Transient enhancement of inhibition following visual cortical lesions in the mouse superior colliculus.

Transient enhancement of inhibition following visual cortical lesions in the mouse superior colliculus.
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小鼠上丘视觉皮质损伤后抑制作用短暂增强。

DOI:
10.1111/j.1460-9568.2012.08224.x
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发表时间:
2012
影响因子:
3.4
通讯作者:
Kaneda K
Kaneda K
中科院分区:
医学3区
文献类型:
--
作者:
稲吉晃;長田 重一;Kaneda K

文献摘要

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许多研究已经调查了初级视皮层(V1)病变对上级丘(sSC)浅层神经元视觉反应的影响,sSC接收来自视网膜和V1的视觉信息。然而,很少有人知道的变化后,接受V1病变的sSC的局部电路动力学。在这里,我们发现,周围的抑制sSC神经元是短暂增强V1病变小鼠,这种增强可能是由于兴奋性和抑制性输入之间的平衡改变sSC神经元。 与正常小鼠相比,在视觉皮层损伤后约1周,sSC神经元对大的视觉刺激的反应短暂减少,并且这种减少在损伤后约1个月时部分恢复。  通过使用从记录前1周接受视觉皮层损伤的小鼠获得的切片制备物中sSC神经元的全细胞膜片钳记录,我们发现兴奋和抑制之间平衡的细胞类型依赖性变化。 在非GABA能细胞中,抑制作用优于兴奋作用,而在GABA能神经元中,兴奋-抑制平衡没有改变。这些结果表明,增强的抑制可能是部分负责减少一些sSC神经元对大的视觉刺激的反应。因此,我们建议,增强环绕抑制视觉皮层病变后不久,可能会防止超兴奋性的sSC本地电路,有助于重建微调的感受野组织的sSC神经元视觉皮层病变后。
Numerous studies have investigated the effects of lesions of the primary visual cortex (V1) on visual responses in neurons of the superficial layer of the superior colliculus (sSC), which receives visual information from both the retina and V1. However, little is known about the changes in the local circuit dynamics of the sSC after receiving V1 lesions. Here, we show that surround inhibition of sSC neurons is transiently enhanced following V1 lesions in mice and that this enhancement may be attributed to alterations in the balance between excitatory and inhibitory inputs to sSC neurons. Extracellular recordingsin vivorevealed that sSC neuronal responses to large visual stimuli were transiently reduced at about 1 week after visual cortical lesions compared with normal mice and that this reduction was partially recovered at about 1 month after the lesions. By using whole‐cell patch‐clamp recordings from sSC neurons in slice preparations obtained from mice that had received visual cortical lesions at 1 week prior to the recordings, we found cell type‐dependent changes in the balance between excitation and inhibition. In non‐GABAergic cells, inhibition predominated over excitation, whereas the excitation–inhibition balance did not change in GABAergic neurons. These results suggest that enhanced inhibition may be partially responsible for the reduced responses to large visual stimuli in some sSC neurons. Thus, we propose that the enhanced surround inhibition shortly after visual cortical lesions may prevent hyperexcitability in the sSC local circuit, contributing to reconstructing the finely tuned receptive field organization of sSC neurons after the visual cortical lesions.