Long-Term Depression of Excitatory Synaptic Transmission in the Rat Amygdala
Long-Term Depression of Excitatory Synaptic Transmission in the Rat Amygdala
复制标题
大鼠杏仁核兴奋性突触传递的长期抑制
作者：
Su;P. Gean
鉴于点燃和恐惧增强惊吓都是通过杏仁核中突触传递的长期增强来表达的，大脑这一区域的突触可塑性特别重要。在这里，我们第一次表明，低频刺激外侧核在1 Hz的15分钟引起了一个长期的抑郁症（LTD）在基底外侧杏仁核（BLA）神经元。LTD特异性表达于外侧-BLA突触，但不表达于腹侧内杯状核-BLA突触。LTD的诱导需要NMDA和代谢型谷氨酸受体的激活。加载细胞与钙离子螯合剂BAPTA或细胞外灌流与蛋白磷酸酶抑制剂防止LTD，这表明LTD可能导致AMPA受体的去磷酸化。同样的刺激方案不能引起LTD的神经元点燃的动物，而神经元从假手术或年龄匹配的对照组大鼠能够表现出LTD。总之，本研究的特点LTD的性质首次在napoliparnave杏仁核切片，并表明癫痫在体内诱导破坏LTD的体外制备。
In view of the fact that both kindling and fear-potentiated startle are expressed by long-term enhancement of synaptic transmission in the amygdala, synaptic plasticity in this area of the brain is of particular importance. Here, we show for the first time that low-frequency stimulation of the lateral nucleus at 1 Hz for 15 min elicited a long-term depression (LTD) in the basolateral amygdala (BLA) neurons. LTD is expressed specifically at the lateral–BLA synapses but not at ventral endopyriform nucleus–BLA synapses. The induction of LTD requires activation of both NMDA and metabotropic glutamate receptors. Loading cells with a Ca2+ chelator BAPTA or extracellular superfusion with protein phosphatase inhibitors prevents LTD, suggesting that LTD may result from dephosphorylation of AMPA receptors. The same stimulating protocol could not elicit LTD in neurons from kindled animals, whereas neurons from sham-operated or age-matched control rats were able to exhibit LTD. Together, this study characterizes the properties of LTD in the naı̈ve amygdala slices for the first time and demonstrates that epileptogenesis in vivoinduces disruption of LTD in the in vitropreparation.
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大鼠脑 G 蛋白偶联谷氨酸受体的克隆、表达和基因结构
影响因子：
56.9
作者：
HOUAMED, KM;KUIJPER, JL;HAGEN, FS
通讯作者：
HAGEN, FS
影响因子：
56.9
作者：
MULKEY, RM;HERRON, CE;MALENKA, RC
通讯作者：
MALENKA, RC
点燃引起基底外侧杏仁核突触传递的持久变化。
影响因子：
2.5
作者：
Rainnie,DG;Asprodini,EK;Shinnick-Gallagher,P
通讯作者：
Shinnick-Gallagher,P
DOI：
10.1073/pnas.86.23.9574
发表时间：
1989-12-01
影响因子：
11.1
作者：
LISMAN, J
通讯作者：
LISMAN, J