Neuroscience letters
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Neuroscience letters · May 2013
Progesterone attenuates early brain injury after subarachnoid hemorrhage in rats.
Although the neuroprotective effects of progesterone against early brain injury (EBI) after trauma have been demonstrated in several studies, whether progesterone reduces EBI after subarachnoid hemorrhage (SAH) remains unknown. In this study, we explored the effect of progesterone on cell apoptosis, stability of the blood-brain barrier (BBB), brain edema, and mortality in male Sprague-Dawley rats subjected to subarachnoid hemorrhage-induced EBI by endovascular perforation. ⋯ Progesterone may reduce EBI after SAH by inhibiting cell apoptosis and stabilizing the BBB.
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Neuroscience letters · May 2013
Neurotropin inhibits axonal transport in cultured mouse dorsal root ganglion neurons.
Axonal transport is a basic neuronal cell function and important for the supply of materials that maintain neuronal cells, and any increase or decrease in axonal transport expresses the state of neurons. Neurotropin is an analgesic agent commonly used for the treatment of chronic pain, but its mechanism of action remains not fully understood. The effects of neurotropin have been investigated in various animal models of nerve injury and chronic pain. ⋯ Movement of organelles in neurites was recorded by real-time video-enhanced microscopy. Neurotropin significantly reduced bidirectional axonal transport in time- and concentration-dependent manners without affecting the diameter of these neurites. This is the first report to show the inhibitory effect of neurotropin on axonal transport, and suggest that this action may mediate, at least in part, the analgesic effects of this agent.
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Neuroscience letters · May 2013
Capsaicin avoidance as a measure of chemical hyperalgesia in orofacial nerve injury models.
Many patients suffer from trigeminal neuralgia and other types of orofacial pain that are poorly treated, necessitating preclininal animal models for development of mechanisms-based therapies. The present study assessed capsaicin avoidance and other nocifensive behavioral responses in three models of orofacial nerve injury in rats: chronic constriction injury (CCI) of the mental nerves, partial tight ligation of mental nerves, and CCI of lingual nerves. We additionally investigated if nerve injury resulted in enhanced capsaicin-evoked activation of neurons in trigeminal caudalis (Vc) or nucleus of the solitary tract (NTS) based on expression of Fos-like immunoreactivity (FLI). ⋯ CCI of lingual nerves did not affect capsaicin avoidance. Counts of FLI in Vc were significantly higher in the lingual sham and mental nerve CCI groups compared to mental shams; FLI counts in NTS did not differ among groups. Mental nerve CCI may have induced central sensitization of chemical nociception since increased capsaicin avoidance was accompanied by greater activation of Vc neurons in response to oral capsaicin.
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Neuroscience letters · May 2013
Spinal neuroimmune activation inhibited by repeated administration of pioglitazone in rats after L5 spinal nerve transection.
Neuroimmune activation contributes to the generation and maintenance of neuropathic pain after peripheral nerve injury. Peroxisome proliferator activated receptor gamma (PPAR-γ) agonists have potential neuroprotection. The current study aimed to determine the effects of a PPAR-γ agonist pioglitazone on mechanical hyperalgesia and neuroimmune activation in a rat model of neuropathic pain induced by L5 spinal nerve transection (SNT). ⋯ Glial fibrillary acidic protein (GFAP) expression, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6 levels, and nuclear factor-kappa B (NF-κB) activity in the lumbar spinal cord were determined on day 14 after operation. The results displayed pioglitazone improved the mechanical hyperalgesia, and attenuated the astrocyte and NF-κB activation and the inflammatory cytokine upregulation in nerve-injured rats, which might be reversed by GW9662. In conclusion, pioglitazone ameliorates the mechanical hyperalgesia induced by L5 SNT via inhibiting the spinal neuroimmune activation in rats, suggesting spinal PPAR-γ signaling pathway may be involved in the pathogenesis of mechanical hyperalgesia.
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Neuroscience letters · May 2013
Role of spinal opioid receptor on the antiallodynic effect of intrathecal nociceptin in neuropathic rat.
The purpose of this study was to examine the effects of intrathecal nociceptin for neuropathic pain and determine the role of spinal opioid receptor types. Neuropathic pain was induced by ligation of L5 and L6 spinal nerves in male Sprague-Dawley rats. Several antagonists were intrathecally administered to evaluate the action mechanisms of nociceptin: nonselective opioid receptor antagonist (naloxone), μ opioid receptor antagonist (CTOP), δ opioid receptor antagonist (naltrindole) and κ opioid receptor antagonist (GNTI). ⋯ Intrathecal nociceptin increased the level of δ opioid receptor protein compared with that of nerve ligated rats, while the levels of μ, and κ opioid receptor proteins were unchanged. These results suggest that intrathecal nociceptin produced antiallodynic effect in spinal nerve ligation-induced neuropathic pain. All three types of spinal μ, δ, and κ opioid receptors were involved in the antiallodynic mechanism of nociceptin.