Deficit of quantal release of GABA in experimental models of temporal lobe epilepsy
| Data(s) |
25/11/2016
25/11/2016
1999
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| Resumo |
Because GABA (gamma-aminobutyric acid) receptor-mediated inhibition controls the excitability of principal neurons in the brain, deficits in GABAergic inhibition have long been favored to explain seizures. In an experimental model of temporal lobe epilepsy, we have identified a deficit of inhibition in presynaptic GABAergic terminals characterized by decreased GABA quantal activity associated with reduced synaptic vesicle density. This decrease in vesicle number primarily seems to affect the reserve pool, rather than the docked or the readily releasable pool. SIN FINANCIACIÓN 7.157 SJR (1999) Q1, 6/97 Neuroscience (miscellaneous) UEM |
| Identificador |
Hirsch, J. C., Agassandian, C., Merchan-Perez, A., Ben-Ari, Y., Defelipe, J., Esclapez, M., y Bernard, C. (1999). Deficit of quantal release of GABA in experimental models of temporal lobe epilepsy. Nature neuroscience, 2(6), 499-500. 10976256 http://hdl.handle.net/11268/6003 10.1038/9142 |
| Idioma(s) |
eng |
| Direitos |
openAccess |
| Palavras-Chave | #Neurociencias #Epilepsia #Neurología #Enfermedad del sistema nervioso |
| Tipo |
article |
