Autor: |
Lintao Qu, Richard Boyce, L. Stan Leung |
Jazyk: |
angličtina |
Rok vydání: |
2010 |
Předmět: |
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Zdroj: |
Neurobiology of Disease, Vol 37, Iss 3, Pp 704-710 (2010) |
Druh dokumentu: |
article |
ISSN: |
1095-953X |
DOI: |
10.1016/j.nbd.2009.12.009 |
Popis: |
Whether seizures in the developing brain cause long-term changes in the mature brain has been debated. We tested the hypothesis that a model of early-life seizures, induced by systemic injection of a GABAB receptor antagonist CGP56999A in immature rats, decreased GABAB receptor-mediated inhibitory postsynaptic currents (IPSCs) in the hippocampus of adolescent rats. Whole-cell recordings were made in CA1 pyramidal cells and dentate gyrus (DG) granule cells in vitro, 30–45 days after the rats had seizures induced by CGP56999A (1–1.5 mg/kg i.p.) or control saline injection on postnatal day 15. GABAB receptor-mediated IPSCs were reduced in DG neurons but not in CA1 neurons of early-life seizure rats as compared to controls. Additionally, hippocampal neurons of early-life seizure rats, as compared to those in control rats, showed a more depolarized resting membrane potential in both CA1 and DG, and a larger input resistance but reduced spike frequency adaptation in DG neurons. In conclusion, early-life seizures result in a long-lasting reduction in GABAB receptor-mediated transmission in DG principal neurons and depolarization in CA1 and DG principal neurons. These alterations are expected to increase seizure susceptibility in the adult brain. |
Databáze: |
Directory of Open Access Journals |
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