Neuroscience letters
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Neuroscience letters · Jun 2013
JNK pathway may be involved in isoflurane-induced apoptosis in the hippocampi of neonatal rats.
Previous studies have demonstrated that isoflurane, a commonly used volatile anesthetic, can induce widespread apoptosis in the neonatal animal brains and result in persistent cognitive impairment. Isoflurane-induced cytosolic Ca(2+) overload and activation of mitochondrial pathway of apoptosis may be involved in this neurodegeneration. The c-Jun N-terminal kinase (JNK) signaling can regulate the expression of the Bcl-2 family members that modulates mitochondrial membrane integrity. ⋯ SP600125 also attenuated isoflurane-induced down-regulation of Bcl-xL and maintained the activated Akt level to increase the phosphorylation of GSK-3β at Ser9. Our results indicate that JNK activation contributes to isoflurane-induced neuroapoptosis in the developing brain. Maintaining Bcl-xL and Akt activation may be involved in the neuroprotective effects of SP600125.
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Neuroscience letters · Jun 2013
A selective inhibitor of Drp1, mdivi-1, protects against cell death of hippocampal neurons in pilocarpine-induced seizures in rats.
Mdivi-1 is a selective inhibitor of a mitochondrial fission protein Drp1. Recent studies demonstrated that inhibition of Drp1 provides neuroprotection in vitro and in vivo. In this study, we examined the role of mdivi-1 in hippocampal neuron death after seizures induced by pilocarpine. ⋯ In addition, the seizures resulted in up-regulation of Drp1 expression and mdivi-1 treatment had no effect on the expression. Moreover, we also found that mdivi-1 (1.25 mg/kg) treatment reversed the release of cytochrome c (CytC), translocation of apoptosis-inducing factor (AIF) induced by seizures while inhibiting the activated caspase-3. Altogether, our data suggested that mdivi-1 exerts neuroprotective effects against cell death of hippocampal neurons induced by seizures, and the underlying mechanism may be through inhibiting CytC release, AIF translocation and suppression of the mitochondrial apoptosis pathway.
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Neuroscience letters · Jun 2013
Artemin-GFRα3 interactions partially contribute to acute inflammatory hypersensitivity.
The expression of artemin (ARTN), a glial cell line-derived neurotrophic factor (GDNF) family ligand, increases in pre-clinical models of nociception and recent evidence suggests this growth factor may play a causative role in inflammatory pain mechanisms. The aim of this study was to demonstrate functional inhibition of ARTN with monoclonal antibodies and to determine whether ARTN neutralisation could reverse inflammatory pain in mice. ⋯ Anti-ARTN antibodies had no effect on hypersensitivity in response to partial nerve ligation in mice. These data suggest that ARTN-GFRα3 interactions partially mediate early stage nociceptive signalling following an inflammatory insult.
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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.