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Previous studies have confirmed that the number of glial fibrillary acidic protein-positive cells significantly increases during morphine tolerance.However,morphine tolerance is reversed with melanocortin receptor antagonists,and analgesic action is enhanced accordingly.However,these mechanisms remain unclear.In the present study,following addition of morphine to Wistar rat spinal cord astrocytes,glutamate levels in the supernatant significantly increased(P < 0.05).At 30-120 minutes following addition of intervention agent to spinal cord astrocytes,naloxone significantly increased glutamate release in morphine-tolerant model cells(P < 0.05),while melanocortin receptor antagonist HS014 decreased glutamate release(P < 0.05).Additional naloxone and HS014 to astrocytes significantly decreased glutamate release compared with additional naloxone alone(P < 0.01).Results from the present study demonstrated that glutamate release was increased in spinal cord astrocytes co-cultured with morphine.Naloxone increased glutamate release,and HS014 reduced glutamate release.
Previous studies have confirmed that the number of glial fibrillary acidic protein-positive cells significantly increased during morphine tolerance. However, morphine tolerance is reversed from melanocortin receptor antagonists, and analgesic action is enhanced accordingly. , following addition of morphine to Wistar rat spinal cord astrocytes, glutamate levels in the supernatant significantly increased (P <0.05) .At 30-120 minutes following addition of intervention agent to spinal cord astrocytes, naloxone significantly increased glutamate release in morphine-tolerant model (P <0.05), while melanocortin receptor antagonist HS014 decreased glutamate release (P <0.05) .Additional naloxone and HS014 to astrocytes significantly decreased glutamate release compared with additional naloxone alone release was increased in spinal cord astrocytes co-cultured with morphine .Naloxone increased glutamate release, and HS014 reduced glutamate release.