Behavioral and electrophysiological (ECoG) effects of haplophyllum robustum and TRPA1 antagonist in adult male wistar rats.

This article aimed to investigate the effects of Haplophyllum robustum hydroalcoholic extract on animals' behavioral and electrocorticographic changes. This plant is mainly found in Turkey, Iran, and Central Asia, and is reported to have convulsive effects. In this article, we worked on the effects of its hydroalcoholic extract on electrocorticography (ECoG), along with changes induced by intracerebroventricular administration of GABAA antagonists. Furthermore, the effects of low doses of this extract on behavioral depression were examined. Four animal sets were used to compare ECoG in Wistar rats. A group of negative control, a group of positive control (PTZ), and two groups received an injection of plant extract (500 mg/kg, ip), with or without administration of Diazepam (5 mg/kg). Also, three sets were applied to compare receiving and not receiving intracerebroventricular (icv) injection of Transient receptor potential ankyrin 1 antagonist (HC-030031) (2 µg/kg) on plant-induced seizure delay and animal death. Two groups of control and a group with plant extract together with TRPA1 antagonist were administrated. Furthermore, in the present study, the forced swimming test (FST) was used as a model of depression. The behaviors of animals in three groups of negative control and positive control (Fluoxetine) and plant extract (200 mg/kg, ip) were compared. According to the ECoG, high doses of extract of plants led to seizures similar to PTZ, which were then reduced by diazepam injection. At this dose, injection of TRPA1 antagonist did not significantly delay the onset of seizures or the death of the animals. Further, a subconvulsive dose of hydroalcoholic plant extracts was equally effective in treating depression as Fluoxetine injections.

Nifedipine suppresses morphine-induced thermal hyperalgesia: evidence for the role of corticosterone.

It has been shown that systemic administration of morphine induced a hyperalgesic response at an extremely low dose. We have examined the effect of nifedipine, as a calcium channel blocker, on morphine-induced hyperalgesia in intact and adrenalectomized rats and on hypothalamic-pituitary-adrenal axis activity induced by ultra-low dose of morphine. To determine the effect of nifedipine on hyperalgesic effect of morphine, nifedipine (2 mg/kg i.p. and 10 microg i.t.) that had no nociceptive effect, was injected concomitant with morphine (1 microg/kg i.p. and 0.01 microg i.t. respectively). The tail-flick test was used to assess the nociceptive threshold, before and 30, 60, 120, 180, 240 and 300 min after drug administration. The data showed that low dose morphine systemic administration could produce hyperalgesic effect in adrenalectomized rats equivalent to sham-operated animals while intrathecal injection of morphine only elicited hyperalgesia in sham-operated animals. Nifedipine could block morphine-induced hyperalgesia in sham and adrenalectomized rats and even a mild analgesic effect was observed in the adrenalectomized group which was reversed by corticosterone replacement. Systemic administration of low dose morphine produced significant increase in plasma level of corticosterone. Nifedipine has an inhibitory effect on morphine-induced corticosterone secretion. Thus, the data indicate that dihydropyridine calcium channels are involved in ultra-low dose morphine-induced hyperalgesia and that both the pattern of morphine hyperalgesia and the blockage of it by nifedipine are modulated by manipulation of the hypothalamic pituitary adrenal axis.