Light exposure induces short- and long-term changes in the excitability of retinorecipient neurons in suprachiasmatic nucleus
Light exposure induces short- and long-term changes in the excitability of retinorecipient neurons in suprachiasmatic nucleus
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DOI：
10.1152/jn.00060.2011
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发表时间：
2011-08-01
影响因子：
2.5
通讯作者：
Witkovsky, Paul
中科院分区：
文献类型：
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作者：
LeSauter, Joseph;Silver, Rae;Witkovsky, Paul
LeSauter J，Silver R，Cloues R，Witkovsky P。光暴露会引起视交叉上核视网膜受体神经元兴奋性的短期和长期变化。 J Neurophysiol 106: 576-588, 2011。首次发表于 2011 年 5 月 18 日； doi:10.1152/jn.00060.2011.-视交叉上核 (SCN) 是下丘脑生物钟的所在地，可将生理和行为反应与每日明暗周期同步。细胞核由功能和肽能不同的细胞群组成，其独特的电化学特性在很大程度上尚未被研究。含有胃泌素释放肽（GRP）的 SCN 神经元通过视网膜下丘脑束接收直接视网膜输入。我们用绿色荧光蛋白 (GFP) 标记物靶向 GRP 神经元，进行全细胞膜片钳。在这些神经元中，我们研究了熄灯后 2 小时 [Zeitgeber 时间 (ZT) 14:00-15:00] 给予 1 小时光脉冲 (LP) 对膜电位和尖峰放电的短期（0.5-1.5 小时）和长期（2-6 小时）影响。在从暴露于光的动物身上采集的脑切片中，细胞去极化，并且在 ZT 15:30 和 16:30 之间尖峰放电率增加。在 ZT 17:00 左右开始的随后 4 小时内，来自受光动物的 GRP 神经元超极化约 15 mV。在未暴露于光的动物的 GRP 神经元或紧邻的非 GRP 神经元中，无论是否暴露于光，均未观察到这些效应。 GRP 神经元的去极化与 GABA(A) 依赖性突触噪声的减少相关，而超极化则伴随着 GABA(A) 驱动的丧失和主要由 Na 携带的 TTX 抗性漏电流的抑制。这表明，在 SCN 中，暴露于光可能会引起由视网膜神经递质和神经肽介导的 GRP 神经元兴奋性的短期增加，随后由于漏电流的抑制而导致长期的膜超极化，这可能是由基因组信号引起的。
LeSauter J, Silver R, Cloues R, Witkovsky P. Light exposure induces short- and long-term changes in the excitability of retinorecipient neurons in suprachiasmatic nucleus. J Neurophysiol 106: 576-588, 2011. First published May 18, 2011; doi:10.1152/jn.00060.2011.-The suprachiasmatic nucleus (SCN) is the locus of a hypothalamic circadian clock that synchronizes physiological and behavioral responses to the daily light-dark cycle. The nucleus is composed of functionally and peptidergically diverse populations of cells for which distinct electrochemical properties are largely unstudied. SCN neurons containing gastrin-releasing peptide (GRP) receive direct retinal input via the retinohypothalamic tract. We targeted GRP neurons with a green fluorescent protein (GFP) marker for whole cell patch-clamping. In these neurons, we studied short (0.5-1.5 h)- and long-term (2-6 h) effects of a 1-h light pulse (LP) given 2 h after lights off [Zeitgeber time (ZT) 14:00-15:00] on membrane potential and spike firing. In brain slices taken from light-exposed animals, cells were depolarized, and spike firing rate increased between ZT 15:30 and 16:30. During a subsequent 4-h period beginning around ZT 17:00, GRP neurons from light-exposed animals were hyperpolarized by similar to 15 mV. None of these effects was observed in GRP neurons from animals not exposed to light or in immediately adjacent non-GRP neurons whether or not exposed to light. Depolarization of GRP neurons was associated with a reduction in GABA(A)-dependent synaptic noise, whereas hyperpolarization was accompanied both by a loss of GABA(A) drive and suppression of a TTX-resistant leakage current carried primarily by Na. This suggests that, in the SCN, exposure to light may induce a short-term increase in GRP neuron excitability mediated by retinal neurotransmitters and neuropeptides, followed by long-term membrane hyperpolarization resulting from suppression of a leakage current, possibly resulting from genomic signals.