INT7458
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
We evaluated the effects of iberiotoxin, an inhibitor of Slo-type Ca2+-activated potassium channels and two inhibitors of Shaker-type voltage-gated potassium channels margatoxin and dendrotoxin on acetylcholine outflow in rat striatal slices. | |||||||||||||||
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Depolarization using 25-100 mM [K+]o resulted in a prompt rise in intracellular calcium concentration, which returned to near resting levels, and this response was sensitive to removal of extracellular calcium and voltage-gated calcium channel antagonists. | |||||||||||||||
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The mechanism of channel block by amiloride and its analogue seems to be different. | |||||||||||||||
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The channel was blocked by lamotrigine and sipatrigine voltage and state dependently, with potencies 5-20 times higher (IC50 12 and 1.8 microM at -80 mV respectively) than the corresponding block of endogenous Na+ channels from neurones and cloned rNa(v)1.2a (rBIIA) alpha-subunits. | |||||||||||||||
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CONCLUSION: Our data show that the hypotensive effect induced by TRPV4 activation attributes to, at least in part, activation of MaxiK channels and CGRP receptors upon CGRP release from sensory nerves.
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This GS-induced relaxation was partially reversed by tetraethylammonium (TEA), an inhibitor of KCa channels; methylene blue (MB), an inhibitor of soluble guanylate cyclase; as well as Nomega-nitro-L-arginine (L-NNA), but not by glybenclamide. | |||||||||||||||
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KCNN3 mRNA was prevalent in cultured microglia and increased after lipopolysaccharide-induced activation; SK3 channel blockade inhibited microglial activation and reduced their ability to kill neurons. | |||||||||||||||
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Effects of apamin on microglia are most likely due to SK3 channel block because KCNN2 was nearly undetectable in LPS-activated microglia, and rodent KCNN1 apparently does not form functional channels [44,45]. | |||||||||||||||
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Because one potential outcome of peroxynitrite formation is nitration of cell proteins, we asked whether blocking the SK3 channel in microglia reduces tyrosine nitration in the target neuron cultures. | |||||||||||||||
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Thus, the activation of dorsal horn neurones by nociceptive and non-nociceptive afferent inputs can be differentiated by the blockade of a lamotrigine/flunarizine-sensitive Na+ channel, at a spinal site. | |||||||||||||||
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PTX-induced analgesia was blocked by selective inhibitors of nitric oxide synthase (L-NMMA), guanylyl cyclase (ODQ), protein kinase G (KT5823) and ATP-sensitive K(+) channel (Kir6) blockers (glybenclamide and tolbutamide). | |||||||||||||||
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Similarly, axotomy reduces KCa channel activity in the small to medium sized DRG neurons, which would also increase membrane excitability [21]. | |||||||||||||||
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Glycosylation alters steady-state inactivation of sodium channel Nav1.9/NaN in dorsal root ganglion neurons and is developmentally regulated. | |||||||||||||||
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It is concluded that protection against veratridine-induced neurotoxicity can be mediated by blocking a veratridine-sensitive Na+ channel. | |||||||||||||||
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We applied paxilline during the preconditioning period, suggesting that mKCa channel inhibition blocks the infarct size reducing effect of preconditioning during the trigger phase. | |||||||||||||||
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To test whether mKCa channels are involved in the phenomenon of preconditioning, the mKCa channel inhibitor, paxilline 1 ? | |||||||||||||||
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The preconditioning effect of ischemia and morphine was attenuated significantly by the mKCa-channel inhibitor, paxilline. | |||||||||||||||
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These disorders are currently managed by drugs that are dampen neuronal hyperexcitability through voltage-gated sodium channel inhibition, modulation of voltage-gated calcium channels and their auxiliary subunits, and inhibitory GABAergic neurotransmission [6]. | |||||||||||||||
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In this study, we sought to elucidate the molecular mechanisms underlying Rg(3)-induced Na(+) channel inhibition. | |||||||||||||||
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These results reveal that Rg(3) is a novel Na(+) channel inhibitor capable of acting on the resting and open states of Na(+) channel via interactions with the S4 voltage-sensor segment of domain II. | |||||||||||||||
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General Comments
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