Chronic forced swim stress inhibits ultra-low dose morphine-induced hyperalgesia in rats

Abstract

Ultra-low doses of morphine (UL-morphine) induce hyperalgesia, which is assumed to be mediated by stimulatory G proteins (G(alphas)) signaling pathway. G(alphas) pathway inhibition and chronic stress both attenuate development of tolerance to analgesic effect of morphine. This study evaluated the effect of chronic stress on UL-morphine-induced hyperalgesia to find out if chronic stress interacts with the G(alphas) signaling pathway. Repeated daily forced swim stress was applied to induce chronic stress. UL-morphine (1 microg/kg, intraperitoneal)-induced hyperalgesia was assessed using the tail-flick test on day 6, in male rats that during days 1-5 received different treatments of swim stress, dexamethasone, swim stress following adrenalectomy (ADX) or swim stress after sham operation. Chronic stress by itself induced hyperalgesia in control and sham-operated rats but inhibited UL-morphine-induced hyperalgesia. In ADX animals, chronic stress did not produce hyperalgesia and could not inhibit UL-morphine-induced hyperalgesia. Chronic dexamethasone produced hyperalgesia but did not change the UL-morphine-induced hyperalgesia. Inhibition of UL-morphine hyperalgesia by chronic stress suggests that chronic stress interacts with the G(alphas) signaling pathway, which is responsible for UL-morphine-induced hyperalgesia. The absence of this effect in the ADX-rats or after repetitive dexamethasone administration demonstrates that hypothalamic-pituitary-adrenal (HPA) axis activation is necessary for controlling UL-morphine-induced hyperalgesia. Finally, the interaction of stress with the G(alphas) signaling pathway may provide an explanation for the inhibitory effect of stress on development of tolerance to the analgesic effect of morphine.

Genotype-dependent responsivity to inflammatory pain: A role for TRPV1 in the periaqueductal grey

“…Furthermore, chronic water avoidance induces changes in transient receptor potential receptor TRPV1 and the cannabinoid (CB 1 ) receptor expression in the spinal cord (Hong et al, 2009, Hong et al, 2011 which were attenuated by the glucocorticoid receptor antagonist (RU-486). The results were consistent with previous work from Fereidoni et al where adrenalectomy diminished forced swim stress-induced hyperalgesia in rats (Fereidoni et al, 2007).…”

Depressive status does not alter renal oxidative and immunological parameters during early diabetic nephropathy in rats

“…This depressive mood increased during the 15 days of FST in both diabetic and control rats, suggesting that chronic experimental depression were development in all FST groups. FST has been considered as one of the most used tools for screening antidepressants (Lucki 1997;Petit-Demouliere et al 2005;de Paulis 2007;Fereidoni et al 2007) and as one of the experimental depression inducer (Takao et al 1995;Carrizo et al 1997). Depressive parameters observed in FST need to be confirmed with some spontaneous locomotor activity studies (PetitDemouliere et al 2005).…”

Behavioral Neurobiology of Chronic Pain

“…Hyperalgesia in the tail-flick test following repeated forced swim stress was abolished in adrenalectomized rats (Fereidoni et al 2007). Hyperalgesia in the tail-flick test following repeated forced swim stress was abolished in adrenalectomized rats (Fereidoni et al 2007).…”

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