Abstract
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.
MeSH terms
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Analgesia*
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Analgesics, Opioid / administration & dosage
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Analgesics, Opioid / antagonists & inhibitors
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Analgesics, Opioid / pharmacology*
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Animals
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Dynorphins / administration & dosage
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Dynorphins / antagonists & inhibitors
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Dynorphins / pharmacology*
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Immersion
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Immobilization
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Injections, Intraventricular
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Male
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Mice
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Mice, Inbred ICR
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Naloxone / pharmacology
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Narcotic Antagonists / pharmacology
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Pain Measurement / drug effects
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Peptide Fragments / administration & dosage
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Peptide Fragments / antagonists & inhibitors
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Peptide Fragments / pharmacology*
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Stress, Psychological / psychology*
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Swimming
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Vibration / adverse effects
Substances
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Analgesics, Opioid
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Narcotic Antagonists
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Peptide Fragments
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Naloxone
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dynorphin (1-13)
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Dynorphins
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dynorphin amide (1-10)