Mechanisms of reorganization in mouse superior colliculus after visual cortical lesions

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，该浅层神经元接收来自视网膜和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。在体内的细胞外记录显示，sSC神经元对大的视觉刺激的反应是短暂的减少约1周后，视觉皮层病变与正常小鼠相比，这种减少是部分恢复约1个月后的病变。为了研究这种减少的局部电路机制，我们进行了全细胞膜片钳记录从sSC神经元的切片制备从小鼠接受视觉皮层病变1周前的记录。我们发现兴奋和抑制之间的平衡的细胞类型依赖性的变化：在非GABA能细胞，抑制占主导地位的兴奋，而兴奋-抑制平衡没有改变GABA能神经元。这些结果表明，增强的抑制可能是部分负责在一些细胞中的大的视觉刺激的反应减少，并提高的可能性，增强的抑制可能会防止过度兴奋的sSC局部电路后不久，视觉皮层病变。

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 the V1. However, little is known about the changes in 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 recordings in vivo revealed that sSC neuronal responses to large visual stimuli were transiently reduced about 1 week after visual cortical lesions compared with normal mice and that this reduction was partially recovered about 1 month after the lesions. To investigate local circuit mechanisms underlying this reduction, we performed whole-cell patch-clamp recordings from sSC neurons in slice preparations obtained from mice that had received visual cortical lesions 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 cells and raise the possibility that the enhanced inhibition may prevent hyperexcitability in the sSC local circuit shortly after the visual cortical lesion.