Sustained cortical metabolic responsivity to physostigmine after nucleus basalis magnocellularis ablation in rats.

Unilateral nucleus basalis magnocellularis (NBM) ablation, which causes partial cholinergic denervation of the ipsilateral anterior neocortex, results in an acute but transient depression of regional cerebral metabolic rates for glucose (rCMRglc) in deafferented areas; rCMRglc normalizes within 2 weeks. To seek possible compensatory changes in cholinergic mechanisms following NBM ablation that could lead to rapid metabolic normalization, we studied rCMRglc responses to the receptor agonists nicotine and arecoline and the cholinesterase inhibitor physostigmine in rats at 2 weeks after unilateral NBM destruction. Physostigmine increased rCMRglc in 10 of 30 cortical areas contralateral to the NBM lesion. Compared to the unlesioned side, rCMRglc after physostigmine in the lesioned cortex was significantly lower in 2, significantly higher in 1 and not different (P < 0.05) in 27 areas. Neither arecoline nor nicotine treatment produced rCMRglc asymmetry in lesioned rats. These results demonstrate that responsivity to physostigmine is maintained in most regions of the rat neocortex after extrinsic cholinergic denervation by NBM ablation. This adaptive response appears not to result from cholinergic receptor upregulation and may reflect instead reorganization of cholinergic synapses.