Impairment in hippocampal GABAA receptors binding after moderate noise exposure

URAN, S.L; CID, M.P; CACERES, L.G; SALVATIERRA, N.A; GUELMAN, L.R

Huerta Grande, Córdoba

Congreso; XXVII Reunión Anual de la Sociedad Argentina de Investigación en Neurociencias; 2012

Sociedad Argentina de Investigación en Neurociencias (SAN)

Moderate noise-induced damage on the hippocampus (HC) may result from the disruption of the balance between excitatory and inhibitory neurotransmission. Changes in the density or ligand affinity may reflect variations in synaptic transmission. The aim of the present work was to investigate if the exposure of developing rats to moderate noise levels induced changes in HC GABA binding that could underlie the previously observed behavioral and histological alterations. Male Wistar rats of 15 days were exposed to white noise (95-97 dB, 2h) for one day or for 15 consecutive days. Hippocampal GABAA binding was measured at 15 and 30 days. Results show that moderate noise induced a significant decrease in HC GABA Bmax at 2 h after the first exposure (56±2.7 %, p< 0.0001), without changes in Kd. In contrast, after 15 days, one day exposure induced an increase in Bmax (174.9±3.4 %, p< 0.001), while no changes were observed in HC GABA Bmax after multiple exposures. These results suggest that noise might induce an imbalance in hippocampal aminoacidergic neurotransmission that could be responsible for the tissue damage. Furthermore, GABAA receptor downregulation could be compensated by a subsequent upregulation. These data suggest that developing GABAA receptors might plastically adapt to a new inhibitory status. Therefore, it might be hypothesized that impaired inhibitory synaptic transmission could contribute to trigger cell death. Since GABA receptors are differentially affected, these results could underlie the changes in anxiety previously reported.