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; UDOVIN, LD; KUSNIER, CF; BUJAN, GE; CAPANI, F; GUELMAN, LR

Chicago, IL

Congreso; Neuroscience 2019; 2019

Society fro Neuroscience (SFN)

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 and neural damage, during the peri-adolescence period. In addition, housing animals in an enriched environment (EE) has shown to be effective in the reversal of most of these alterations. As the involvement of excitotoxicity has been proposed in different brain injuries, the aim of the present work was to test the effects of early noise exposure on aminoacidergic neurotransmission. In addition, considering that glial cells might influence neuronal environment and integrity, hippocampal histology was 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) or five (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 blot experiments were performed to evaluate the levels of GAD 65/67 (a marker of GABAergic neurotransmission) and EAAT-1 (glutamate transporter, a marker of glutamatergic neurotransmission). GFAP reactive area was studied through immunohistochemical procedures to evaluate the presence of reactive gliosis. Results showed that although an increase in EAAT-1 levels and GFAP reactive area was induced only in rats exposed to N5 at PND 7 when compared with non-exposed rats, housing these animals in an EE was effective in restoring these differences. In contrast, no significant changes were observed in GAD 65/67 levels in neither group. These findings suggest that early noise exposure might differentially affect rats by inducing excitotoxicity, demonstrating a high vulnerability of repeated exposures (N5) at earlier ages (PND7). Furthermore, the associated increase of the GFAP reactive area might suggest reactive gliosis as a mechanism aimed to protect HC against excitotoxicity. In consequence, it could be proposed that this defensive response could have been produced in reaction to a previous excitotoxic extra-cellular challenge in order to prevent neuronal damage. Finally, EE has shown to be an effective strategy to reverse all the alterations found, suggesting that visual, social and physical stimulation during the peri-adolescence period could be an effective strategy to prevent HC-related molecular and histological changes.