Actin cytoskeleton changes after perinatal asphyxia in the rat neostriatum are prevented using hypothermia treatment

E. SARACENO1, V. BOTI1, L. AON1, L. GIRALDEZ2, C. LOIDL1, H. COIRINI3, *F. CAPANI1;

San Diego

Congreso; Society for Neurocience; 2006

Several proteins involved in synaptic functions are damaged during hypoxia-ischemia. These alterations might destroy synaptic transmission and then induce neurologic deficits. Dendritic spines are highly concentrated in F-actin being this protein involved in the movements and shape changes of these structures. Previously we have shown that hypothermia reduced the neuronal and synaptic damage induced by perinatal asphyxia (PA). In the present studied we have investigated the effect of low temperature (15 °C) on actin cytoskeleton distribution in neostriatum from 60 days old rats subjected to 20 minutes of PA (severe PA) at 37 °C by using correlative phalloidin photoconvertion and 3-D serial sections reconstructions. Under severe PA conditions confocal microscopy for phalloidin showed an increment of F-actin fluorescent. Reducing the temperature from 37 °C to 15 °C dramatically reduced the intensity of F-actin staining. In addition, electron microcopy and 3-D reconstruction confirmed these observations showing a decreased of F-actin concentration under hypothermia conditions in comparison with PA neostriatal excitatory synapses. Therefore since F-actin is highly concentrated in excitatory synapses we think that actin changes could be related with the increment in the release of excitatory aminoacids, and then in the neuronal death. Decreasing temperature from 37 ° C to 15 °C might reduce actin polymerization and proctects the neurons against the hypoxia damage.