Cumulative effects of glutamate microstimulation on Ca(2+) responses of CA1 hippocampal pyramidal neurons in slice.
Cumulative effects of glutamate microstimulation on Ca(2+) responses of CA1 hippocampal pyramidal neurons in slice.
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谷氨酸微刺激对切片中 CA1 海马锥体神经元 Ca(2) 反应的累积影响。
DOI：
10.1152/jn.2000.83.1.90
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发表时间：
2000
期刊：
影响因子：
--
通讯作者：
Cormier,RJ
中科院分区：
文献类型：
--
作者：
Connor,JA;Cormier,RJ
采用微电极离子导入谷氨酸刺激脑片海马CA 1区神经元。施加5个脉冲（15 μA，10 s持续时间，以1 min间隔重复），电极尖端位于放射层中，靠近充满Ca 2+指示剂fura-2的神经元的树突。一个单一的刺激组产生的Ca 2+升高，范围从几百nM到几μM，在所有，但少数神经元，恢复1分钟内的刺激终止。随后相同的刺激产生的Ca 2+升高持续了几分钟的局部谷氨酸盐升高，判断在相邻细胞或同一神经元的其他部分的响应恢复。这些长的反应最终恢复，但持续长达10分钟，并在中间和远端树突最突出。对于扩散至索马的应答，未观察到恢复。升高的Ca 2+水平伴随着膜去极化，但似乎并不依赖于去极化。高分辨率图像显示仅涉及几μm树突的响应区域。我们的研究结果证实了先前从分离的和细胞培养的神经元中的一般发现，即谷氨酸刺激，如果超过一定范围，会导致持久的Ca 2+升高。在成熟的原位神经元的反应特点是显着不同的时间过程和可逆性。我们认为，延长Ca 2+升高可能不仅作为延迟性神经元死亡的触发器，但在更多的空间限制，作为局部树突重塑的信号。
Glutamate stimulation of hippocampal CA1 neurons in slice was delivered via iontophoresis from a microelectrode. Five pulses (∼5 μA, 10 s duration, repeated at 1 min intervals) were applied with the electrode tip positioned in the stratum radiatum near the dendrites of a neuron filled with the Ca2+indicator fura-2. A single stimulus set produced Ca2+elevations that ranged from several hundred nM to several μM and that, in all but a few neurons, recovered within 1 min of stimulus termination. Subsequent identical stimulation produced Ca2+elevations that outlasted the local glutamate elevations by several minutes as judged by response recoveries in neighboring cells or in other parts of the same neuron. These long responses ultimately recovered but persisted for up to 10 min and were most prominent in the mid and distal dendrites. Recovery was not observed for responses that spread to the soma. The elevated Ca2+levels were accompanied by membrane depolarization but did not appear to depend on the depolarization. High-resolution images demonstrated responsive areas that involved only a few μm of dendrite. Our results confirm the previous general findings from isolated and cell culture neurons that glutamate stimulation, if carried beyond a certain range, results in long-lasting Ca2+elevation. The response characterized here in mature in situ neurons was significantly different in terms of time course and reversibility. We suggest that the extended Ca2+elevations might serve not only as a trigger for delayed neuron death but, where more spatially restricted, as a signal for local remodeling in dendrites.
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影响因子：
4.7
作者：
A. Mitani;Y. Andou;S. Matsuda;T. Arai;M. Sakanaka;K. Kataoka
通讯作者：
A. Mitani;Y. Andou;S. Matsuda;T. Arai;M. Sakanaka;K. Kataoka
青年和老年时兴奋毒素介导的神经元死亡。
影响因子：
--
作者：
Olney,JW
通讯作者：
Olney,JW
缺血诱导的 Ca2+/钙调蛋白依赖性蛋白激酶 II 易位：在神经元损伤中的潜在作用
影响因子：
4.7
作者：
J. Aronowski;J. Grotta;M. Waxham
通讯作者：
M. Waxham
影响因子：
56.9
作者：
Wang, HG;Pathan, N;Reed, JC
通讯作者：
Reed, JC
影响因子：
8.3
作者：
HATAKEYAMA, T;MATSUMOTO, M;YANAGIHARA, T
通讯作者：
YANAGIHARA, T