Kainate receptor-mediated heterosynaptic facilitation in the amygdala
Kainate receptor-mediated heterosynaptic facilitation in the amygdala
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DOI：
10.1038/88432
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发表时间：
2001-06-01
影响因子：
25
通讯作者：
Rogawski, MA
中科院分区：
文献类型：
--
作者：
Li, H;Chen, AQ;Rogawski, MA
长时间的低频刺激基底外侧杏仁核神经元的兴奋性传入导致兴奋性突触反应的持久增强。这种形式的突触可塑性的诱导被GluR5红藻氨酸受体的选择性拮抗剂消除，并且可以被GluR5激动剂ATPA模拟。红藻氨酸受体介导的突触易化概括为包括靶神经元上的非活性传入突触，因此与输入途径特异性的其他类型的活性依赖性持久突触易化形成对比。这种突触易化的异突触传播可以解释触发杏仁核依赖性行为反应的关键内部和外部刺激的适应性和病理性扩张。
Prolonged low-frequency stimulation of excitatory afferents to basolateral amygdala neurons results in enduring enhancement of excitatory synaptic responses. The induction of this form of synaptic plasticity is eliminated by selective antagonists of GluR5 kainate receptors and can be mimicked by the GluR5 agonist ATPA. Kainate receptor-mediated synaptic facilitation generalizes to include inactive afferent synapses on the target neurons, and therefore contrasts with other types of activity-dependent enduring synaptic facilitation that are input-pathway specific. Such heterosynaptic spread of synaptic facilitation could account for adaptive and pathological expansion in the set of critical internal and external stimuli that trigger amygdala-dependent behavioral responses.