Inhibition of transmitter release and long-term depression in the avian hippocampus

被引:4
作者
Margrie, TW
Rostas, JAP
Sah, P
机构
[1] Australian Natl Univ, John Curtin Sch Med Res, Div Neurosci, Canberra, ACT 2601, Australia
[2] Univ Newcastle, Fac Med & Hlth Sci, Neurosci Grp, Callaghan, NSW 2308, Australia
基金
英国医学研究理事会;
关键词
long-term depression; transmitter release; protein kinase; gamma-aminobutyric acids;
D O I
10.1016/S0304-3940(00)00992-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Long-term depression has recently been shown to occur at glutamatergic synapses in the avian hippocampus and requires activation of calcium/calmodulin-dependent protein kinase II in the nerve terminal. Here using whole cell and intracellular recordings from brain slices, we show that the N-type calcium channel contributes significantly to glutamate release in the avian hippocampus. Activation of the metabotrobic gamma-aminobutyric acid (GABA)(B) receptor by the specific agonist baclofen blocks synaptic transmission. The action of baclofen was associated with a change in paired pulse facilitation indicating that it resulted from a reduction in the probability of transmitter release, In contrast, no change in paired pulse facilitation was observed following the induction of long-term depression. These results show that activation of GABA(B) receptors and long-term depression reduce transmitter release by distinct mechanisms. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:17 / 20
页数:4
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