INVESTIGADORES
BIGNANTE Elena anahi
artículos
Título:
Erk activation in the amygdala and hippocampus induced by fear conditioning in ethanol withdrawn rats: Modulation by mk-801
Autor/es:
BERTOTTO MARIA EUGENIA; MALDONADO NOELIA MARTINA; BIGNANTE ELENA ANAHI; GOROSITO SILVANA VANESA; CAMBIASSO MARIA JULIA; MOLINA VICTOR ALEJANDRO; MARTIJENA IRENE DELIA
Revista:
EUROPEAN NEUROPSYCHOFARMACOLOGY
Editorial:
ELSEVIER SCIENCE BV
Referencias:
Año: 2011 vol. 21 p. 892 - 904
ISSN:
0924-977X
Resumen:
Abstract
The extracellular signal-regulated kinase (ERK) pathway, which can be activated by NMDA receptor
stimulation, is involved in fear conditioning and drug addiction. We have previously shown that
withdrawal from chronic ethanol administration facilitated the formation of contextual fear
memory. In order to explore the neural substrates and the potential mechanism involved in this
effect, we examined: 1) the ERK1/2 activation in the central (CeA) and basolateral (BLA) nuclei of
the amygdala and in the dorsal hippocampus (dHip), 2) the effect of the NMDA receptor antagonist
MK-801 on fear conditioning and ERK activation and 3) the effect of the infusion of U0126, a MEK
inhibitor, into the BLA on fear memory formation in ethanol withdrawn rats.Rats made dependent
via an ethanol-containing liquid diet were subjected to contextual fear conditioning on day 3 of
ethanol withdrawal. High basal levels of p-ERK were found in CeA and dHip fromethanol withdrawn
rats. ERK activation was significantly increased both in control (60 min) and ethanol withdrawn rats
(30 and 60 min) in BLA after fear conditioning. Pre-training administration of MK-801, at a dose that
had no effect on control rats, prevented the increase in ERK phosphorylation in BLA and attenuated
the freezing response 24 h later in ethanol withdrawn rats. Furthermore, the infusion of U0126 into
the BLA, but not the CeA, before fear conditioning disrupted fearmemory formation. These results
suggest that the increased fear memory can be linked to changes in ERK phosphorylation, probably
due to NMDA receptor activation in BLA in ethanol withdrawn rats.
© 2011 Elsevier B.V. and ECNP. All rights reserved.
⁎ Corresponding author at: IFEC-CONICET, Departamento de Farmacología, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba,Corresponding author at: IFEC-CONICET, Departamento de Farmacología, Facultad de Ciencias Químicas, Universidad Nacional de Córdoba,