Early chronic noise exposure can induce aminoacidergic neurotransmission changes and reactive gliosis in the hippocampus of adolescent rats. Influence of enriched environment housing

MOLINA, SJ; BUJÁN, GE; UDOVIN, LD; CAPANI, F; KUSNIER, C; GUELMAN, LR

Chicago

Congreso; Neuroscience 2019, October 19-23; 2019

Society for Neuroscience

We have previously shown that exposure of immature rats to moderate noise can induce hippocampus(HC)-related behavioral, molecular and histological alterations, including oxidative imbalance andneural damage, during the peri-adolescence period. In addition, housing animals in an enrichedenvironment (EE) has shown to be effective in the reversal of most of these alterations. As theinvolvement of excitotoxicity has been proposed in different brain injuries, the aim of the present workwas to test the effects of early noise exposure on aminoacidergic neurotransmission. In addition,considering that glial cells might influence neuronal environment and integrity, hippocampal histologywas also evaluated. Finally, the possibility that EE could prevent these changes was further considered.Male Wistar rats of 7 and 15 postnatal days (PND) were exposed to noise (95-97 dB, 2h) for one (N1) orfive (N5) consecutive days. After weaning, rats were transferred to an EE, consisting of toys, a wheel,plastic tunnels and ramps, whereas others were placed in standard cages. One week later, western blotexperiments were performed to evaluate the levels of GAD 65/67 (a marker of GABAergicneurotransmission) and EAAT-1 (glutamate transporter, a marker of glutamatergic neurotransmission).GFAP reactive area was studied through immunohistochemical procedures to evaluate the presence ofreactive gliosis. Results showed that although an increase in EAAT-1 levels and GFAP reactive area wasinduced only in rats exposed to N5 at PND 7 when compared with non-exposed rats, housing theseanimals in an EE was effective in restoring these differences. In contrast, no significant changes wereobserved in GAD 65/67 levels in neither group. These findings suggest that early noise exposure mightdifferentially affect rats by inducing excitotoxicity, demonstrating a high vulnerability of repeatedexposures (N5) at earlier ages (PND7). Furthermore, the associated increase of the GFAP reactive areamight suggest reactive gliosis as a mechanism aimed to protect HC against excitotoxicity. Inconsequence, it could be proposed that this defensive response could have been produced in reactionto a previous excitotoxic extra-cellular challenge in order to prevent neuronal damage. Finally, EE hasshown to be an effective strategy to reverse all the alterations found, suggesting that visual, social andphysical stimulation during the peri-adolescence period could be an effective strategy to prevent HCrelated molecular and histological changes.