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PubMed1989

Effect of repeated versus single electroconvulsive seizures on adrenergic-mediated phosphatidylinositol hydrolysis in rat neocortex.

Adrenergic-stimulated phosphatidylinositol (PI) hydrolysis was measured in cortical slices obtained from adult rats following electroconvulsive seizures (ECS). One group of animals received ECS daily for 15 days and a second group received a single ECS. Rats were then sacrificed at intervals of 15 min, 60 min, 4 h, and 24 h after the last ECS. Inositol 1-monophosphate (IP1) accumulation was transiently reduced (20%, P less than 0.01), at 15 min, in repeatedly shocked versus sham-shocked control animals. No changes were observed at later intervals nor at any time in rats submitted to a single ECS. These findings suggest that repeated but not single convulsive seizures transiently desensitize adrenergic-mediated PI metabolism. Although repeated ECS significantly increased the density (Bmax) of alpha 1 recognition sites in cortical slices at 15 min, 4 h, and 24 h, this upregulation was not coupled to a functional change in PI hydrolysis.

Animals↗
PubMed1982

Choline acetyltransferase activity and histopathology of frontal neocortex from biopsies of demented patients.

Cortical biopsies were taken from the frontal lobe of 25 patients with presenile dementia. Choline acetyltransferase (ChAT) activity, and in some specimens the high affinity uptake of choline, was used to estimate loss of cholinergic nerve terminals. Of the 15 samples with varying degrees of histological evidence of Alzheimer's disease (AD) 14 were from clinically suspected examples of the disease. There was significant loss of ChAT in 10 of the 15 compared with control and the mean activity was also highly significantly reduced (to 41% of control). The deficit was found in patients examined within a year of onset of symptoms. In 6 biopsies from clinically suspected cases of AD without diagnostic histological features there was loss of activity in only one, subsequently shown to have Jakob-Creutzfeldt disease. The remaining samples were two of vascular dementia (no loss of ChAT), one probable disorder of white matter (no loss of activity) and one undiagnosed disorder (with loss of ChAT activity). Thus most patients without histologically demonstrated AD had no evidence of a presynaptic cholinergic defect. It was concluded that suspected cases of AD particularly suitable for putative cholinergic therapy were those with an onset of the disease at 55 to 65 and an absence of family history.

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