto, Japan. Email: akaike{at}kumamoto-hsu.ac.jp

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