Théorĕt Y, Davies M F, Esplin B, Capek R
Neuroscience. 1985 Mar;14(3):798-806.
Effects of ammonia on excitatory synaptic transmission were studied in the rat hippocampal slice preparation. Population spikes, elicited by orthodromic or antidromic stimulation, were recorded in the cell body layer of the CA1, CA3 and dentate regions. Perfusion with 5 mM ammonium chloride induced a profound and reversible depression of orthodromically evoked population spikes in all three regions. Antidromic population spikes were not depressed in any of the regions, indicating that neither axonal conduction nor electrical excitability were affected by ammonia. The paired-pulse test revealed a transient disinhibition during the early phase of perfusion. Iontophoretic application of glutamate evoked unit firing even when the synaptically evoked responses were reduced by ammonia, indicating that the postsynaptic sensitivity to the putative transmitter was not depressed. Depression of release of the excitatory transmitter, probably because of depletion following the block of transmitter synthesis, is the likely explanation of these findings. It is suggested that ammonia-induced depression of excitatory transmission may account for coma and other symptoms of central nervous system depression encountered in hyperammonemic states.
在大鼠海马脑片标本中研究了氨对兴奋性突触传递的影响。通过顺向或逆向刺激诱发的群体峰电位，在CA1、CA3和齿状回区域的细胞体层进行记录。用5 mM氯化铵灌注可在所有三个区域引起顺向诱发群体峰电位的显著且可逆性抑制。在任何区域，逆向群体峰电位均未受到抑制，这表明轴突传导和电兴奋性均未受氨的影响。双脉冲试验显示在灌注早期存在短暂的去抑制。即使氨使突触诱发反应减弱，离子电渗法施加谷氨酸仍能诱发单位放电，这表明对假定递质的突触后敏感性未受抑制。兴奋性递质释放的抑制，可能是由于递质合成受阻后的耗竭，是这些发现的可能解释。有人提出，氨诱导的兴奋性传递抑制可能是高氨血症状态下昏迷和中枢神经系统抑制的其他症状的原因。
