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The Journal of Neurophysiology Vol. 82 No. 2 August 1999, pp. 1059-1062
Copyright ©1999 by the American Physiological Society
RAPID COMMUNICATION
Department of Neurosurgery, Yale University Medical School, New Haven, Connecticut 06520
Liu, Qing-Song,
Peter R. Patrylo,
Xiao-Bing Gao, and
Anthony N. van den Pol.
Kainate Acts at Presynaptic Receptors to Increase GABA Release
From Hypothalamic Neurons. J. Neurophysiol. 82: 1059-1062, 1999. Recent reports suggest that kainate
acting at presynaptic receptors reduces the release of the inhibitory
transmitter GABA from hippocampal neurons. In contrast, in the
hypothalamus in the presence of
-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and
N-methyl-D-aspartate (NMDA) receptor
antagonists [1-(4-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine
(GYKI 52466) and D,L-2-amino-5-phosphonopentanoic acid
(AP5)], kainate increased GABA release. In the presence of
tetrodotoxin, the frequency, but not the amplitude, of GABA-mediated
miniature inhibitory postsynaptic currents (IPSCs) was enhanced by
kainate, consistent with a presynaptic site of action. Postsynaptic
activation of kainate receptors on cell bodies/dendrites was also
found. In contrast to the hippocampus where kainate increases
excitability by reducing GABA release, in the hypothalamus where a much
higher number of GABAergic cells exist, kainate-mediated activation of
transmitter release from inhibitory neurons may reduce the level of
neuronal activity in the postsynaptic cell.
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