Acute noise exposure during adolescence induce sex-specific hippocampal aminoacidergic neurotransmission changes that can be partially prevented by prior ethanol intake

MOLINA, SJ; CARREIRA CARO, CS; LIETTI, AE; BUJÁN, GE; GUELMAN, LR

Congreso; 23rd Biennial Meeting of the International Society of Developmental Neuroscience (ISDN2021); 2021

Adolescents often attend recreational events where they consume ethanol (EtOH) and are exposed to noise of high intensities, two environmental stimuli that could affect the developing central nervous system (CNS). Animal models studies have shown that both stimuli presented separately might have detrimental effects on the hippocampus (HC), a CNS structure related to cognitive functions, including neurotransmission alterations. Therefore, the aim of this work was to investigate the effects of EtOH intake in conjunction with noise exposure during adolescence on hippocampal aminoacidergic neurotransmission. Wistar rats (28-days-old) were subjected to 10% ethanol 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 GAD 65/67 (marker of GABAergic neurotransmission) and EAAT-1 (excitatory amino acid transporter-1, marker of glutamatergic neurotransmission) levels. Results showed a significant decrease in females and an increase in males in both glycosylated and active multimeric forms of EAAT-1 after noise exposure, without differences when rats consumed EtOH alone or followed by noise exposure. In addition, a significant increase in GAD 65/67 levels was found in males exposed to noise and to both stimuli (EtOH+Noise group), without differences in females.These findings suggest that noise might affect HC in a sex-dependent way. Given that glutamate transporters play a crucial role in the removal of the excess of glutamate to limit its neurotoxic effects, a decrease in EAAT-1, as observed in females, could imply a greater vulnerability to the harmful effects of excitotoxicity, whereas an increase in both markers, as observed in males, could indicate a defensive response against a possible increase in extra-cellular glutamate. Additionally, EtOH intake before noise exposure prevented most noise-induced disturbances. Finally, these findings demonstrate the high vulnerability of developing brain to environmental stressors.