Author:

Keywords:

Science & Technology, Life Sciences & Biomedicine, Anatomy & Morphology, Neurosciences, Neurosciences & Neurology, Adulthood, Cortical plasticity, Multimodal, Somatostatin interneurons, Optogenetic stimulation, Dark exposure, OCULAR DOMINANCE PLASTICITY, CROSS-MODAL PLASTICITY, TOPOGRAPHIC MAP REORGANIZATION, DENSE INHIBITORY CONNECTIVITY, EARLY GENE-EXPRESSION, SOMATOSENSORY CORTEX, NEURONAL-ACTIVITY, RETINAL LESIONS, AUDITORY-CORTEX, ADULT-MOUSE, Animals, Blindness, Channelrhodopsins, Disease Models, Animal, Early Growth Response Protein 1, Eye Enucleation, Female, Functional Laterality, Gene Expression Regulation, Interneurons, Male, Mice, Mice, Transgenic, Neuronal Plasticity, Optic Nerve, Optogenetics, Recovery of Function, Sensory Deprivation, Somatostatin, Vibrissae, Visual Cortex, 1109 Neurosciences, 1116 Medical Physiology, 1702 Cognitive Sciences, Developmental Biology, Neurology & Neurosurgery, 3208 Medical physiology, 3209 Neurosciences

Abstract:

Unilateral vision loss through monocular enucleation (ME) results in partial reallocation of visual cortical territory to another sense in adult mice. The functional recovery of the visual cortex occurs through a combination of spared-eye potentiation and cross-modal reactivation driven by whisker-related, somatosensory inputs. Brain region-specific intracortical inhibition was recently recognized as a crucial regulator of the cross-modal component, yet the contribution of specific inhibitory neuron subpopulations remains poorly understood. Somatostatin (SST)-interneurons are ideally located within the cortical circuit to modulate sensory integration. Here we demonstrate that optogenetic stimulation of visual cortex SST-interneurons prior to eye removal decreases ME-induced cross-modal recovery at the stimulation site. Our results suggest that SST-interneurons act as local hubs, which are able to control the influx and extent of cortical cross-modal inputs into the deprived cortex. These insights critically expand our understanding of SST-interneuron-specific regulation of cortical plasticity induced by sensory loss.