Cortical influences on rapid brainstem plasticity.
Cortical contributions to brainstem plasticity in the somatosensory system are poorly understood. Tactile receptive fields (RFs) of brainstem dorsal column nuclei (DCN) neurons rapidly enlarge when peripheral inputs are disrupted by local anesthetic blocks with lidocaine (LID). Cortical inputs appear to influence this plasticity because enlargements have been shown to be greater when cortical inputs are disrupted. Like disruptions of peripheral inputs, disruptions of DCN inhibition by DCN administration of the GABAA receptor antagonist bicuculline methiodide (BMI) also cause rapid enlargements of DCN RFs when cortical inputs are intact. These findings leave questions about interactions between cortical inputs, DCN inhibition, and DCN RF plasticity. To study potential interactions, the present experiments evaluated RF sizes of DCN tactilely responsive neurons in anesthetized rats following DCN microinjection of BMI when cortical inputs were acutely disrupted or intact. These tests were also supplemented by subsequent LID tests to directly compare post-BMI and post-LID effects on the same RF. BMI caused DCN RF enlargements when cortical inputs were disrupted or intact; however, enlargements after cortical input disruption were greater than when cortical inputs were intact. Following RF enlargement and retraction after BMI, LID often caused a second enlargement of the same RF, across skin that partially matched skin involved in the enlargement after BMI. This occurred when cortical inputs were disrupted or intact. We hypothesize that cortical inputs are not required for BMI and LID to initiate partially matching enlargements in individual DCN tactile RFs, however, cortical inputs constrain magnitudes of these enlargements.