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Traumatic brain injury to primary visual cortex produces long-lasting circuit dysfunction

ABSTRACT: Primary sensory areas of the mammalian neocortex have a remarkable degree of plasticity, allowing neural circuits to adapt to dynamic environments. However, little is known about the effects of traumatic brain injury on visual circuit function. Here we used anatomy and in vivo electrophysiological recordings in adult mice to quantify neuron responses to visual stimuli two weeks and three months after mild controlled cortical impact injury to primary visual cortex (V1). We found that, although V1 remained largely intact in brain-injured mice, there was ~35% reduction in the number of neurons that affected inhibitory cells more broadly than excitatory neurons. V1 neurons showed dramatically reduced activity, impaired responses to visual stimuli and weaker size selectivity and orientation tuning in vivo. Our results show a single, mild contusion injury produces profound and long-lasting impairments in the way V1 neurons encode visual input. These findings provide initial insight into cortical circuit dysfunction following central visual system neurotrauma. Jan Frankowski and Andrzej Foik et al. characterized neuroanatomical, electrophysiological, and functional deficits in the primary visual cortex of mice after traumatic brain injury (TBI). Their results suggest that TBI produces long-lasting impairments to V1 neurons, and provide further insight into circuit dysfunction following injury of the visual cortex.

SUBMITTER: Frankowski J

PROVIDER: S-EPMC8599505 | biostudies-literature |

REPOSITORIES: biostudies-literature

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