Journal
NEUROMOLECULAR MEDICINE
Volume 12, Issue 3, Pages 270-276Publisher
HUMANA PRESS INC
DOI: 10.1007/s12017-010-8113-y
Keywords
Parkin; PARK2; Hippocampus; LTP; Plasticity; EPSP; Mouse; Compensatory; Aging; CA1
Categories
Funding
- National Institute of Mental Health [MH065541]
- G. Harold and Leila Y. Mathers Charitable Foundation
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We examined synaptic function in the hippocampus of aged mice deficient for the Parkinson's disease-linked protein, parkin. Surprisingly, heterozygous but not homozygous parkin-deficient mice exhibited impairments in basal excitatory synaptic strength. Similarly heterozygous mice exhibited broad deficits in paired-pulse facilitation, while homozygous parkin-deficient mice exhibited more restricted deficits. In contrast to the measurements of basal synaptic function, synaptic plasticity was not altered in aged heterozygous parkin-deficient mice, but was enhanced in aged homozygous parkin-deficient mice, due to an absence of age-related decline. These findings of differential synaptic phenotypes in heterozygous vs. homozygous parkin deficiency suggest compensatory responses to genetic abnormalities could play an important role during the development of pathology in response to parkin deficiency.
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