高低頻電針刺激合骨穴引發大鼠差異性之交感神經系統活性

To address the effect of electroacupuncture (Ea) on autonomic nerve activity, the responses of rhythmic micturition contraction (RMC), urine excretion (UE), blood pressure (BP), renal sympathetic nerve activity (RNA ) and pelvic parasympathetic nerve activity (PNA) to Ea were investigated in urethane-anesthetized rats. The acupoint Hoku (Li-4) was tested with two different stimulation frequencies (2 Hz and 20 Hz). Elongation of the RMC cycle and an increase in UE associated with the elevation of BP and RNA was elicited during Ea at Hoku. However, the pressor response induced by low frequency Ea (LFEa) was different from that by high frequency Ea ( HFEa), i.e. a tonic effect was elicited by LFEa, while a phasic one was induced by HFEa . These results imply that: (1) Ea at Hoku may selectively activate the sympathetic, but not the parasympathetic nervous system, (2) Ea at Hoku with a different stimulation frequency may elicit a distinct mechanism to activate the sympathetic nervous system and (3) Ea at Hoku may ameliorate the hyperactive bladder in clinical therapy

Melatonin relieves neuropathic allodynia through spinal MT2enhanced PP2Ac and downstream HDAC4 shuttling-dependent epigenetic modi?cation of hmgb1 transcription

[[abstract]]Melatonin (MLT; N-acetyl-5-methoxytryptamine) exhibits analgesic properties in chronic pain conditions. While researches linking MLT to epigenetic mechanisms have grown exponentially over recent years, very few studies have investigated the contribution of MLT-associated epigenetic modification to pain states. Here, we report that together with behavioral allodynia, spinal nerve ligation (SNL) induced a decrease in the expression of catalytic subunit of phosphatase 2A (PP2Ac) and enhanced histone deacetylase 4 (HDAC4) phosphorylation and cytoplasmic accumulation, which epigenetically alleviated HDAC4-suppressed hmgb1 gene transcription, resulting in increased high-mobility group protein B1 (HMGB1) expression selectively in the ipsilateral dorsal horn of rats. Focal knock-down of spinal PP2Ac expression also resulted in behavioral allodynia in association with similar protein expression as observed with SNL. Notably, intrathecal administration with MLT increased PP2Ac expression, HDAC4 dephosphorylation and nuclear accumulation, restored HDAC4-mediated hmgb1 suppression and relieved SNL-sensitized behavioral pain; these effects were all inhibited by spinal injection of 4P-PDOT (a MT2 receptor antagonist, 30 minutes before MLT) and okadaic acid (OA, a PP2A inhibitor, 3 hr after MLT). Our findings demonstrate a novel mechanism by which MLT ameliorates neuropathic allodynia via epigenetic modification. This MLT-exhibited anti-allodynia is mediated by MT2-enhanced PP2Ac expression that couples PP2Ac with HDAC4 to induce HDAC4 dephosphorylation and nuclear import, herein increases HDAC4 binding to the promoter of hmgb1 gene and upregulates HMGB1 expression in dorsal horn neurons

Melatonin relieves neuropathic allodynia through spinal MT2enhanced PP2Ac and downstream HDAC4 shuttling-dependent epigenetic modi?cation of hmgb1 transcription

[[abstract]]Melatonin (MLT; N-acetyl-5-methoxytryptamine) exhibits analgesic properties in chronic pain conditions. While researches linking MLT to epigenetic mechanisms have grown exponentially over recent years, very few studies have investigated the contribution of MLT-associated epigenetic modification to pain states. Here, we report that together with behavioral allodynia, spinal nerve ligation (SNL) induced a decrease in the expression of catalytic subunit of phosphatase 2A (PP2Ac) and enhanced histone deacetylase 4 (HDAC4) phosphorylation and cytoplasmic accumulation, which epigenetically alleviated HDAC4-suppressed hmgb1 gene transcription, resulting in increased high-mobility group protein B1 (HMGB1) expression selectively in the ipsilateral dorsal horn of rats. Focal knock-down of spinal PP2Ac expression also resulted in behavioral allodynia in association with similar protein expression as observed with SNL. Notably, intrathecal administration with MLT increased PP2Ac expression, HDAC4 dephosphorylation and nuclear accumulation, restored HDAC4-mediated hmgb1 suppression and relieved SNL-sensitized behavioral pain; these effects were all inhibited by spinal injection of 4P-PDOT (a MT2 receptor antagonist, 30 minutes before MLT) and okadaic acid (OA, a PP2A inhibitor, 3 hr after MLT). Our findings demonstrate a novel mechanism by which MLT ameliorates neuropathic allodynia via epigenetic modification. This MLT-exhibited anti-allodynia is mediated by MT2-enhanced PP2Ac expression that couples PP2Ac with HDAC4 to induce HDAC4 dephosphorylation and nuclear import, herein increases HDAC4 binding to the promoter of hmgb1 gene and upregulates HMGB1 expression in dorsal horn neurons

Prevalence and Risk Factors for the Development of Venous Thromboembolism After Spinal Tumor Surgery

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