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The Journal of Neuroscience, August 15, 2001, 21(16):5962-5972
Contribution of the Na-K-Cl Cotransporter on GABAA
Receptor-Mediated Presynaptic Depolarization in Excitatory Nerve
Terminals
Il-Sung
Jang,
Hyo-Jin
Jeong, and
Norio
Akaike
Cellular and System Physiology, Graduate School of Medical
Sciences, Kyushu University, Fukuoka 812-8582, Japan
GABAA receptor-mediated responses manifest as either
hyperpolarization or depolarization according to the intracellular
Cl concentration
([Cl ]i). Here, we report a
novel functional interaction between the Na-K-Cl cotransporter (NKCC)
and GABAA receptor actions on glutamatergic presynaptic
nerve terminals projecting to ventromedial hypothalamic (VMH) neurons.
The activation of presynaptic GABAA receptors depolarizes the presynaptic nerve terminals and facilitates spontaneous glutamate release by activating TTX-sensitive Na+ channels and
high-threshold Ca2+ channels. This depolarizing
action of GABA was caused by an outwardly directed
Cl driving force for GABAA receptors;
that is, the [Cl ]i of glutamatergic
nerve terminals was higher than that predicted for a passive
distribution. The higher [Cl ]i was
generated by bumetanide-sensitive NKCCs and was responsible for the
GABA-induced presynaptic depolarization. Thus, GABAA
receptor-mediated modulation of spontaneous glutamatergic transmission
may contribute to the development and regulation of VMH function as
well as to the excitability of VMH neurons themselves.
Key words:
sEPSCs; presynaptic GABAA receptors; intraterminal Cl concentration; NKCC; mechanical
dissociation; VMH; GABA-induced depolarization
Copyright © 2001 Society for Neuroscience 0270-6474/01/21165962-11$05.00/0
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