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

MOLINA, SJ; BUJÁN, GE; GUELMAN, LR

Córdoba, Argentina

Congreso; IX LASBRA INTERNATIONAL MEETING: Determinants of Alcoholism: bridging the gap between epidemiologic and basic research.; 2019

Latin American Society for Biomedical Research on Alcoholism (LASBRA)

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 different environmental factors. Alcohol is one of the chemical compounds most used for recreational purposes by human adolescents and it has the ability to affect the CNS. In addition, alcohol consumption usually occurs in the presence of high noise intensities in different entertainment places. In previous studies, we demonstrated that early exposure to noise can cause hippocampal (HC)-related behavioral and biochemical alterations during adolescence, including changes in aminoacidergic neurotransmission. So, considering that both alcohol consumption and noise are capable of affecting the CNS, the aim of this work was to investigate the possible changes induced by voluntary alcohol intake in conjunction with noise exposure on aminoacidergic neurotransmission during adolescence. Female Wistar rats (28-days-old) consumed 10% ethanol or 1% sucrose using two-bottle choice drinking in the dark paradign, during 4h/day for 4 days. After last session, animals were exposed to noise (95-97 dB, 2h) and HC tissue was dissected for Western Blot experiments to evaluate the levels of GAD 65/67 (a marker of GABAergic neurotransmission) and EAAT-1 (Excitatory amino acid transporter 1, a marker of glutamatergic neurotransmission). Results showed no significant changes on GAD 65/67 enzyme and EAAT-1 multimers levels between neither groups. However, a decrease in glycosylated EAAT-1 was found in animals exposed to noise which was prevented on animals that consumed alcohol before noise exposure. These findings suggest that exposure to physical and chemical agents during adolescence could induce HC-related biochemical alterations, demonstrating a high vulnerability of the developing brain to these clinically relevant agents. Glutamate transporters play a crucial role in removing the excess of glutamate to limit its neurotoxic effects and a decrease in EAAT-1 glycosylation sites, which are important for the generation of its active multimeric forms and extra-cellular expression of EAAT-2 (Excitatory amino acid transporter 2), could lead to future difficulties in preventing glutamate increases especially if the individual continues to be exposed to these agents. Finally, these results highlight the importance of future research to understand the mechanisms involved.