NRSF and CCR5 Established Neuron-glia Communication during Acute and Chronic Stresses

Abstract

It has been reported that traumatic stress resulted in immune-suppression. Src kinase activation in the prefrontal cortex was believed to initiate cellular-reorganization at the recover stage of trauma. Herein, we reported that NRSF and CCR5 expression were consistently increased in the prefrontal cortex of SD rats when exposed to traumatic stress, in which CCR5 was activated mostly in neurons and targeted by astrocyte NRSF. Moreover, HPA axis activation could be acutely and sustainably triggered by traumatic stress and PSS at post-trauma respectively, both NRSF and CCR5 had inhibitory effect in the former event, while NRSF could block the scenario in the later event. Intriguingly, the effect of NRSF was mostly converged on multiple mechanisms that associated with GR activity, and the optimal preservation of neuroligin-1 formed neuron-astrocyte communication was achieved by NRSF. Therefore, the present results argue for the dichotomy of NRSF regulatory complexes, whose inhibition in HPA hyper-reactivity during acute and chronic stresses have significant potential for the development of therapeutic approaches in posttraumatic stress-related disorders.