Neuroscience letters
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Neuroscience letters · Feb 2013
Activation of JAK-STAT3 signaling pathway in chronic subdural hematoma outer membranes.
Chronic subdural hematoma (CSDH) is an inflammatory disease, the mechanism of which still remains to be elucidated. Interleukin-6 (IL-6), one of the inflammatory cytokines regulating janus kinase (JAK)-signal transducer and activator of transcription (STAT) signaling pathway, is expressed in human CSDH fluid. The status of this signaling pathway in human CSDH outer membranes was examined in the present study using outer membranes obtained during trepanation surgery. ⋯ In some cases, p-STAT3 at Ser(727) could also be detected, while p-STAT1 at Ser(727) could not. The localizations of STAT1 and STAT3 were revealed to be present in fibroblasts in human CSDH outer membranes, especially when p-STAT3 at Tyr(705) was in the nuclei of fibroblasts. These findings suggest that JAK1-STAT3 signaling is dominantly activated in fibroblasts of human CSDH outer membranes compared with STAT1 and indicate the possibility that this JAK1-STAT3 pathway might be activated by IL-6 and play a critical role in progression of human CSDH.
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Neuroscience letters · Feb 2013
The effects of menthol on cold allodynia and wind-up-like pain in upper limb amputees with different levels of phantom limb pain.
The mechanisms underlying phantom limb pain are not fully known, but hypersensitivity appears to be a central element. Menthol has previously been suggested as a model for hypersensitivity, but it has not yet been investigated if different levels of neuropathic pain may influence the effects of menthol or if topical application of menthol may act as a model for hypersensitivity in patients with phantom limb pain. In the present study, menthol (l-menthol 40%) was applied to the affected and non-affected sides in 24 upper-limb amputees with different levels of phantom limb pain to test if menthol could induce cold allodynia and exacerbate wind-up-like pain. ⋯ After application of menthol, the level of phantom limb pain was only related to wind-up-like pain following brush (P=0.011) but not pinprick stimulation (P=0.233). This study indicates that menthol does influence hypersensitivity in phantom limb pain patients, and it is the first study to show that menthol may exacerbate wind-up-like pain in this group of neuropathic pain patients. The findings suggest that menthol may act as a model for studying sensitization in phantom limb patients.
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Neuroscience letters · Feb 2013
Involvement of central cholinergic mechanisms on sodium intake induced by gabaergic activation of the lateral parabrachial nucleus.
Bilateral injections of the GABA(A) agonist muscimol into the lateral parabrachial nucleus (LPBN) disrupt satiety and induce strong ingestion of water and 0.3M NaCl in fluid-replete rats by mechanisms not completely clear. In the present study, we investigated the effects of the blockade of central muscarinic cholinergic receptors with atropine injected intracerebroventricularly (i.c.v.) on 0.3M NaCl and water intake induced by muscimol injections into the LPBN in fluid-replete rats. Male Holtzman rats with stainless steel cannulas implanted bilaterally into the LPBN and unilaterally into the lateral ventricle (LV) were used. ⋯ The i.c.v. injection of atropine did not affect 0.3M NaCl (26.8±6.2mL/2h, vs. saline i.c.v.: 36.5±9.8mL/2h) or water intake (14.4±2.5mL/2h, vs. saline i.c.v.: 15.6±4.8mL/2h) in rats treated with furosemide+captopril subcutaneously combined with bilateral injections of moxonidine (α(2)-adrenoceptor/imidazoline agonist, 0.5nmol/0.2μL) into the LPBN, suggesting that the effect of atropine was not due to non-specific inhibition of ingestive behaviors. The results show that active central cholinergic mechanisms are necessary for the hypertonic NaCl and water intake induced by the blockade of the inhibitory mechanisms with injections of muscimol into the LPBN in fluid-replete rats. The suggestion is that in fluid-replete rats the action of LPBN mechanisms inhibits facilitatory signals produced by the activity of central cholinergic mechanisms to maintain satiety.
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Neuroscience letters · Feb 2013
Treadmill running and static stretching improve long-lasting hyperalgesia, joint limitation, and muscle atrophy induced by cast immobilization in rats.
The effects of exercise on chronic pain induced by immobilization are incompletely understood. The purpose of this study was to investigate whether 30min of treadmill running (TR; active exercise) and 10min of static stretching (SS; passive exercise) of the immobilized hindlimb reduce widespread chronic pain, joint limitation, and hindlimb muscle atrophy induced by cast immobilization in rats. One hindlimb of Sprague Dawley (SD) rats was immobilized for 2 weeks with a cast, and remobilization was conducted for 7 weeks. ⋯ Both forms of exercise significantly inhibited mechanical hyperalgesia in the calf and hindpaw in immobilized rats. Range-of-motion limitations in the knee and ankle joints and calf muscle atrophy after cast removal were also decreased by both TR and SS. This study is the first to demonstrate the beneficial effect of TR and SS on widespread chronic pain, joint limitation, and muscle atrophy in a cast-immobilized rat model.
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Neuroscience letters · Feb 2013
Repeated exposure to propofol potentiates neuroapoptosis and long-term behavioral deficits in neonatal rats.
Previous studies have shown that exposure of the immature brain to drugs that block NMDA glutamate receptors or drugs that potentiate GABA(A) receptors can trigger widespread neuroapoptosis. Almost all currently used general anesthetics have either NMDA receptor blocking or GABA(A) receptor enhancing properties. Propofol, a new intravenous anesthetic, is widely used in pediatric anesthesia and intensive care practice whose neurotoxicity on brain development remains unknown. ⋯ This treatment also produced a remarkable reduction in the levels of excitatory neurotransmitters in the cortex and the hippocampus as measured by high performance liquid chromatography. Repeated exposure to propofol induced exposure-time dependent neuroapoptosis and long-term neurocognitive deficits in neonatal rats. The neurocognitive deficits may be attributed to neuronal loss and a reduction of excitatory neurotransmitter release in the cortex and hippocampus.