Abstract
The nicotinic α7 agonist dimethoxybenzilidene anabaseine (DMXB) and cholinesterase inhibitor tetrahydroaminoacridine (THA) were investigated in a trans-synaptic model for neocortical atrophy and degeneration following nucleus basalis lesions. Bilateral lesions reduced parietal neuronal density in layers II–V 8 months later. DMXB administered i.p. daily to rats for 3 months attenuated this loss in layers II–V at a 1 mg/kg i.p. dose. A lower, 0.2 mg/kg i.p. dose, was neuroprotective in layer IV only. THA (1 mg/kg i.p.) also protected against neocortical Nissl-staining deficits.
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