Neuronal mechanisms underlying transhemispheric diaschisis following focal cortical injuries

Abstract

Unilateral cortical lesions cause disturbances often spreading into the hemisphere contralateral to the injury. The functional alteration affecting the contralesional cortex is called transhemispheric diaschisis and is believed to contribute to neurological deficits and to processes of functional reorganization post-lesion. Despite the profound implications for recovery, little is known about the cellular mechanisms that underlie this phenomenon. In the present study, transhemispheric diaschisis was investigated with an in vivo-ex vivo model of unilateral lesions, induced by an infrared laser in rat visual cortex. Visually evoked cortical activity was evaluated by the expression level of the cellular activity marker zif268, which showed an elevation in the cortex contralateral to the lesion. In vitro patch-clamp recordings from layer 2/3 pyramidal neurons revealed a shift in the excitatory–inhibitory balance in favor of excitability, particularly expressed in the undamaged hemisphere. Layer 5 principal neurons displayed an increased spontaneous firing rate contralateral to the lesion, while cells of the injured cortex displayed a reduced firing upon somatic current injection. These data suggest that a cortical lesion triggers an enhanced neuronal activity in the hemisphere contralateral to the damage. Our findings constitute an important step toward the understanding of transhemispheric diaschisis on the cellular level.