INVESTIGADORES
CID Mariana Paula
congresos y reuniones científicas
Título:
Participacion del sistema gabaergico en la liberacion de glutamato en sinaptosomas provenientes de animales con encefalomielitis autoinmune experimental (EAE),
Autor/es:
CID MARIANA PAULA; VILCAES ALDO ALEJANDRO; ROTH GERMAN ALFREDO
Reunión:
Jornada; Segundo encuentro de jóvenes investigadores en neurociencias de Córdoba; 2010
Resumen:
Recent reports
have
been showed a deficit in expression of proteins associated with GABAergic
neurotransmission in neocortex of Multiple Sclerosis (MS). Interestingly, it had been described that the activation
of GABAA receptors led to an inhibition of glutamate release. Recently, we found in synaptosomes isolated
from cerebral cortex that the glutamate release was decreased during of EAE,
the animal model of MS. In order to evaluate the potential
events that may affect neuronal function in EAE synaptosomes, we analyzed the
possible participation of the GABAergic system on the glutamate release. For this, synaptosomes from CFA and EAE
animals were incubated in the presence of GABA followed by the addition of 4AP
to trigger release. In synaptosomes from CFA rats, the glutamate release was
decreased by GABA. To confirm that the observed inhibition of glutamate release
from CFA synaptosomes was indeed mediated by GABAA receptors, we
incubated synaptosomes with a GABAA antagonist, prior to the
addition of GABA. The inhibition of glutamate release by GABA was abolished by
the antagonist in CFA synaptosomes. However, the glutamate release was
unaffected when EAE synaptosomes were incubated with GABA prior to induction of
the release. On the other hand, GABAA R density was measured ex vivo in
neocortex cerebral synaptosomes by 3[H]-flunitrazepam binding assay at 4º C.
The Bmax in synaptosomes from EAE rats was 591 fmol/mg proteins, whereas the
Bmax fmol/mg proteinsin CFA syanptosomes was 1101 fmol/mg proteins. Ours results suggest that the
diminution of the flunitrazepan sensitive GABAA R density could
explain the observed failure in the GABAergic regulation on the glutamate
release of synaptosomes of neocoxtex from EAE rats.