Regulation of glutamate release by presynaptic kainate receptors in the hippocampus
Regulation of glutamate release by presynaptic kainate receptors in the hippocampus
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DOI：
10.1038/379078a0
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发表时间：
1996-01-04
期刊：
影响因子：
64.8
通讯作者：
Henley, JM
中科院分区：
文献类型：
--
作者：
Chittajallu, R;Vignes, M;Henley, JM
大多数报道的海因酸盐的作用是由AMPA （α -氨基-3-羟基-5-甲基3-异唑烯丙酸）受体介导的（1,2）。在这里，我们报道，与AMPA刺激不同，海碱盐引起大鼠海马突触体中l -谷氨酸释放的剂量依赖性减少，并抑制谷氨酸能突触传递。短暂暴露于盐酸盐可抑制Ca2+依赖性[H-3] l -谷氨酸释放高达80%。kainate拮抗剂可逆转抑制作用，但ampa选择性非竞争性拮抗剂1-（4-氨基苯基）-4-甲基-7,8-亚甲二氧基- 5h -2,3-苯二氮卓（GYKI 52466）不能逆转抑制作用（3-7）。当GYKI 52466阻断AMPA受体时，观察到相应的可逆性海碱盐诱发的NMDA （n -甲基- d -天冬氨酸）受体介导的兴奋性突触后电流（e.p.s.cs）的抑制。突触抑制之前是短暂的增强释放，也观察到一个小的内向电流。代谢性谷氨酸（mGlu）、GABA(A)、GABA(B)、甘氨酸和腺苷受体拮抗剂不影响海因酸盐的作用。这些结果表明，盐酸盐自受体可以直接调节谷氨酸的释放。
MOST reported actions of kainate are mediated by AMPA (alpha-amino-3-hydroxy-5-methyl 3-isosazolepropionate) receptors(1,2). Here we report that, unlike AMPA which stimulates, kainate elicits a dose-dependent decrease in L-glutamate release from rat hippocampal synaptosomes and also depresses glutamatergic synaptic transmission. Brief exposure to kainate inhibited Ca2+-dependent [H-3]L-glutamate release by up to 80%. Inhibition was reversed by kainate antagonists but not by the AMPA-selective noncompetitive antagonist 1-(4-aminophenyl)-4-methyl-7,8-methylenedioxy-5H-2,3- benzodiazepine (GYKI 52466)(3-7). A corresponding reversible kainate-evoked depression of NMDA (N-methyl-D-aspartate) receptor-mediated excitatory postsynaptic currents (e.p.s.cs) was observed when AMPA receptors were blocked by GYKI 52466. The synaptic depression was preceded by a brief period of enhanced release and a small inward current was also observed. The effects of kainate were unaffected by metabotropic glutamate (mGlu), GABA(A), GABA(B), glycine and adenosine receptor antagonists. These results indicate that glutamate release can be modulated directly by kainate autoreceptors.