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低阈值钙离子通道介导小猫视觉皮层中长时程增强的诱导。

Low-threshold Ca2+ channels mediate induction of long-term potentiation in kitten visual cortex.

作者信息

Komatsu Y, Iwakiri M

机构信息

Department of Physiology, Kyoto Prefectural University of Medicine, Japan.

出版信息

J Neurophysiol. 1992 Feb;67(2):401-10. doi: 10.1152/jn.1992.67.2.401.

DOI:10.1152/jn.1992.67.2.401
PMID:1349036
Abstract
  1. The induction mechanism of long-term potentiation (LTP) in developing visual cortex was studied by recording intracellular responses from layer III-IV cells in slice preparations of kitten visual cortex at 30-40 days after birth. 2. Strong stimulation of white matter produced a late depolarizing response after an orthodromic action potential. This depolarizing response was abolished by membrane depolarization or hyperpolarization caused by current injection through the recording electrode. In addition, this response was reduced by bath application of a low concentration (100 microM) of Ni2+ without any changes in the rising slope of the excitatory postsynaptic potential (EPSP) or orthodromic action potential. This suggests that this response is mediated by low-threshold Ca2+ channels (LTCs). 3. The involvement of LTCs in the induction of LTP was tested. White matter was stimulated at 2 Hz for 15 min as a conditioning stimulus to induce LTP, and the resultant changes in EPSPs were tested by low-frequency (0.1 Hz) stimulation of white matter. Conditioning stimulation produced a large N-methyl-D-aspartate (NMDA) receptor-mediated depolarizing response in these cells, which obscured the presence of the late depoliarzation. Therefore the test was conducted in a solution containing an NMDA antagonist 2-amino-5-phosphonovalerate (APV). 4. Weak conditioning stimulation, which evoked no LTC responses, never induced LTP; whereas strong conditioning stimulation, which evoked LTC responses, always induced LTP. Strong conditioning stimulation failed to induce LTP when LTC responses were prevented either by membrane depolarization or hyperpolarization or by a bath application of 100 microM Ni2+. 5. In a solution without APV, the application of Ni2+ also prevented the induction of LTP. 6. When cells were impaled by an electrode containing a Ca2+ chelator 1,2-bis-(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), LTP was never induced, even though LTC responses were evoked by conditioning stimulation. These results indicate that Ca2+ influx into postsynaptic cells through LTCs induces the LTP. 7. The responses mediated by LTCs, which were evoked by the injection of current pulses into the cells, were maximum at the critical period of visual cortical plasticity, suggesting that LTCs in postsynaptic cells regulate the plastic changes in developing visual cortex.
摘要
  1. 通过记录出生后30 - 40天小猫视觉皮层切片标本中III - IV层细胞的细胞内反应,研究了发育中视觉皮层长期增强(LTP)的诱导机制。2. 对白质的强刺激在顺向动作电位后产生了晚期去极化反应。这种去极化反应可通过经记录电极注入电流引起的膜去极化或超极化而消除。此外,通过浴加低浓度(100微摩尔)的Ni2 +可使该反应减弱,而兴奋性突触后电位(EPSP)或顺向动作电位的上升斜率无任何变化。这表明该反应是由低阈值Ca2 +通道(LTCs)介导的。3. 测试了LTCs在LTP诱导中的作用。以2赫兹刺激白质15分钟作为条件刺激来诱导LTP,然后通过对白质的低频(0.1赫兹)刺激来测试EPSP的变化。条件刺激在这些细胞中产生了大量N - 甲基 - D - 天冬氨酸(NMDA)受体介导的去极化反应,这掩盖了晚期去极化的存在。因此,测试在含有NMDA拮抗剂2 - 氨基 - 5 - 磷酸戊酸(APV)的溶液中进行。4. 未引发LTC反应的弱条件刺激从未诱导出LTP;而引发LTC反应的强条件刺激总是能诱导出LTP。当通过膜去极化或超极化或浴加100微摩尔Ni2 +阻止LTC反应时,强条件刺激未能诱导出LTP。5. 在没有APV的溶液中,施加Ni2 +也能阻止LTP的诱导。6. 当用含有Ca2 +螯合剂1,2 - 双 -(邻氨基苯氧基)乙烷 - N,N,N',N' - 四乙酸(BAPTA)的电极刺入细胞时,即使条件刺激引发了LTC反应,也从未诱导出LTP。这些结果表明,Ca2 +通过LTCs流入突触后细胞诱导了LTP。7. 通过向细胞内注入电流脉冲引发的由LTCs介导的反应,在视觉皮层可塑性的关键期达到最大值,这表明突触后细胞中的LTCs调节发育中视觉皮层的可塑性变化。

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