NEUROCHEMICAL AND ELECTROPHYSIOLOGICAL STUDIES ON THE INHIBITORY EFFECT OF AMMONIUM-IONS ON SYNAPTIC TRANSMISSION IN SLICES OF RAT HIPPOCAMPUS - EVIDENCE FOR A POSTSYNAPTIC ACTION

被引:65
作者
FAN, P
LAVOIE, J
LE, NLO
SZERB, JC
BUTTERWORTH, RF
机构
[1] DALHOUSIE UNIV,DEPT PHYSIOL & BIOPHYS,HALIFAX B3H 4H2,NS,CANADA
[2] UNIV MONTREAL,HOP ST LUC,CTR RECH CLIN ANDRE VIALLET,NEUROCHIM LAB,MONTREAL H3C 3J7,QUEBEC,CANADA
关键词
D O I
10.1016/0306-4522(90)90403-Q
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
To elucidate the mechanisms involved in the inhibition of synaptic transmission by ammonium ions, the effects of NH4Cl on glutamate release and on synaptic transmission from Schaffer collaterals to CA1 pyramidal cells were measured in fully submerged slices of rat hippocampus. The large, Ca2+-dependent release of glutamate evoked by electrical-field stimulation or by 56 mM K+ was not reduced by 5 mM NH4Cl. In contrast, 5 mM NH4Cl decreased the smaller, field stimulation-induced release of glutamate observed in the presence of low concentrations of Ca2+ (0.1 mM), as well as the spontaneous release of glutamate both in normal and low Ca2+. Unlike the Ca2+-dependent release of glutamate, synaptic transmission was reversibly depressed even by 1 mM NH4 Cl. Firing of CA1 pyramidal cells evoked by iontophoretically applied glutamate was significantly inhibited by 2 or 5 mM NH4Cl. This depression was increased in the presence of 25 μ M bicuculline. Results suggest that ammonium ions do not depress the Ca2+-dependent release of glutamate originating from synaptic vesicles, which is involved in synaptic transmission. Rather, ammonium ions inhibit synaptic transmission by a postsynaptic action, a conclusion strengthened by the inhibitory effect of NH4Cl on glutamate-induced firing. However, NH4Cl may inhibit the formation of cytoplasmic glutamate, the source of spontaneous and Ca2+-independent release. © 1990.
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页码:327 / 334
页数:8
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