INT9968
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Gabazine also reversed EA inhibition of cardiovascular premotor sympathetic rVLM neurons. | |||||||||||||||
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Treatment with the glutamate antagonists MK-801 (1 mg kg-1) and NBQX (30 mg kg-1 x 2) did not significantly change this, although MK-801 tended to reduce the size of the metabolic penumbra calculated as the difference between ischemic cortex with reduced PS and ischemic cortex with reduced rCMRglc. | |||||||||||||||
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In control rats, clonidine caused a significant reduction in MAP that continued for at least 6 h and was associated with reductions in SDMAP and SDRR but not rMSSD, suggesting inhibition of central sympathetic tone. | |||||||||||||||
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In control rats, clonidine caused a significant reduction in MAP that continued for at least 5 h and was associated with significant reductions in SDMAP, SDRR, and rMSSD, responses that are consistent with the inhibition of central sympathetic tone. | |||||||||||||||
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The clonidine-induced reductions in SDMAP, SDRR, and rMSSD were also significantly attenuated by ethanol. | |||||||||||||||
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These results suggest that an acute inhibition of TTX-R I(Na) by LY333531 attenuates the exaggerated excitability of DRG neurons in the diabetic state, which appears to be related at least partly to anti-hyperalgesic actions of the drug in diabetic neuropathy. | |||||||||||||||
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Bath application of LY333531 acutely inhibited TTX-R I(Na) in both control and diabetic DRG neurons, and the degree of inhibition by the drug at concentrations of 1, 10 and 100 nM was significantly greater in diabetic DRG neurons than in control DRG neurons. | |||||||||||||||
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M, thiopental abolished SPW-R activity in two out of ten slices.
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Neuronal activity in the rVLM induced by splanchnic nerve stimulation was reduced for 50 (or more) min after termination of EA in 7 of 12 rVLM neurons. | |||||||||||||||
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These outcomes indicate that HD-MTX and the reduced rCMRGlc that follows this treatment do not contribute to the hypnotic action of phenobarbital. | |||||||||||||||
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The mechanism by which hepatic SOD, catalase, Se-GSHpx, GSSG-R, and G-6-PDH activities are reduced with liver injury development in rats treated with ANIT has not been elucidated. | |||||||||||||||
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Oral administration of TJ-10 (1.3 or 2.6 g/kg BW) to ANIT-treated rats at an early stage of liver injury significantly attenuated the decreases in hepatic SOD, catalase, Se-GSHpx, GSSG-R, and G-6-PDH activities found at a progressed stage of liver injury. | |||||||||||||||
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Our previous reports have shown that, in rats treated once with ANIT, hepatic SOD and GSSG-R activities decrease with injury formation and progression, while catalase, and Se-GSHpx activities decrease with liver injury progression [79]. | |||||||||||||||
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We determined whether the altered neuronal function after HD-MTX [such as the reduced regional cerebral metabolic glucose rate (rCMRGlc) and slow electroencephalographic pattern] affects the sensitivity of the CNS to centrally acting drugs: the depressant phenobarbital, which reduces rCMRGlc, and the analeptic agent pentylenetetrazol (PTZ), which elevates rCMRGlc. | |||||||||||||||
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Mean TTX-R sodium current density was decreased from 504 +/- 77 pA/pF to 307 +/- 61 pA/pF in control versus NGF-deprived neurons, respectively. | |||||||||||||||
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Therefore, it seems likely that the enhanced decreases in hepatic SOD and GSSG-R activities and the decrease in hepatic catalase, Se-GSHpx, and G-6-PDH activities found at a progressed stage of liver injury in ANIT-treated rats are due to ROS derived from neutrophils accumulating in the tissue. | |||||||||||||||
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Sensory neuron specific TTX-R sodium channel NaV1. 8 transcript was down-regulated after antisense oligonucleotide injection at the dosage of 45 microg as compared with that in CCI group (P < 0.01), and it was even greater at the dosage of 90 microg. | |||||||||||||||
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In the ANIT-treated group, further decreases in hepatic SOD and GSSG-R activities occurred with decreases in hepatic catalase, Se-GSHpx, and G-6-PDH activities at 48 h after the treatment (Figs. 6 and 7). | |||||||||||||||
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These data suggest that EA attenuates BK-induced visceral sympathoexcitatory reflexes through opioid-mediated inhibition of Glu's action in the rVLM. | |||||||||||||||
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