Brain research bulletin
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Brain research bulletin · Jan 2010
Sensitization of voltage activated calcium channel currents for capsaicin in nociceptive neurons by tumor-necrosis-factor-alpha.
It is known that application of tumor-necrosis-factor-alpha (TNF-alpha) sensitizes neuronal calcium channels for heat stimuli in rat models of neuropathic pain. This study examines whether TNF-alpha modulates the capsaicin-induced effects after transient receptor potential vanilloid (TRPV)-1 receptor activation on voltage activated calcium channel currents (I(Ca(V))). TRPV-1 receptors are activated by heat and play an important role in the pathogenesis of thermal hyperalgesia in neuropathic pain syndromes, while voltage activated channels are essential for transmission of neuronal signals. ⋯ While L-type (36.6+/-5.2%) and P/Q-type currents (35.6+/-4.1%) are also sensitized by TRPV-1 activation, N-type channel currents are most sensitive (74.5+/-7.3%). The capsaicin-induced shift towards the hyperpolarizing voltage range does not occur when TNF-alpha is applied. Summarizing, TNF-alpha sensitizes nociceptive neurons for capsaicin.
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Brain research bulletin · Dec 2009
The effects of acute stress and acute corticosterone administration on the immobility response in rats.
The immobility response is an innate antipredatory behavior in a broad variety of species. The immobility response varies in its postural components but in general is characterized by an absence of movement and a relative unresponsiveness to stimuli. Experimentally in rats, clamping the neck followed by body inversion and manual restrain elicits a response called "immobility by clamping the neck". ⋯ We observed that either previous acute stress caused by forced exposure to elevated open platform or application of a heat-pain stimulus to the rat's tail during the immobility increased the duration of the immobility response caused by clamping the neck. Also, the corticosterone produced a rapid increase (15 min after injection) in the duration of this immobility response. Our results show that the acute stress, in rats, is a facilitator of the immobility response and suggest a possible nongenomic rapid action of corticosterone over brain structures that control this behavior.
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Brain research bulletin · Dec 2009
Effect of puerarin on P2X3 receptor involved in hyperalgesia after burn injury in the rat.
The study investigated the effects of puerarin on P2X(3) receptor involved in hyperalgesia after burn injury in the rat. Superficial second degree burn injury models were adopted. Mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) were measured and the P2X(3) receptor expressions in dorsal root ganglion (DRG) from burn injury models rats were detected by immunohistochemistry, in situ hybridization, RT-PCR and western blot. ⋯ At day 3 post-burn, the expressions of P2X(3) protein and mRNA in DRG neurons in untreated superficial second degree back burn group were increased significantly compared with sham back burn group, puerarin-treated back unburned control group, blank back control group, while in puerarin-treated superficial second degree back burn group, the P2X(3) protein and mRNA expressions were decreased markedly. There is no significant difference in sham back burn group, puerarin-treated back unburned control group, blank back control group. Therefore, puerarin may reduce the nociceptive transmission of burn injury pain mediated by P2X(3) receptor and alleviate P2X(3) receptor involved in hyperalgesia after burn injury in the rats.
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Brain research bulletin · Aug 2009
Cerebellar peduncle injury in patients with ataxia following diffuse axonal injury.
No diffusion tensor imaging (DTI) study has yet investigated ataxia in diffuse axonal injury (DAI). In the current study, we used DTI to investigate cerebellar peduncle lesions of patients who showed severe ataxia following DAI. Six patients with severe ataxia following DAI and six age-and sex-matched control subjects were recruited. ⋯ In each of the 20 cerebellar peduncles, all the lesions displaying the lowest FA values relative to that of normal controls (11 peduncles; 55%) were located in the junction between brain stem and cerebellum and post-junctional area (nine peduncles; 45%). The junction and peri-junctional areas between the brain stem and cerebellum appear to be the most vulnerable area by DAI, with the order of incidence SCP, ICP, and MCP. Evaluation of the cerebellar peduncles using DTI can be helpful in patients with ataxia following DAI.
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Brain research bulletin · Aug 2009
N-Methyl-D-aspartate receptor antagonist d-AP5 prevents pertussis toxin-induced alterations in rat spinal cords by inhibiting increase in concentrations of spinal CSF excitatory amino acids and downregulation of glutamate transporters.
Recently, we found that intrathecal (i.t.) pertussis toxin (PTX) injection produces thermal hyperalgesia and is associated with increasing concentrations of excitatory amino acids (EAAs) in spinal cerebrospinal fluid (CSF) dialysates; a reduction in the antinociceptive effects of morphine and glutamate transporters (GTs) was also observed. The reduction in the morphine-induced analgesic effects is directly related to increased extracellular EAA levels, which are maintained by GTs at physiological levels. In this study, we aimed to examine the role of GT isoforms in thermal hyperalgesia, determine the EAA concentrations in CSF dialysates, and elucidate the role of N-methyl-d-aspartate (NMDA) receptors in PTX-induced reduction in the antinociceptive effects of morphine. ⋯ The microdialysis probe was used to collect CSF dialysates for EAA measurements by high-performance liquid chromatography. Intrathecal morphine failed to produce antinociceptive effects in PTX-treated rats, and d-AP5 coinfusion prevented the PTX-induced reduction in the antinociceptive effect and associated downregulation of the GTs. We conclude that NMDA receptor suppression inhibits EAA excitation and reduces the morphine-induced antinociception in PTX-treated rats.