Mechanisms of reorganization in mouse superior colliculus after visual cortical lesions

许多研究已经研究了初级视觉皮质(V1)损伤对上丘(SSC)浅层神经元视觉反应的影响，SSC接受来自视网膜和V1的视觉信息。然而，对于接受V1损毁后SSc局部回路动力学的变化知之甚少。在这里，我们表明，在小鼠的V1损伤后，SSC神经元的周围抑制被瞬时增强，这种增强可能归因于SSC神经元兴奋性和抑制性输入之间的平衡的改变。活体细胞外记录显示，与正常小鼠相比，视皮质损伤后约1周，SSc神经元对大的视觉刺激的反应一过性降低，并在损伤后约1个月部分恢复。为了研究这种减少的局部电路机制，我们对SSC神经元进行了全细胞膜片钳记录，这些记录来自于在记录前一周接受视觉皮质损伤的小鼠的切片准备。我们发现兴奋和抑制之间的平衡随细胞类型的变化而变化：在非GABA能细胞中，抑制占主导地位，而在GABA能神经元中，兴奋-抑制平衡没有改变。这些结果表明，增强的抑制作用可能是某些细胞对大的视觉刺激的反应减弱的部分原因，并增加了增强的抑制作用可能在视觉皮质损伤后不久阻止SSC局部回路的过度兴奋性的可能性。

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.