CEFYBO   02669
CENTRO DE ESTUDIOS FARMACOLOGICOS Y BOTANICOS
Unidad Ejecutora - UE
congresos y reuniones científicas
Título:
Enriched environment is able to counteract some of the histological alterations induced by early noise exposure.
Autor/es:
SAINT MARTIN, M; MOLINA, SJ; CAPANI, F; GUELMAN, LR
Lugar:
Montreal
Reunión:
Congreso; 20th Biennial Meeting of the International Society for Developmental Neuroscience and the 5th Annual NeuroDevNet Brain Development Conference; 2014
Institución organizadora:
International Society for Developmental Neuroscience
Resumen:
Although noise exposure can induce hearing loss, few data are available regarding its effects on extra-auditory structures. Previous studies of our laboratory showed that exposure of immature rats to moderate noise for two hours can induce hippocampus (HC)-related behavioral, biochemical and histological alterations, including an increase in number of cells in all layers, mainly due to an increase in pyknotic cells. The aim of the present work was to test if a non-pharmacological strategy, the enriched environment housing (EE) can prevent noise-induced histological changes. Fifteen-days-old rats were exposed to 95-97 dB of white noise for two hours, using an ?ad-hoc? sound camera. After weaning, groups of 3-4 rats were transferred to an enriched cage, consisting of different toys, a wheel, plastic tunnels and ramps. Other groups were placed in standard cages. One week later, animals were subjected to perfusion and histological hippocampal assessment was performed in hematoxilin-eosin slices. Results show that although no changes in hippocampal layers width were found in noise-exposed animals, an increase in the number of pyknotic cells was found in all layers. In particular, animals reared in EE showed the same number of pyknotic cells in DG and CA3 layer than rats reared in a standard cage, whereas in CA1 layer its number reestablished, reaching control values. These findings suggest that visual, social and physical stimulation during the peri-adolescence period after exposure to noise might reverse the process of neuronal injury by interfering with some of the previously reported biochemical mechanisms triggered by noise. The difference observed between CA1 and the other layers might be attributed to the different roles that these areas play, the developmental stage at which the animal is exposed to noise and to EE and their consequent differential vulnerability.