Within the past two decades, our meager understanding of how the adult brain can change has grown exponentially. The accessibility of somotosensory cortical areas and the highly reliable central representation of the body surface have provided a particularly fertile model by which to study adult neural plasticity. Manipulations of afferent stimulation patterns are accompanied by (now) predictable alterations in the topographic representation of the dermal surface. It is likely that many of the mechanisms by which somatosensory areas """"""""learn"""""""" new responses after nerve injury are evolutionarily conserved in other brain areas as well. These changes can be beneficial or detrimental in nature and may manifest themselves as the ability to consolidate memory, or in the progression of a pathological disease. While injury induced reorganization in the somatosensory cortex has been extensively studied the mechanisms responsible for cortical plasticity have not been fully elucidated. In the present application, it is proposed that the neurochemical changes that occur during cortical reorganization be monitored and then compared to any neurochemical changes that might occur in response to deprivation alone. Such a subtractive analysis permits the identification of the neurochemical changes that are causal and those that are epiphenomenal.
