Permanent receptor organ damage can cause plasticity of topographic cortical maps of that receptor surface while temporary receptor organ damage, and conditions mimicking such damage, can unmask new excitatory inputs in central sensory neurons receiving input from that receptor surface. Cortical plasticity is associated with an anatomically or pharmacologically defined decrease in inhibition in cortex. It is therefore widely proposed that a reduction incentral inhibition underlies cortical neural plasticity. Here I demonstrate that small receptor organ damage results, in primary auditory cortical (A1) neurons, in loss of one component of functionally defined afferent inhibition but unmasking of another component of afferent inhibition along with new excitatory responses. Overall, there did not appear to be any change in the strength of afferent inhibition or in the strength of excitation. Thus, auditory receptor organ damage can unmask new excitatory inputs as well as inhibitory inputs from within the receptive field of the neurons.
