engleski

The anticonvulsive effect of swim stress in mice

A recent study (Peričić and Bujas, Brain Res., 752:279-284, 1997) has shown that swim stress enhances the threshold doses of bicuculline producing convulsive signs. It has been suggested that stress-induced release of glucocorticoids from the adrenal glands could be responsible for the observed anticonvulsive effect of stress. The objective of this study was a further elucidation of the anticonvulsive effect of swim stress. The convulsive signs (myoclonic twitch, running/bouncing clonus, tonic hindlimb extensor convulsion, death) were studied in male CBA mice following a constant i.v. infusion of convulsants. Mice were subjected to stress (10 min swimming at 18-19 0 C) 15 min prior to the beginning of infusion. Stress postponed the onset of convulsive signs produced by GABA related (picrotoxin, pentylenetetrazole) and GABA unrelated (strychnine) convulsants. The effect of stress on picrotoxin-induced convulsions could not be mimicked by corticosterone, or blocked by aminoglutethimide (50 mg/kg s.c.), which blocks the synthesis of adrenocortical steroids. Furthermore, the effect could not be prevented by flumazenil (10 mg/kg i.p.), the antagonist of benzodiazepine receptors, or by haloperidol (0.2 mg/kg i.p. ), a dopamine and sigma receptor antagonist. The effect of stress was potentiated by propranolol (10 mg/kg i.p.), a non-selective b-adrenoceptor and 5-HT1 antagonist, and by betaxolol (20 mg/kg i.p.), a selective b1-adrenoceptor antagonist, but also by isoproterenol (10 mg/kg i.p.), a b-adrenoceptor agonist, all given in doses ineffective in control animals. The results do not support the involvement of glucocorticoids, and among the receptors under study, only b-adrenoceptors appear to interfere with the anticonvulsive effect of swim stress.

stress; convulsions; mice

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