Abstract
236 Alzheimer’s disease (AD) is characterized by extensive cholinergic denervation in both cortex and hippocampus. However, cholinergic therapies are of limited value. We investigated choline@ mechanisms in hippocampus which was denervated by a fimbriafomix lesion. Denervated pyramidal cells were found to be hypersensitive to carbachol, responding to a given dose with larger depolarizing currems and with a more pronounced blockade of the after-hyperpolarizing (AHP) current. Also, in denervated hippocampus, depolarization blockade was induced by lower concentrations of carbachol. In some cells this blockade could be reversed by addition of clonidine. It is suggested that treatment failure in AD is due to the induction of depolarization blockade and that combined treatment with a hyperpolarizing agent may enhance the therapeutic effects of cholinergic agents in this disease.
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