BEHAVIORAL, HISTOLOGICAL AND BIOCHEMICAL CHANGES INDUCED ON HIPPOCAMPUS AFTER NEONATAL X RADIATION EXPOSURE

CÁCERES, LG; SARACENO E; AÓN L; ZORRILLA ZUBILETE, M.A; CAPANI, F; GUELMAN, L.R

Washington DC, USA

Congreso; 38th Annual Meeting of the Society for Neuroscience (SFN); 2008

Society for Neuroscience (SFN)

Developing Central Nervous System (CNS), in particular cerebellum, has been found to be extremely vulnerable to ROS-mediated, ionizing radiation damage. The aim of the present work was to test the radiosensitivity of the hippocampus (Hip), a CNS region mainly involved in mechanisms of learning and memory. Neonatal rats were X-irradiated with 5 Gy in their cephalic ends, up to 48hs of postnatal life, and were subjected to a passive avoidance test (PA) 30 days after birth in order to evaluate short and long term hippocampal-related memory. Moreover, the basal and induced (by NMDA) levels of ROS -main mediators of radiation-induced damage- as well as the levels of PKC -a protein involved in the memory mechanism- were determined in the hippocampus and histological and morphological assessments were also performed. The irradiated animals showed a better performance in the PA test compared with control when tested at short term (rate T2/T1: C= 28.93 ± 6.71; Rx= 51.62 ± 8.22, p< 0.05). while there were no differences between irradiated and control animals when tested at long term. The histology showed no gross changes in the hippocampal. However, an increase in the number of dendritic spines was observed in Hip of irradiated animals. The basal/induced ratio of ROS levels were increased in irradiated animals (C= 0.334 ± 0.016; Rx= 0.450 ± 0.006, p< 0.01), together with PKC levels (pmolPKC/mg of tissue, C= 39.20 ± 1.70; Rx= 96.97 ± 10.87, p< 0.05) These data suggest that increased basal ROS levels found in irradiated animals could trigger the increase in PKC levels. Likewise, this increase could be responsible for the improvement in the performance of irradiated animals observed in the PA test at short term. Even more, stimulated PKC signaling pathway would regulate dendritic spines density in the Hip. Taken together, although no cytoarchitectural damage was induced to Hip, these results could suggest the existence of hippocampal plastic compensatory mechanism to counteract ROS attack, and could be proposed that ROS can be considered as small messenger molecules critical for neuronal signaling.