Back to Search
Start Over
Enhanced Synaptic Potentiation in Transgenic Mice Expressing presenilin 1 Familial Alzheimer's Disease Mutation Is Normalized with a Benzodiazepine
- Source :
- Neurobiology of Disease, Vol 7, Iss 1, Pp 54-63 (2000)
- Publication Year :
- 2000
- Publisher :
- Elsevier, 2000.
-
Abstract
- 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.
- Subjects :
- Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
Subjects
Details
- Language :
- English
- ISSN :
- 1095953X
- Volume :
- 7
- Issue :
- 1
- Database :
- Directory of Open Access Journals
- Journal :
- Neurobiology of Disease
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.4a07cc601e48c090c626dec1e6f359
- Document Type :
- article
- Full Text :
- https://doi.org/10.1006/nbdi.1999.0271