Plasticity of excitation and inhibition in the receptive field of primary auditory cortical neurons after limited receptor organ damage

Permanent receptor organ damage can cause plasticity of topographic cortica l maps of that receptor surface white temporary receptor organ damage, and conditions mimicking such damage, can unmask new excitatory inputs in centr al sensory neurons receiving input from that receptor surface. Cortical pla sticity is associated with an anatomically or pharmacologically defined dec rease in inhibition in cortex. It is therefore widely proposed that a reduc tion in central inhibition underlies cortical neural plasticity. Here I dem onstrate that small receptor organ damage results, in primary auditory cort ical (A1) neurons, in loss of one component of functionally defined afferen t inhibition but unmasking of another component of afferent inhibition alon g with new excitatory responses. Overall, there did not appear to be any ch ange in the strength of afferent inhibition or in the strength of excitatio n. Thus, auditory receptor organ damage can unmask new excitatory inputs as well as inhibitory inputs from within the receptive field of the neurons.