Regulation of the rebound depolarization and spontaneous firing patterns of deep nuclear neurons in slices of rat cerebellum
Regulation of the rebound depolarization and spontaneous firing patterns of deep nuclear neurons in slices of rat cerebellum
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DOI：
10.1152/jn.1999.82.4.1697
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发表时间：
1999-10-01
影响因子：
2.5
通讯作者：
Linden, DJ
中科院分区：
文献类型：
--
作者：
Aizenman, CD;Linden, DJ
电流钳记录从12至15日龄大鼠的小脑深核（DCN），以了解介导的内在自发放电模式的因素。所有记录的细胞都是自发活动的，其尖峰模式从规则尖峰到自发爆发，前者占主导地位。在超极化电流注入的偏移后，引起了一个强大的反弹去极化（RD），导致Na+尖峰爆发。RD的电压和时间依赖性与低阈值电压门控Ca 2+通道的介导一致。此外，RD的诱导也可能受到超极化激活的阳离子电流I-h的激活的影响。刺激浦肯野细胞轴突诱发的抑制性突触后电位（IPSPs）的短暂高频爆发后，可以有效地诱发RD。IPSP驱动的RD通常比由幅度和持续时间近似匹配的直接超极化脉冲引起的RD大得多且长得多。细胞内灌注Ca ~（2+）缓冲液双-（邻氨基苯氧基）-N，N，N '，N'-四乙酸（BAPTA）显著增强RD及其相关的尖峰，有时导致持续数百毫秒的平台电位。BAPTA的作用可以部分地通过应用apamin来模拟。一种小电导钙门控钾通道的阻滞剂，但不能被paxilline阻断，paxilline阻断大电导钙门控钾通道。应用BAPTA和apamin，而不是paxilline，导致细胞定期尖峰自发爆裂。综上所述，我们的数据表明，有一个强大的DCN细胞之间的关系，以引起RD和他们的倾向自发爆发的能力。RD可以通过T型Ca 2+通道的开放触发，并具有超极化激活电流I-h的额外贡献。RD持续时间由小电导Ca 2+门控K+通道调节。RD也由抑制性输入进行紧张性调制。所有这些因素反过来又受到外部调节性神经递质的改变，并且至少部分地负责确定DCN神经元的放电模式。
Current-clamp recordings were made from the deep cerebellar nuclei (DCN) of 12- to 15-day-old rats to understand the factors that mediate intrinsic spontaneous firing patterns. All of the cells recorded were spontaneously active with spiking patterns ranging continuously from regular spiking to spontaneous bursting with the former predominating. A robust rebound depolarization (RD) leading to a Na+ spike burst was elicited after the offset of hyperpolarizing current injection. The voltage and time dependence of the RD was consistent with mediation by low-threshold voltage-gated Ca2+ channels. Tn addition, induction of a RD also may be affected by activation of a hyperpolarization-activated cation current, I-h. A RD could be evoked efficiently after brief high-frequency bursts of inhibitory postsynaptic potentials (IPSPs) induced by stimulation of Purkinje cell axons. IPSP-driven RDs were typically much larger and longer than those elicited by direct hyperpolarizing pulses of approximately matched amplitude and duration. Intracellular perfusion of the Ca2+ buffer bis-(o-aminophenoxy)-N,N,N',N'-terraacetic acid (BAPTA) dramatically enhanced the RD and its associated spiking, sometimes leading to a plateau potential that lasted several hundred milliseconds. The effects of BAPTA could be mimicked partly by application of apamin. a blocker of small conductance Ca2+-gated K+ channels, but not by paxilline, which blocks large conductance Ca2+-gated K+ channels. Application of both BAPTA and apamin, but not paxilline, caused cells that were regularly spiking to burst spontaneously. Taken together, our data suggest that there is a strong relationship between the ability of DCN cells to elicit a RD and their tendency burst spontaneously. The RD can be triggered by the opening of T-type Ca2+ channels with an additional contribution of hyperpolarization-activated current I-h. RD duration is regulated by small-conductance Ca2+-gated K+ channels. The RD also is modulated tonically by inhibitory inputs. All of these factors are in turn subject to alteration by extrinsic modulatory neurotransmitters and are, at least in part, responsible for determining the firing modes of DCN neurons.