Stress rapidly dysregulates the glutamatergic synapse in the prefrontal cortex of cocaine‐withdrawn adolescent rats

摘要: Although several lines of evidence have shown that chronic cocaine use is associated with stress system dysregulation, the underlying neurochemical mechanisms are still elusive. To investigate whether rapid stress-induced response glutamatergic synapse was influenced by a previous history cocaine, rats were exposed to repeated injections during adolescence [from postnatal day (PND) 28–42], subjected single swim (5 minutes) three days later (PND 45) and sacrificed 15 minutes after end this stressor. Critical determinants homeostasis measured in medial prefrontal cortex (mPFC) whereas circulating corticosterone levels plasma. Exposure saline-treated animals did not show changes crucial synapse. Conversely, cocaine-treated animals, dynamically altered by: (1) enhancing presynaptic vesicular mediators glutamate release; (2) reducing transporters responsible for clearance; (3) increasing postsynaptic responsiveness N-methyl-D-aspartate subunit GluN1; (4) causing hyperresponsive spines as evidenced increased activation cdc42-Pak pathway. These findings indicate exposure sensitizes mPFC synapses stress. It suggested signaling may contribute sensitivity observed users. Moreover, processes play an important role reinstatement seeking.