Saiepour M Hadi, Rajendran Rajeev, Omrani Azar, Ma Wen-Pei, Tao Huizhong W, Heimel J Alexander, Levelt Christiaan N
Department of Molecular Visual Plasticity, The Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences (KNAW), Meibergdreef 47, 1105 BA Amsterdam, the Netherlands.
Zilkha Neurogenetic Institute, Department of Cell & Neurobiology, University of Southern California, 1501 San Pablo Street, ZNI 439, Los Angeles, CA 90033, USA.
Curr Biol. 2015 Mar 16;25(6):713-721. doi: 10.1016/j.cub.2015.01.024. Epub 2015 Mar 5.
To ensure that neuronal networks function in a stable fashion, neurons receive balanced inhibitory and excitatory inputs. In various brain regions, this balance has been found to change temporarily during plasticity. Whether changes in inhibition have an instructive or permissive role in plasticity remains unclear. Several studies have addressed this question using ocular dominance plasticity in the visual cortex as a model, but so far, it remains controversial whether changes in inhibition drive this form of plasticity by directly affecting eye-specific responses or through increasing the plasticity potential of excitatory connections.
We tested how three major classes of interneurons affect eye-specific responses in normally reared or monocularly deprived mice by optogenetically suppressing their activity. We find that in contrast to somatostatin-expressing or vasoactive intestinal polypeptide-expressing interneurons, parvalbumin (PV)-expressing interneurons strongly inhibit visual responses. In individual neurons of normal mice, inhibition and excitation driven by either eye are balanced, and suppressing PV interneurons does not alter ocular preference. Monocular deprivation disrupts the binocular balance of inhibition and excitation in individual neurons, causing suppression of PV interneurons to change their ocular preference. Importantly, however, these changes do not consistently favor responses to one of the eyes at the population level.
Monocular deprivation disrupts the binocular balance of inhibition and excitation of individual cells. This disbalance does not affect the overall expression of ocular dominance. Our data therefore support a permissive rather than an instructive role of inhibition in ocular dominance plasticity.
为确保神经网络以稳定的方式运作，神经元会接收平衡的抑制性和兴奋性输入。在各个脑区中，已发现这种平衡在可塑性过程中会暂时发生变化。抑制作用的变化在可塑性中是起指导性作用还是允许性作用仍不清楚。有几项研究以视觉皮层中的眼优势可塑性为模型来探讨这个问题，但到目前为止，抑制作用的变化是通过直接影响眼特异性反应还是通过增加兴奋性连接的可塑性潜能来驱动这种可塑性形式，仍存在争议。
我们通过光遗传学抑制三种主要类型的中间神经元的活性，测试了它们如何影响正常饲养或单眼剥夺小鼠的眼特异性反应。我们发现，与表达生长抑素或血管活性肠肽的中间神经元不同，表达小白蛋白（PV）的中间神经元强烈抑制视觉反应。在正常小鼠的单个神经元中，由任何一只眼睛驱动的抑制和兴奋是平衡的，抑制PV中间神经元不会改变眼偏好。单眼剥夺会破坏单个神经元中抑制和兴奋的双眼平衡，导致对PV中间神经元的抑制改变其眼偏好。然而，重要的是，在群体水平上，这些变化并不一致地有利于对其中一只眼睛的反应。
单眼剥夺会破坏单个细胞中抑制和兴奋的双眼平衡。这种失衡不会影响眼优势的整体表达。因此，我们的数据支持抑制在眼优势可塑性中起允许性作用而非指导性作用。
