Hydrogen sulfide-induced mechanical hyperalgesia and allodynia require activation of both Cav3.2 and TRPA1 channels in mice.
about
The TRPA1 channel in migraine mechanism and treatmentNeuropathic pain: role for presynaptic T-type channels in nociceptive signaling.Epigenetic modification of DRG neuronal gene expression subsequent to nerve injury: etiological contribution to complex regional pain syndromes (Part I).Expression and Regulation of Cav3.2 T-Type Calcium Channels during Inflammatory Hyperalgesia in Mouse Dorsal Root Ganglion Neurons.Interaction of H2S with Calcium Permeable Channels and Transporters.Hydrogen sulfide-induced itch requires activation of Cav3.2 T-type calcium channel in mice.Involvement of the endogenous hydrogen sulfide/Ca(v) 3.2 T-type Ca2+ channel pathway in cystitis-related bladder pain in mice.Hydrogen sulfide induces hypersensitivity of rat capsaicin-sensitive lung vagal neurons: role of TRPA1 receptors.TRP channels: sensors and transducers of gasotransmitter signals.The transient receptor potential channel TRPA1: from gene to pathophysiology.Transient receptor potential ion channels in primary sensory neurons as targets for novel analgesics.Receptor Mechanisms Mediating the Pro-Nociceptive Action of Hydrogen Sulfide in Rat Trigeminal Neurons and Meningeal AfferentsInflammatory acidic pH enhances hydrogen sulfide-induced transient receptor potential ankyrin 1 activation in RIN-14B cells.AKAP-dependent sensitization of Ca(v) 3.2 channels via the EP(4) receptor/cAMP pathway mediates PGE(2) -induced mechanical hyperalgesiaTRPA1 detects environmental chemicals and induces avoidance behavior and arousal from sleep.Roles of Cav3.2 and TRPA1 channels targeted by hydrogen sulfide in pancreatic nociceptive processing in mice with or without acute pancreatitis.Mechanisms underlying transient receptor potential ankyrin 1 (TRPA1)-mediated hyperalgesia and edema.Possible involvement of transient receptor potential ankyrin 1 in Ca2+ signaling via T-type Ca2+ channel in mouse sensory neurons.TRPA1 channels: molecular sentinels of cellular stress and tissue damage.Involvement of NF-κB in the upregulation of cystathionine-γ-lyase, a hydrogen sulfide-forming enzyme, and bladder pain accompanying cystitis in mice.Cinnamaldehyde promotes root branching by regulating endogenous hydrogen sulfide.Reduced excitability of gp130-deficient nociceptors is associated with increased voltage-gated potassium currents and Kcna4 channel upregulation.
P2860
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P2860
Hydrogen sulfide-induced mechanical hyperalgesia and allodynia require activation of both Cav3.2 and TRPA1 channels in mice.
description
2012 nî lūn-bûn
@nan
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
2012年论文
@zh
2012年论文
@zh-cn
name
Hydrogen sulfide-induced mecha ...... .2 and TRPA1 channels in mice.
@ast
Hydrogen sulfide-induced mecha ...... .2 and TRPA1 channels in mice.
@en
type
label
Hydrogen sulfide-induced mecha ...... .2 and TRPA1 channels in mice.
@ast
Hydrogen sulfide-induced mecha ...... .2 and TRPA1 channels in mice.
@en
prefLabel
Hydrogen sulfide-induced mecha ...... .2 and TRPA1 channels in mice.
@ast
Hydrogen sulfide-induced mecha ...... .2 and TRPA1 channels in mice.
@en
P2093
P2860
P1476
Hydrogen sulfide-induced mecha ...... .2 and TRPA1 channels in mice.
@en
P2093
Atsufumi Kawabata
Fumiko Sekiguchi
Kazumasa Okubo
Maho Matsunami
Midori Matsumura
Yasumasa Okawa
Yudai Kawaishi
P2860
P304
P356
10.1111/J.1476-5381.2012.01886.X
P407
P577
2012-07-01T00:00:00Z