Homeostatic synapse-driven membrane plasticity in nucleus accumbens neurons.
Homeostatic synapse-driven membrane plasticity in nucleus accumbens neurons.
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DOI：
10.1523/jneurosci.5703-08.2009
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发表时间：
2009-05-06
期刊：
影响因子：
--
通讯作者：
Dong Y
中科院分区：
文献类型：
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作者：
Ishikawa M;Mu P;Moyer JT;Wolf JA;Quock RM;Davies NM;Hu XT;Schlüter OM;Dong Y
稳定的大脑功能依赖于单个神经元功能输出的稳态维持。一般来说，神经元通过将突触输入转换为动作电位放电的输出来发挥作用。为了确定平衡这种输入-输出/突触-膜相互作用的稳态机制，我们专注于伏隔核（NAc）神经元，并证明了突触到膜稳态调节的一种新形式，即稳态突触驱动的膜可塑性（hSMP）。通过 hSMP，NAc 神经元调整其膜兴奋性，以在功能上补偿兴奋性突触输入的基础变化。此外，hSMP 由突触 N-甲基-D-天冬氨酸受体 (NMDAR) 触发，并通过 SK 型 Ca2+ 激活钾通道的修饰来表达。此外，在重复腹膜内注射可卡因（15 mg/kg/天，5天）的短期（2天）或长期（21天）戒断期间，NAc神经元中的hSMP被消除。这些结果表明 hSMP 是突触-膜稳态可塑性的一种新形式，hSMP 的失调可能导致可卡因诱导的 NAc 细胞改变。
Stable brain function relies on homeostatic maintenance of the functional output of individual neurons. In general, neurons function by converting synaptic input to output as action potential firing. To determine homeostatic mechanisms that balance this input-output/synapse-membrane interaction, we focused on nucleus accumbens (NAc) neurons and demonstrated a novel form of synapse-to-membrane homeostatic regulation, homeostatic synapse-driven membrane plasticity (hSMP). Through hSMP, NAc neurons adjusted their membrane excitability to functionally compensate for basal shifts in excitatory synaptic input. Furthermore, hSMP was triggered by synaptic N-methyl-D-aspartate receptors (NMDARs) and expressed by the modification of SK-type Ca2+-activated potassium channels. Moreover, hSMP in NAc neurons was abolished in rats during a short- (2 days) or long-term (21 days) withdrawal from repeated intraperitoneal injections of cocaine (15 mg/kg/day, 5 days). These results suggest that hSMP is a novel form of synapse-to-membrane homeostatic plasticity and dysregulation of hSMP may contribute to cocaine-induced cellular alterations in the NAc.