Neuroscience letters
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Neuroscience letters · Jul 2012
Altered gene expression in cultured microglia in response to simulated blast overpressure: possible role of pulse duration.
Blast overpressure has long been known to cause barotrauma to air-filled organs such as lung and middle ear. However, experience in Iraq and Afghanistan is revealing that individuals exposed to explosive munitions can also suffer traumatic brain injury (TBI) even in the absence of obvious external injury. The interaction of a blast shock wave with the brain in the intact cranial vault is extremely complex making it difficult to conclude that a blast wave interacts in a direct manner with the brain to cause injury. ⋯ Microarray analysis revealed increases in expression of a number of microglial genes relating to immune function and inflammatory responses to include Saa3, Irg1, Fas and CxCl10. All changes in gene expression were dependent on pulse duration and were independent of pressure. These results indicate that microglia are mildly activated by blast overpressure and uncover a heretofore undocumented role for pulse duration in this process.
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Neuroscience letters · Jul 2012
Comparative StudyPromazine and chlorpromazine for prolonged spinal anesthesia in rats.
Though promazine and chlorpromazine elicited cutaneous anesthesia, no study of spinal anesthesia with chlorpromazine and promazine has been reported. This study was to examine whether chlorpromazine and promazine produce spinal anesthesia. Using a rat model via intrathecal injection, we tested spinal blockades of motor function and nociception by promazine, chlorpromazine or bupivacaine, and so were dose-response studies and durations. ⋯ On an equipotent basis (25% effective dose [ED(25)], ED(50), and ED(75)), the block duration caused by chlorpromazine or promazine was longer than that caused by the long-lasting local anesthetic bupivacaine (P<0.01 for the differences). Chlorpromazine and promazine, as well as bupivacaine, showed longer duration of sensory block than that of motor block. Our data reported that intrathecal promazine and chlorpromazine with a more sensory-selective action over motor blockade had less potent and longer-lasting spinal blockades when compared with bupivacaine.
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Neuroscience letters · Jul 2012
Simvastatin mobilizes bone marrow stromal cells migrating to injured areas and promotes functional recovery after spinal cord injury in the rat.
This study investigated the therapeutic effects of simvastatin administered by subarachnoid injection after spinal cord injury (SCI) in rats; explored the underlying mechanism from the perspective of mobilization, migration and homing of bone marrow stromal cells (BMSCs) to the injured area induced by simvastatin. Green fluorescence protein labeled-bone marrow stromal cells (GFP-BMSCs) were transplanted into rats through the tail vein for stem cell tracing. Twenty-four hours after transplantation, spinal cord injury (SCI) was produced using weight-drop method (10g 4cm) at the T10 level. ⋯ Immunofluorescence revealed that simvastatin increased the number of GFP-positive cells in the injured spinal cord, and the number of cells double positive for GFP/NeuN or GFP/GFAP was larger in the simvastatin treated group than the control group. Western blot and immunohistochemistry showed higher expression of BDNF and VEGF in the simvastatin treated group than the control group. In conclusion, simvastatin can help to repair spinal cord injury in rat, where the underlying mechanism appears to involve the mobilization of bone marrow stromal cells to the injured area and higher expression of BNDF and VEGF.
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Neuroscience letters · Jul 2012
Striatal μ-opioid receptor availability predicts cold pressor pain threshold in healthy human subjects.
Previous PET studies in healthy humans have shown that brain μ-opioid receptor activation during experimental pain is associated with reductions in the sensory and affective ratings of the individual pain experience. The aim of this study was to find out whether brain μ-opioid receptor binding at the resting state, in absence of painful stimulation, can be a long-term predictor of experimental pain sensitivity. We measured μ-opioid receptor binding potential (BP(ND)) with μ-opioid receptor selective radiotracer [(11)C]carfentanil and positron emission tomography (PET) in 12 healthy male subjects. ⋯ We used both voxel-by-voxel and region-of-interest image analyses to examine the potential associations between μ-opioid receptor BP(ND) and psychophysical measures. The results show that striatal μ-opioid receptor BP(ND) predicts cold pressor pain threshold, but not cold pressor pain tolerance or tactile sensitivity. This finding suggests that striatal μ-opioid receptor density is involved in setting individual pain threshold.
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Neuroscience letters · Jul 2012
Mechanisms of Bv8-induced biphasic hyperalgesia: increased excitatory transmitter release and expression.
Bv8 is a pronociceptive peptide that binds to two G-protein coupled prokineticin receptors, PK-R1 and PK-R2. These receptors are localized in the dorsal horn of the spinal cord and dorsal root ganglia (DRG) of nociceptive neurons in rodents. Systemic administration of Bv8 elicits a biphasic reduction in nociceptive thresholds to thermal and mechanical stimuli. ⋯ These data suggest that Bv8 induces hyperalgesia by direct release of excitatory transmitters in the spinal cord, consistent with the first phase of hyperalgesia. Additionally, Bv8 elicits a subsequent, protein-synthesis dependent increase in expression and release of excitatory transmitters that may underlie the long-lasting second phase of hyperalgesia. Activation of prokineticin receptors may therefore contribute to persistent hyperalgesia occurring as a consequence of tissue injury further suggesting that these receptors are attractive targets for development of therapeutics for pain treatment.