Long lasting increase in nociçeptive threshold induced in mice by forced swimming: involvement of an endorphinergic mechanism

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Abstract

Mice submitted to forced swimming session(s) displayed a long lasting modification in their nociceptive threshold, assessed through their jump latency from a hot plate (55°C). Thus two forced swimming sessions (6 min each, 8h apart), in water at 33°C, increased by about 50% the jump latency when the hot plate test was performed 14 hours, 3 days or 6 days thereafter. The water temperature (16°C vs 33°C) had no critical influence in this respect. To be clearly effective (at 33°C) the swimming session had tp.be performed twice (when performed only once it was irregularly effective); it apparently culminated for a 6 min duration, since its effectiveness was not significantly increased by extending the swimming time to 12 min or 18 min. Performing 2 forced swimming sessions (6 min each, 8h apart), 5 consecutive days, resulted in a suppression of the increase in jump latency in the hot plate test. The two forced swimming episodes-induced analgesia was prevented by the s.c. administration of diazepam (from 0.125 mg/kg) or morphine (from 5 mg/kg) or scopolamine (1 mg/kg) before each forced swimming episode. Morphine (7.5 mg/kg) was uneffective to prevent the induction of two forced swimming episodes-induced analgesia when it was administered immediately after each forced swimming session. Finally this analgesia was dose dependently reversed by naloxone (ID50 = 0.14 mg/kg, s.c., 30 min before the hot plate test). It is hypothetized that the handling of mice immediately before the hot plate test induces the remembrance of the stress induced by previous forced swimming episodes, triggering a fear reaction which increases the nociceptive threshold. © 2000 OPA (Overseas Publishers Association) Amsterdam U.V. Published by license under the Gordon and Breach Publishers imprint.

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Suaudeau, C., & Costentin, J. (2000). Long lasting increase in nociçeptive threshold induced in mice by forced swimming: involvement of an endorphinergic mechanism. Stress, 3(3), 221–227. https://doi.org/10.3109/10253890009001126

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