RESUMEN
Excitotoxin lesion of the nucleus basalis of the rat causes a substantial reduction in the K+-evoked release of [3H]acetylcholine (ACh) from tissue slices of ipsilateral frontal and parietal cortex. Decreases in the K+-evoked release of [3H]ACh (nCi/mg protein) of 71% and 47% are seen 21 days after lesion in the frontal and parietal cortex respectively. However, in later periods a considerable reversal of this deficit occurred which was complete in parietal cortex at 102 days, when the K+-evoked release of [3H]ACh was not significantly different from the controls. In the frontal cortex where a greater decrease in acetylcholinesterase (AChE) is obtained, a similar but attenuated reversal occurred, the K+-evoked release of [3H]ACh reaching 75% of the control value at 128 days after lesion. The compensatory changes in [3H]ACh release were paralleled by changes in AChE in both regions. Despite the reduced level of release following lesion, the K+-evoked release of [3H]ACh was responsive to the inhibitory effect of the cholinergic agonist, oxotremorine. Lesions outside the nucleus basalis produced no changes in the release of [3H]ACh from frontal or parietal cortex. All lesions were verified histologically. The compensatory changes reported are discussed in terms of the growth of 'sprouts' from the spared cholinergic axons. This study clearly demonstrates that compensatory changes in complex systems such as transmitter release which markedly affect cholinergic function do occur in response to lesion in common with other presynaptic parameters.