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Spontaneous voltage oscillations in striatal projection neurons in a rat corticostriatal slice

机译:大鼠皮质纹状体切片中纹状体投射神经元的自发电压振荡

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摘要

In a rat corticostriatal slice, brief, suprathreshold, repetitive cortical stimulation evoked long-lasting plateau potentials in neostriatal neurons. Plateau potentials were often followed by spontaneous voltage transitions between two preferred membrane potentials. While the induction of plateau potentials was disrupted by non-NMDA and NMDA glutamate receptor antagonists, the maintenance of spontaneous voltage transitions was only blocked by NMDA receptor and L-type Ca2+ channel antagonists. The frequency and duration of depolarized events, resembling up-states described in vivo, were increased by NMDA and L-type Ca2+ channel agonists as well as by GABAA receptor and K+ channel antagonists. NMDA created a region of negative slope conductance and a positive slope crossing indicative of membrane bistability in the current–voltage relationship. NMDA-induced bistability was partially blocked by L-type Ca2+ channel antagonists. Although evoked by synaptic stimulation, plateau potentials and voltage oscillations could not be evoked by somatic current injection – suggesting a dendritic origin. These data show that NMDA and L-type Ca2+ conductances of spiny neurons are capable of rendering them bistable. This may help to support prolonged depolarizations and voltage oscillations under certain conditions.
机译:在大鼠皮层皮质片中,短暂,超阈值的重复皮层刺激引起新纹状体神经元的持久高原电位。高原电位之后通常是两个优选膜电位之间的自发电压跃迁。虽然非NMDA和NMDA谷氨酸受体拮抗剂破坏了高原电位的诱导,但自发电压转换的维持仅被NMDA受体和L型Ca 2 + 通道拮抗剂阻断。 NMDA和L型Ca 2 + 通道激动剂以及GABAA受体和K + 增加了类似于体内描述的上态状态的去极化事件的频率和持续时间。 sup>通道拮抗剂。 NMDA创建了一个负斜率电导和正斜率交叉的区域,该区域指示了电流-电压关系中的膜双稳性。 NMDA诱导的双稳态被L型Ca 2 + 通道拮抗剂部分阻断。尽管由突触刺激引起,但体细胞注射不能引起高原电位和电压振荡,这提示树突状起源。这些数据表明,棘突神经元的NMDA和L型Ca 2 + 电导能够使其呈双稳态。在某些情况下,这可能有助于支持长时间的去极化和电压振荡。

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