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BioMed Research International
Volume 2015, Article ID 734367, 6 pages
http://dx.doi.org/10.1155/2015/734367
Research Article

Postnatal Administration of Allopregnanolone Modifies Glutamate Release but Not BDNF Content in Striatum Samples of Rats Prenatally Exposed to Ethanol

1Instituto de Investigaciones Biomédicas (INBIOMED-IMBECU-CONICET), Facultad de Ciencias de la Salud, Universidad de Mendoza, Paseo Dr. Emilio Descotte 720, 5500 Mendoza, Argentina
2Área de Farmacología, Facultad de Ciencias Médicas, Universidad Nacional de Cuyo, Avenidad del Libertador 80, 5500 Mendoza, Argentina
3Laboratorio de Neurobioquímica, Facultad de Ciencias Químicas y Farmacéuticas, Universidad de Chile, Calle Sergio Livingstone Polhammer 1007, 8380492 Santiago de Chile, Chile

Received 15 December 2014; Revised 10 February 2015; Accepted 11 February 2015

Academic Editor: Abdel A. Abdel-Rahman

Copyright © 2015 Roberto Yunes et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Ethanol consumption during pregnancy may induce profound changes in fetal CNS development. We postulate that some of the effects of ethanol on striatal glutamatergic transmission and neurotrophin expression could be modulated by allopregnanolone, a neurosteroid modulator of receptor activity. We describe the acute pharmacological effect of allopregnanolone (65 μg/kg, s.c.) administered to juvenile male rats (day 21 of age) on the corticostriatal glutamatergic pathway, in both control and prenatally ethanol-exposed rats (two ip injections of 2.9 g/kg in 24% v/v saline solution on gestational day 8). Prenatal ethanol administration decreased the K+-induced release of glutamate regarding the control group. Interestingly, this effect was reverted by allopregnanolone. Regarding BDNF, allopregnanolone decreases the content of this neurotrophic factor in the striatum of control groups. However, both ethanol alone and ethanol plus allopregnanolone treated animals did not show any change regarding control values. We suggest that prenatal ethanol exposure may produce an alteration of receptors which blocks the GABA agonist-like effect of allopregnanolone on rapid glutamate release, thus disturbing normal neural transmission. Furthermore, the reciprocal interactions found between GABAergic neurosteroids and BDNF could underlie mechanisms operating during the neuronal plasticity of fetal development.