Lesions of basal forebrain cholinergic nuclei projecting to neocortex have recently been employed as an animal model for the cholinergic deficits in Alzheimer's desease. However, unlike Alzheimer's patients, whose deterioration appears to be progressive and irreversible, basalis lesioned rats usually recover both behaviorally and neurochemically within several months after the lesion. We now demonstrate that this recovery may be a function of the age of the rat and that cholinergic deficits re-occur in the aged rat. Choline acetyltransferase (ChAT) activity and [3H]hemicholinium-3 ([3H]HCh-3) binding are reduced in cortex ipsilateral to ibotenic acid lesions in the 12-month postlesion rat following an initial recovery to normal levels by about 3 months postlesion. The recurrence of decrease of cholinergic markers is not a consequence of a non-specific age-related decline since the activity of glutamic acid decarboxylase remains constant between 3 and 12 months postlesion.
- Aged rat
- Choline acetyltransferase, [H]Hemicholinium-3
- Glutamic acid decarboxylase
- Nucleus basalis magnocellularis (NBM) lesion
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