Loss of sensory input from peripheral organ damage, sensory deprivation, or brain damage can result in adaptive or maladaptive changes in sensory cortex. In previous research, we found that auditory cortical tuning and tonotopy were impaired by cross-modal invasion of visual inputs. Sensory deprivation is typically associated with a loss of inhibition. To determine whether inhibitory plasticity is responsible for this process, we measured pre- and postsynaptic changes in inhibitory connectivity in ferret auditory cortex (AC) after cross-modal plasticity. We found that blocking GABAA receptors increased responsiveness and broadened sound frequency tuning in the cross-modal group more than in the normal group. Furthermore, expression levels of glutamic acid decarboxylase (GAD) protein were increased in the cross-modal group. We also found that blocking inhibition unmasked visual responses of some auditory neurons in cross-modal AC. Overall, our data suggest a role for increased inhibition in reducing the effectiveness of the abnormal visual inputs and argue that decreased inhibition is not responsible for compromised auditory cortical function after cross-modal invasion. Our findings imply that inhibitory plasticity may play a role in reorganizing sensory cortex after cross-modal invasion, suggesting clinical strategies for recovery after brain injury or sensory deprivation. 1. Introduction Loss of sensory drive as a result of deprivation or deafferentation can lead to a compensatory plastic reorganization of the affected sensory cortex. For example, a homeostatic downregulation of inhibition makes cortical neurons more sensitive to any remaining inputs (see [1], for review). Although the plastic response to the loss of drive can be limited to a single modality, sprouting of inputs responding to other sensory modalities into the deafferented area often results in cross-modal plasticity. For example, in deaf and blind subjects, the spared sensory cortex can be taken over by sensory inputs from other sensory modalities [2–4]. Such cross-modal inputs replace the lost inputs to some extent; thus the mechanisms of recovery might be different from recovery from manipulations affecting a single modality [5]. Because sensory inputs have been changed rather than lost entirely, the loss of inhibition seen after unimodal deprivation may be mitigated. It is important to understand whether cross-modal plasticity has similar or different effects on inhibition than within-modality plasticity because of the prevalence of cross-modal plasticity in patients suffering from
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