The consequences of epileptic seizures related to postictal inhibition in early postictal period include postictal analgesia. We studied this phenomenon over 96 h following flurothyl-induced seizures in adult male Wistar rats. Nociception of control (no seizure) and seizured groups were tested using the plantar and von Frey hair tests. We determined latency of forepaw and hind paw reactions using plantar tests and the number of von Frey hairs reactions. Shortly after seizures, longer plantar test latencies were seen relative to the control group. Before the seizures the plantar test reaction times were significantly shorter in forepaws than in hind paws. The effect disappeared post-seizure and surprisingly, it also disappeared at the corresponding time in controls; it reappeared after 48 h in the seizure group and after 24 h in controls. Differences in the von Frey hairs test occurred at 5 and 60 min post-seizure, however, these differences could not be explained by limb anatomy; although, different thermal and mechanical nociception mechanisms could be significant. The unexpected reactions in controls could be related to brief social and physical interactions between the two groups. and J. Mareš, R. Rokyta.
The rationale for the topical application of capsaicin and other vanilloids in the treatment of pain is that such compounds selectively excite and subsequently desensitize nociceptive neurons. This desensitization is triggered by the activation of vanilloid receptors (TRPV1), which leads to an elevation in intracellular free Ca2+ levels. Depending on the vanilloid concentration and duration of exposure, the Ca2+ influx via TRPV1 desensitizes the channels themselves, which may represent not only a feedback mechanism protecting the cell from toxic Ca2+ overload, but also likely contributes to the analgesic effects of capsaicin. This review summarizes the current state of knowledge concerning the mechanisms that underlie the acute capsaicin-induced Ca2+-dependent desensitization of TRPV1 channels and explores to what extent they may contribute to capsaicin-induced analgesia. In view of the polymodal nature of TRPV1, we illustrate how the channels behave in their desensitized state when activated by other stimuli such as noxious heat or depolarizing voltages. We also show that the desensitized channel can be strongly reactivated by capsaicin at concentrations higher than those previously used to desensitize it. We provide a possible explanation for a high incidence of adverse effects of topical capsaicin and point to a need for more accurate clinical criteria for employing it as a reliable remedy., L. Vyklický, K. Nováková-Toušová, J. Benedikt, A. Samad, F. Touška, V. Vlachová., and Obsahuje bibliografii a bibliografické odkazy
The analgesic effects of intracerebroventricularly (i.c.v.) administered dynorphin A(l-13) and its analog dynorphin A(l-10)amide using the hot plate test were studied in mice. Both dynorphins applied i.c.v. by the freehand method had an analgesic effect but no effect was seen when applied i.c.v. through an implanted cannula. Moreover, freehand i.c.v. injection of saline increased the time of immobility in the forced swimming test and glycaemia levels compared with intact mice. In contrast to the freehand injection, saline administration through an implanted cannula did not influence the immobility of animals in forced swimming test when compared with the intact controls. These results suggest that 1) the freehand method is very stressful procedure of administration which could influence the effects of dynorphins in the hot plate test and 2) dynorphins exert an analgesic effect in the hot plate test only when combined with a stressor (freehand i.c.v. injection).
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.