ISDN2014_0034: The immunological and neuroimmunological response to spreading depression in Wistar rats

This study was undertaken in order test the hypothesis that early insult of the mediodorsal nucleus of the thalamus (MD) leads to morphological abnormalities of dendrites and spines of neurons in prefrontal cortex (PFC) possibly as a result of alterations in the calcium/calmodulin dependent signaling pathway, as well as causes stereotypic behaviours present in many developmental disorders involving the frontal cortex. Pregnant Long Evans dams were obtained from Cadi Ayyad University’s central animal care facilities. Date of birth was designated as postnatal day 0 (P0). On the day P4, the pups received a bilateral electrolytic lesion. One group of animals received a sham lesion to act as a control to verify that alterations observed are due to the loss of cells in the thalamus and not to the operation itself. Seven weeks post surgery the animals will be trained in the behavioral paradigms and assessed for behavior and at P60, the animals were sacrificed. The PFC was dissected out for Golgi impregnation and placed in Golgi-Cox solution. In the behavioral study, we reported that the lesion induced several changes that mimic schizophrenia and autism symptoms. Indeed, at the pubertal age, animals showed a significant decrease in the number of social interactions, anxiety, learning impairment and highly increase in the locomotor activity compared to controls. The Golgi techniques demonstrated the neonatal thalamic lesion induced pronounced alterations in dendritic branching and spine density of both projection neurons and local circuit neurons in PFC at adulthood stage. This concerned particularly PFC pyramidal neuron dendritic morphology, with a loss of dendritic spines and a decrease in dendritic complexity. These data provide insight into whether disruption of thalamocortical pathways could produce the changes in the PFC related to developmental disorders such as Autism and Schizophrenia.