Brain research
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The effect of 17beta-estradiol on the secondary damage following spinal cord injury (SCI) was examined in male rats subjected to moderate compression. Two doses of 17beta-estradiol (0.1 or 4 mg/kg) were injected i.p. immediately after spinal cord compression. Functional outcome was observed during 4 weeks following injury with two different tests. ⋯ These results suggest that 17beta-estradiol protects the spinal cord by stimulating early cytokines release and astroglial responses. These stimulations may prevent the area of damage from expanding and inflammatory cells to spread in the surrounding tissue during the critical first week following SCI. Although transient, these effects improved the locomotor recovery that was sustained over 4 weeks after injury.
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Bilobalide, a constituent of Ginkgo biloba, has neuroprotective properties. Its mechanism of action is unknown but it was recently found to interact with neuronal transmission mediated by glutamate, gamma-aminobutyric acid (GABA) and glycine. The goal of this study was to test the interaction of bilobalide with glycine in assays of neuroprotection. ⋯ In this model, glycine release was induced by ischemia, an effect that was strongly reduced by bilobalide. We conclude that bilobalide does not interact with glycine receptors in neurochemical assays but it significantly reduces the release of glycine under ischemic conditions. This effect likely contributes to bilobalide's neuroprotective effects in assays of excitotoxicity and ischemia.
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Vanilloid receptor 1 (VR1) is a noxious receptor and a novel target for pain therapy. Cochinchinenin B (6-hydroxy-7-methoxy-3-(4'-hydroxybenzyl) chromone; CB) is one of the small-molecular components from the flavonoids of Dragon's Blood, a well-known herbal medicine to treat various types of pain. Using whole-cell patch clamp technique, we found that capsaicin (CAP)-activated currents (ICAP) was inhibited by CB with an IC50 of 0.92 mM in acutely isolated rat dorsal root ganglion (DRG) neurons. ⋯ The bind site was on the extracellular part of the channel since intracellular application of CB did not alter the inhibition effect on ICAP. In addition, CB inhibited CAP-evoked depolarization under current-clamp condition. Our findings indicate that CB may be a candidate in developing new analgesic drugs targeting the VR1 receptor.
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The present study aims to investigate changes of spinal cord AMPA receptor GluR1 and its phosphorylation in inflammatory and neuropathic pain. Complete Freund's adjuvant (CFA) injection into the hind paw produced inflammatory thermal hyperalgesia that was assessed by decreased response latency to radiant heat; spinal nerve ligation (SNL) was used to induce mechanical allodynia that was evaluated with von Frey hairs. ⋯ In contrast, neither GluR1 nor pGluR1 showed any significant change in rats following SNL. These results suggest that phosphorylated GluR1 (pGluR1-Ser845 and pGluR1-Ser831) might play a role in the induction of inflammatory but not neuropathic pain.