Glutamate receptors regulate actin-based plasticity in dendritic spines
Glutamate receptors regulate actin-based plasticity in dendritic spines
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DOI：
10.1038/78791
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发表时间：
2000-09-01
影响因子：
25
通讯作者：
Matus, A
中科院分区：
文献类型：
--
作者：
Fischer, M;Kaech, S;Matus, A
兴奋性突触处的树突棘经历快速的、肌动蛋白依赖的形状变化，这可能有助于脑回路的可塑性。在这里，我们表明，肌动蛋白动力学的棘被有效地抑制AMPA或NMDA亚型谷氨酸受体的激活。任一受体类型的激活抑制肌动蛋白为基础的从脊椎头部的扩张活动。这种运动性的阻断导致脊柱变圆，使得脊柱形态变得更加稳定和规则。AMPA受体对脊髓运动的抑制依赖于突触后膜去极化和通过电压激活通道的Ca 2+内流。结合以前的研究，我们的研究结果表明，一个两步的过程中，棘最初形成响应于NMDA受体激活，随后由AMPA受体稳定。
Dendritic spines at excitatory synapses undergo rapid, actin-dependent shape changes which may contribute to plasticity in brain circuits. Here we show that actin dynamics in spines are potently inhibited by activation of either AMPA or NMDA subtype glutamate receptors. Activation of either receptor type inhibited actin-based protrusive activity from the spine head. This blockade of motility caused spines to round up so that spine morphology became both more stable and more regular. Inhibition of spine motility by AMPA receptors was dependent on postsynaptic membrane depolarization and influx of Ca2+ through voltage-activated channels. In combination with previous studies, our results suggest a two-step process in which spines initially formed in response to NMDA receptor activation are subsequently stabilized by AMPA receptors.