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海马切片中突触诱发的内在光学信号成像。

Imaging of synaptically evoked intrinsic optical signals in hippocampal slices.

作者信息

MacVicar B A, Hochman D

机构信息

Neuroscience Research Group, University of Calgary, Alberta, Canada.

出版信息

J Neurosci. 1991 May;11(5):1458-69. doi: 10.1523/JNEUROSCI.11-05-01458.1991.

Abstract

Imaging analysis techniques were used to examine changes in the intrinsic optical properties in hippocampal brain slices that occurred during synaptic activity evoked by Schaffer collateral stimulation in CA1. Repetitive synaptic activity was associated with an increase in light transmission in the synaptic region in stratum radiatum. The effect was seen at wavelengths of light between 450 and 800 nm but was of greater amplitude at longer wavelengths. Blocking synaptic transmission with either Ca(2+)-free EGTA perfusate or kynurenic acid (an excitatory amino acid antagonist) blocked the optical signal, indicating that it resulted from postsynaptic activation of the cells and was not due to presynaptic fiber volleys or transmitter release alone. Because the optical changes were blocked by reducing extracellular Cl- (by replacement with gluconate) or by furosemide (an anion transport inhibitor), increased Cl- transport (conceivably Na-K-2Cl cotransport) may generate these signals possibly by causing cellular swelling and thereby less light scattering. These optical changes were not blocked, however, by bicarbonate-free solution, indicating that bicarbonate transport may not be involved. Changes in the intrinsic optical signal could be related to glial swelling due to K+ released during neuronal activity because high-K(+)-induced swelling of cultured astrocytes is blocked by furosemide and low-Cl- solution. Intrinsic optical signals of neuronal tissue should be considered when voltage- or ion-sensitive dyes are used.

摘要

采用成像分析技术检测在CA1区由Schaffer侧支刺激诱发的突触活动期间海马脑片内在光学特性的变化。重复性突触活动与辐射层突触区域光传输的增加相关。在450至800nm的光波长下可观察到该效应,但在较长波长下幅度更大。用无钙EGTA灌流液或犬尿喹啉酸(一种兴奋性氨基酸拮抗剂)阻断突触传递可阻断光信号,表明其源于细胞的突触后激活,而非仅由于突触前纤维冲动或递质释放。由于通过用葡萄糖酸盐替代来降低细胞外Cl-或用呋塞米(一种阴离子转运抑制剂)可阻断光学变化,因此增加的Cl-转运(可能是Na-K-2Cl协同转运)可能通过引起细胞肿胀从而减少光散射来产生这些信号。然而,无碳酸氢盐溶液并未阻断这些光学变化,表明碳酸氢盐转运可能未参与其中。内在光学信号的变化可能与神经元活动期间释放的K+导致的胶质细胞肿胀有关,因为呋塞米和低Cl-溶液可阻断高K+诱导的培养星形胶质细胞肿胀。当使用电压或离子敏感染料时应考虑神经元组织的内在光学信号。

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