CEFYBO   02669
CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Noise exposure of adolescent female rats induce hippocampal aminoacidergic neurotransmission changes that can be prevented by prior ethanol intake
Autor/es:
MOLINA, SJ; BUJÁN, GE; GUELMAN, LR
Lugar:
Córdoba
Reunión:
Congreso; IX INTERNATIONAL MEETING of the Latin American Society for Biomedical Research on Alcoholism (LASBRA); 2019
Institución organizadora:
Latin American Society for Biomedical Research on Alcoholism (LASBRA)
Resumen:
Adolescence constitutes a critical period in the maturation of the Central Nervous System (CNS) and its normal development can be altered by the presence of harmful environmental factors. Ethanol 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, ethanol consumption usually occurs in the presence of high noise intensities in different entertainment places. Therefore, the use of an animal model of ethanol intake combined with noise exposure could be clinically relevant. We have previously demonstrated that rats exposed to noise at childhood can induce hippocampal (HC)-related behavioral and biochemical alterations, including changes in aminoacidergic neurotransmission. In consequence, the aim of the present work was to investigate possible changes that voluntary ethanol intake in conjunction with noise exposure during early adolescence might induce on hippocampal aminoacidergic neurotransmission. Female Wistar rats (28-days-old) were subjected to 10% ethanol or 1% sucrose using the two-bottle choice drinking in the dark paradigm, 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 either 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. Glycosylated EAAT-1 is important for the generation of the active multimeric forms and for the extra-cellular expression of other glutamate transporters. Therefore, considering that glutamate transporters play a crucial role in the removal of the excess of glutamate to limit its neurotoxic effects, the observed decrease in glycosylated EAAT-1 could lead to difficulties in preventing harmful glutamate increase, especially if the individual is being continuously exposed to pro-excitotoxic agents. Finally, 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.