SCOPOLAMINE FACILITATES RECOVERY OF FUNCTION FOLLOWING UNILATERAL ELECTROLYTIC SENSORIMOTOR CORTEX LESIONS IN THE RAT

Following brain injury there is an excessive release of excitatory neu rotransmitters that may lead to secondary cell death. Although much re search has focused on glutamate-NMDA receptor interactions, acetylchol ine-muscarinic receptor interactions may also prove to be important fo r an understanding of the pathophysiological events that lead to secon dary degeneration after brain damage. Previous experiments have shown that the muscarinic receptor antagonist scopolamine facilitates recove ry from very transient (1 h-10 days) behavioral deficits after fluid p ercussion injury. The present study extends these findings by investig ating whether scopolamine can facilitate recovery from the more enduri ng behavioral deficits (14-60 days) that follow electrolytic lesions o f the rat somatic sensorimotor cortex (SMC). Rats received unilateral lesions of the SMC and a regimen of scopolamine (1 mg/kg) or saline be ginning 15 min after surgery. Following SMC lesions rats exhibited an impairment in placing the forelimb contralateral to the lesion as well as an ipsilateral somatosensory asymmetry on a bilateral tactile stim ulation test. Rats treated with scopolamine showed a reduction in the initial magnitude of the contralateral placing deficit and an accelera ted rate of recovery compared with saline-treated control rats. In con trast, scopolamine had no effect on recovery from the ipsilateral soma tosensory asymmetry. These data are consistent with the idea that musc arinic receptor stimulation plays a role in the production of secondar y brain damage, that blockade of this receptor leads to a facilitation of recovery on some behavioral tasks, and that electrolytic lesions m ay trigger some of the same posttraumatic events described in other mo dels of neural trauma.