MECHANISMS OF DAMAGE-INDUCED CORTICAL PLASTICITY

点击翻译按钮获取中文摘要

Representations of the body surface in the brain, including those of craniofacial structures, an change rapidly as a function of peripheral damage or experience. Experiments in the trigeminal system have demonstrated that destruction of a portion of the vibrissae follicles or loss of normal functional input from them results in expansion of the representations of the unaltered whispers in the primary somatosensory cortex (S-I). While rapid reorganization of cortical maps appears often after peripheral damage or deafferentation there appear to be distinct spatial limits to these changes. These limits may be particularly relevant in the rodent cortex where different portions of the body (face, forelimb, hindlimb) are represented in distinct histologically and cytochemically demonstrable compartments. Thus, it is important to understand, particularly in the context of this Program Project, whether "rules" for experience-induced cortical reorganization based on results derived from studies of changes within a given compartment (the craniofacial representation) also apply across compartments. During the previous funding period, we showed that neonatal amputation of the forelimb results in subcortical anatomical and functional reorganization in the brainstem and thalamus that is only expressed in the S-I when gamma- aminobutyric acid (GABA) receptors are blocked. The hey feature of the functional reorganization observed subcortically and in the cortex after GABA receptor blockade is neurons with receptive fields that include both the forelimb stump and the hindlimb (split Rfs) in regions where only the forelimb would normally be represented. The overall goal of the experiments in this application is to answer four questions regarding both the reorganization and cortical suppression of sensory information observed after neonatal forelimb removal in the rat: 1) What are the substrates for the split Rfs expressed by S-I neurons after GABA receptor blockade in neonatally amputated rats? 2) What is the mechanism underlying suppression of hindlimb information in the cortices of neonatally amputated animals? 3) What are the necessary conditions for development of neurons with split Rfs in S-I of neonatally amputated rats? 4) What are the necessary conditions for the functional suppression of split Rfs? We will employ a wide range of both physiological and anatomical methods to answer all of these questions.