Molecular correlates of impaired prefrontal plasticity in response to chronic stress

摘要: Disturbed adaptations at the molecular and cellular levels following stress could represent compromised neural plasticity that contributes to pathophysiology of stress-induced disorders. Evidence illustrates atrophy cell death stress-vulnerable neurones in prefrontal cortex. Reduced may be realized through destabilized function selective proteins involved organizing neuronal skeleton translating neurotrophic signals. To elucidate mechanisms underlying these effects, rats were exposed chronic footshock stress. Patterns c-fos, phospho-extracellular-regulated protein kinases 1/2 (ERK1/2), calcineurin phospho-cyclic-AMP response-element binding (CREB) expression subsequently investigated. The results indicate impairments cingulate signal transduction cascades plasticity. medial cortex, demonstrated functional hyperactivity dendritic phospho-ERK1/2 hyperphosphorylation, while reduced c-fos immunoreactivity occurred Significantly phospho-CREB both cortical regions, considering its implication brain-derived factor (BDNF) transcription, suggests synaptic This data confirms damaging effect on activity, a level. Due association markers regulation BDNF signalling, findings suggest central role for intracellular neurotrophin members pathways actions brain.