NOISE EXPOSURE OF ADOLESCENT FEMALE RATS CAN INDUCE AMINOACIDERGIC NEUROTRANSMISSION CHANGES ON HIPPOCAMPUS THAT CAN BE PREVENTED BY PREVIOUS ALCOHOL INTAKE

MOLINA, SJ; BUJAN, GE; GUELMAN, LR

Cordoba

Congreso; IX INTERNATIONAL MEETING of the Latin American Society for Biomedical Research on Alcoholism (LASBRA); 2019

LASBRA INTERNATIONAL MEETING

Adolescence constitutes a critical period in the maturation of the Central Nervous System(CNS) and its normal development can be altered by the appearance of differentenvironmental factors. Alcohol is one of the chemical compounds most used forrecreational purposes by human adolescents and it has the ability to affect the CNS. Inaddition, alcohol consumption usually occurs in the presence of high noise intensities indifferent entertainment places. In previous studies, we demonstrated that early exposureto noise can cause hippocampal (HC)-related behavioral and biochemical alterationsduring adolescence, including changes in aminoacidergic neurotransmission. So,considering that both alcohol consumption and noise are capable of affecting the CNS, theaim of this work was to investigate the possible changes induced by voluntary alcoholintake in conjunction with noise exposure on aminoacidergic neurotransmission duringadolescence.Female Wistar rats (28-days-old) consumed 10% ethanol or 1% sucrose using two-bottlechoice drinking in the dark paradign, during 4h/day for 4 days. After last session, animalswere exposed to noise (95-97 dB, 2h) and HC tissue was dissected for Western Blotexperiments to evaluate the levels of GAD 65/67 (a marker of GABAergicneurotransmission) and EAAT-1 (Excitatory amino acid transporter 1, a marker ofglutamatergic neurotransmission).Results showed no significant changes on GAD 65/67 enzyme and EAAT-1 multimerslevels between neither groups. However, a decrease in glycosylated EAAT-1 was found inanimals exposed to noise which was prevented on animals that consumed alcohol beforenoise exposure.These findings suggest that exposure to physical and chemical agents during adolescencecould induce HC-related biochemical alterations, demonstrating a high vulnerability of thedeveloping brain to these clinically relevant agents. Glutamate transporters play a crucialrole in removing the excess of glutamate to limit its neurotoxic effects and a decrease inEAAT-1 glycosylation sites, which are important for the generation of its active multimericforms and extra-cellular expression of EAAT-2 (Excitatory amino acid transporter 2), couldlead to future difficulties in preventing glutamate increases especially if the individualcontinues to be exposed to these agents. Finally, these results highlight the importance offuture research to understand the mechanisms involved.