NEUROCHEMICAL AND ELECTROPHYSIOLOGICAL STUDIES ON THE INHIBITORY EFFECT OF AMMONIUM-IONS ON SYNAPTIC TRANSMISSION IN SLICES OF RAT HIPPOCAMPUS - EVIDENCE FOR A POSTSYNAPTIC ACTION
NEUROCHEMICAL AND ELECTROPHYSIOLOGICAL STUDIES ON THE INHIBITORY EFFECT OF AMMONIUM-IONS ON SYNAPTIC TRANSMISSION IN SLICES OF RAT HIPPOCAMPUS - EVIDENCE FOR A POSTSYNAPTIC ACTION
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DOI：
10.1016/0306-4522(90)90403-q
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发表时间：
1990-01-01
期刊：
影响因子：
3.3
通讯作者：
BUTTERWORTH, RF
中科院分区：
文献类型：
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作者：
FAN, P;LAVOIE, J;BUTTERWORTH, RF
为了阐明铵离子抑制突触传递的机制，我们在大鼠海马全浸没切片中测量了NH4Cl对谷氨酸释放和Schaffer络向CA1锥体细胞突触传递的影响。由电场刺激或56 mM K+引起的谷氨酸的大量Ca2+依赖性释放不会被5 mM NH4Cl减少。相比之下，在低浓度Ca2+ (0.1 mM)下，5mm NH4Cl降低了较小的场刺激诱导的谷氨酸释放，以及在正常和低Ca2+下谷氨酸的自发释放。不像Ca2+。与谷氨酸的Ca2+依赖性释放不同，即使1mm NH4Cl也可可逆地抑制突触传递。2、5 mM NH4Cl可显著抑制谷氨酸离子连接引起的CA1锥体细胞放电。这种洼地在25亩的土地上增加了。荷包牡丹碱。结果表明，铵离子不抑制来自突触囊泡的谷氨酸的Ca2+依赖性释放，这参与了突触传递。相反，铵离子通过突触后作用抑制突触传递，NH4Cl对谷氨酸激发的抑制作用强化了这一结论。然而，NH4Cl可能抑制细胞质谷氨酸的形成，谷氨酸是自发和Ca2+独立释放的来源。
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+. Unlike the Ca2+-dependent release of glutamate, synaptic transmission was reversibly depressed even by 1 mM NH4Cl. 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 .mu.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.