Journal
NEUROBIOLOGY OF DISEASE
Volume 7, Issue 1, Pages 54-63Publisher
ACADEMIC PRESS INC
DOI: 10.1006/nbdi.1999.0271
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- NIA NIH HHS [1PO1AG14248] Funding Source: Medline
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Mutations in presenilin 1(PS1) are the most common causes of familial Alzheimer's disease (FAD). We examined synaptic physiology in hippocampal brain slices of transgenic mice expressing the FAD-linked PS1 deletion of exon 9 variant. Basal excitatory transmission and paired-pulse facilitation in PS1 mutant mice were unchanged. Short- and long-term potentiation of excitatory transmission following high-frequency stimulation were greater in transgenic mice expressing mutant PS1. Mutants had enhanced synaptic inhibition, which may be a compensatory change offsetting an abnormally sensitized plasticity of excitatory transmission. Increasing inhibitory transmission in mutant animals even more with a benzodiazepine reverted synaptic potentiation to the levels of controls. These results support the potential use of benzodiazepines in the treatment of familial Alzheimer's disease. (C) 2000 Academic Press.
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