
Dynorphin A (1-13) and its analog dynorphin A (1-10) amide were applied intracerebroventricularly in male ICR mice. Both dynorphins did not reveal any analgesic activity in tail-flick test under normal (non-stressed) conditions. However, in combination with stress (forced swimming or whole body vibration) both dynorphins prolonged tail-flick latencies when compared with stressed saline controls. Naloxone inhibited the effect of dynorphins in forced swimming test. Neither dynorphin A (1-13) nor dynorphin A (1-10) amide increased tail-flick latencies when combined with weak immobilization stress. Our results suggest that the analgesic effects of dynorphins are potentiated by strong stressors.
Male, Mice, Inbred ICR, Naloxone, Narcotic Antagonists, Dynorphins, Vibration, Peptide Fragments, Analgesics, Opioid, Immobilization, Mice, Immersion, Animals, Analgesia, Stress, Psychological, Swimming, Injections, Intraventricular, Pain Measurement
Male, Mice, Inbred ICR, Naloxone, Narcotic Antagonists, Dynorphins, Vibration, Peptide Fragments, Analgesics, Opioid, Immobilization, Mice, Immersion, Animals, Analgesia, Stress, Psychological, Swimming, Injections, Intraventricular, Pain Measurement
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