Blockade of amino acid‐induced depolarizations and inhibition of excitatory post‐synaptic potentials in rat dentate gyrus.
Blockade of amino acid‐induced depolarizations and inhibition of excitatory post‐synaptic potentials in rat dentate gyrus.
复制标题
阻断氨基酸诱导的去极化和抑制大鼠齿状回兴奋性突触后电位。
DOI:
10.1113/jphysiol.1983.sp014829
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发表时间:
1983
期刊:
影响因子:
--
通讯作者:
J. Kelly
中科院分区:
文献类型:
--
作者:
V. Crunelli;S. Forda;J. Kelly
Excitatory post‐synaptic potentials (e.p.s.p.s) evoked by stimulation of the medial perforant path and depolarizations induced by excitatory amino acids were recorded from granule cells in the preparation of the hippocampal slice from the rat. The effects of (+/‐)‐2‐amino‐5‐phosphonovalerate (APV), gamma‐D‐glutamylglycine (gamma DGG) and cis‐2,3‐piperidinedicarboxylate (PDA), antagonists of excitatory amino acids on these phenomena were compared. gamma DGG was the most effective antagonist of the e.p.s.p. Its action was reversible and not associated with any change in the passive membrane properties of the granule cells or in the apparent reversal potential of the e.p.s.p. Quantal analysis showed that the reduction in the e.p.s.p. paralleled the decrease in quantal size rather than quantal content, confirming a post‐synaptic site of the action of gamma DGG. The potency of gamma DGG against the exogenous agonists was N‐methyl‐D‐aspartate greater than kainate greater than or equal to quisqualate. APV had very little effect on the e.p.s.p. but was a selective antagonist of N‐methyl‐D‐aspartate‐induced depolarizations. PDA depolarized granule cells and increased their membrane input resistance. Although gamma DGG was a potent antagonist of both glutamate‐ and aspartate‐induced depolarizations, no clear pattern of specificity could be found. The action of glutamate was unaffected by APV. These results indicate that the receptor for the transmitter at the synapses formed by the fibres of the perforant path with the granule cells is of the quisqualate and/or kainate type. The present data are consistent with the biochemical evidence that glutamate may be the endogenous transmitter at his synapse.
影响因子:
2.5
作者:
T. H. Brown;R. Fricke;D. Perkel
通讯作者:
T. H. Brown;R. Fricke;D. Perkel