Neuroreport
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Glutamate transporter-1 (GLT-1) reduction causes dysregulation of excitatory-inhibitory balance, contributing toward neuropathic pain development. However, the mechanisms underlying GLT-1 downregulation are still unclear. Histone acetylation plays a pivotal role in the regulation of gene expression. ⋯ Immunofluorescent histochemistry showed that both GLT-1 and AcH3 had high expressions in the dorsal horn. Double staining indicated that several GLT-1-positive cells were colocalized with AcH3. Our data provide evidence that histone deacetylation may contribute toward the loss of GLT-1 and this could be a new consideration for the development of more effective strategies for treating neuropathic pain.
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In cranial and spinal nerve ganglia, both axotomized primary sensory neurons without regeneration (axotomy-nonregenerative neurons) and spared intact primary sensory neurons adjacent to axotomized neurons (axotomy-spared neurons) have been definitely shown to participate in pain transmission in peripheral neuropathic pain states. However, whether axotomized primary sensory neurons with regeneration (axotomy-regenerative neurons) would be integral components of neural circuits underlying peripheral neuropathic pain states remains controversial. In the present study, we utilized an adult rat sciatic nerve crush model to systematically analyze pain behaviors on the glabrous plantar surface of the hindpaw sural nerve skin territories. ⋯ To our surprise, Protein Gene Product 9.5-immunoreactive nerve fibers with regular and large varicosities ectopically emigrated into the upper dermis of the glabrous sural nerve skin territories after adult rat sciatic nerve crush. Our results indicated that axotomy-regenerative primary sensory neurons could be critical elements in neural circuits underlying peripheral neuropathic pain states. Besides, our results implied that peripheral neuropathic pain transmitted by axotomy-regenerative primary sensory neurons alone might be a new dimension in the clinical therapy of peripheral nerve trauma beyond regeneration.
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It is unknown whether normobaric oxygen (NBO) therapy exerts neuroprotective effects against human intracerebral hemorrhage (ICH). In this study, the potential of NBO therapy for salvaging brain damage following ICH was investigated in a rodent model with oxygen delivered at different concentrations. A total of 164 male Sprague-Dawley rats were induced with ICH using a collagenase injection and divided randomly into one ICH control group (no treatment, n=86) and three NBO treatment groups (35, 50, or 90% oxygen, n=26/group). ⋯ ICH rats also showed higher contents of brain water, HIF-1α, and VEGF (peaked at 72 h) in the ipsilateral perihematoma tissue than in the contralateral brain tissue. Compared with the ICH control group, all NBO groups showed improved NSSs, decreased contents of brain water, HIF-1α and VEGF, and fewer apoptotic cells in the perihematoma at 72 h after ICH, but statistical significance of these changes was achieved only with oxygen delivered at 90% (P<0.05, two-way analysis of variance). These results suggest that NBO therapy with oxygen delivered at 90% conferred best neuroprotection to ICH rats, potentially through amelioration of brain edema by suppressing HIF-1α and VEGF expression in the perihematoma.
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Event-related potentials (ERPs) were recorded to explore, for the first time, the electrophysiological correlates of the shape Stroop effect. Fifteen healthy individuals were presented with a frame and a name of an object with a typical shape in life and asked to categorize the object's typical shape in life as a 'circle', a 'square,' or a 'triangle' by pressing the relevant button as quickly as possible. ⋯ N430 is a critical sign of conflict detection in the early stage, whereas late positive component reflects the response conflict in the late stage. The results provided evidence for the dissociation between conflict detection and conflict resolution in the shape Stroop effect.
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P2X3 receptor plays a role in nociception transmission of orofacial pain in temporomandibular disorder patients. A previous study found that P2X3 receptors in masseter muscle afferent neurons and the trigeminal ganglia were involved in masseter muscle pain induced by inflammation caused by chemical agents or eccentric muscle contraction. In this study, we attempted to investigate changes in P2X3 receptors in the trigeminal subnucleus caudalis (Vc) and midbrain periaqueductal gray (PAG) in relation to the hyperalgesia of masseter muscles induced by occlusal interference. ⋯ We found that mechanical pain threshold of bilateral masseter muscles decreased significantly after occlusal interference, which remained for the entire experimental period. The mRNA expression of the P2X3 receptor increased significantly and the number of P2X3R-positive neurons increased markedly in Vc and PAG accordingly. These results indicate that the upregulated expression of P2X3 receptors in Vc and PAG may contribute toward the development of orofacial pain induced by occlusal interference and P2X3 receptors in the PAG may play a key role in the supraspinal antiociception effect.