Cell-specific alterations of T-type calcium current in painful diabetic neuropathy enhance excitability of sensory neurons.
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The Physiology, Pathology, and Pharmacology of Voltage-Gated Calcium Channels and Their Future Therapeutic PotentialRedox regulation of neuronal voltage-gated calcium channelsDiabetic neuropathic pain: Physiopathology and treatmentT-type calcium channels contribute to colonic hypersensitivity in a rat model of irritable bowel syndromeNeuronal T-type calcium channels: what's new? Iftinca: T-type channel regulationTargeting of CaV3.2 T-type calcium channels in peripheral sensory neurons for the treatment of painful diabetic neuropathyAn integrated perspective on diabetic, alcoholic, and drug-induced neuropathy, etiology, and treatment in the US.Is Diabetic Nerve Pain Caused by Dysregulated Ion Channels in Sensory Neurons?Painful Diabetic Neuropathy: Prevention or Suppression?Inhibition of CaV3.2 T-type calcium channels in peripheral sensory neurons contributes to analgesic properties of epipregnanolone.Reversal of neuropathic pain in diabetes by targeting glycosylation of Ca(V)3.2 T-type calcium channelsImmunohistological demonstration of CaV3.2 T-type voltage-gated calcium channel expression in soma of dorsal root ganglion neurons and peripheral axons of rat and mouse.CaV3.2 T-type calcium channels in peripheral sensory neurons are important for mibefradil-induced reversal of hyperalgesia and allodynia in rats with painful diabetic neuropathy.Presynaptic Cav3.2 channels regulate excitatory neurotransmission in nociceptive dorsal horn neuronsTTA-P2 is a potent and selective blocker of T-type calcium channels in rat sensory neurons and a novel antinociceptive agent.T-type voltage-gated calcium channels as targets for the development of novel pain therapies.Characterization of the gating brake in the I-II loop of CaV3 T-type calcium channels.Molecular mechanisms of lipoic acid modulation of T-type calcium channels in pain pathway.Selective T-type calcium channel blockade alleviates hyperalgesia in ob/ob mice.In vivo silencing of the Ca(V)3.2 T-type calcium channels in sensory neurons alleviates hyperalgesia in rats with streptozocin-induced diabetic neuropathy.Role of voltage-gated calcium channels in ascending pain pathwaysUpregulation of the T-type calcium current in small rat sensory neurons after chronic constrictive injury of the sciatic nerveI-II loop structural determinants in the gating and surface expression of low voltage-activated calcium channels.Neuropathic pain: role for presynaptic T-type channels in nociceptive signaling.Physiological basis of tingling paresthesia evoked by hydroxy-alpha-sanshool.CRMP-2 peptide mediated decrease of high and low voltage-activated calcium channels, attenuation of nociceptor excitability, and anti-nociception in a model of AIDS therapy-induced painful peripheral neuropathyCharacterization of novel cannabinoid based T-type calcium channel blockers with analgesic effects.Hyperglycemia induces oxidative stress and impairs axonal transport rates in mice.Determinants of synaptic integration and heterogeneity in rebound firing explored with data-driven models of deep cerebellar nucleus cells.Alpha-lipoic Acid suppresses P2X receptor activities and visceral hypersensitivity to colorectal distention in diabetic rats.ACTH induces Cav3.2 current and mRNA by cAMP-dependent and cAMP-independent mechanisms.Reduction in voltage-gated K+ channel activity in primary sensory neurons in painful diabetic neuropathy: role of brain-derived neurotrophic factorOptogenetic and potassium channel gene therapy in a rodent model of focal neocortical epilepsy.Gastrodin inhibits allodynia and hyperalgesia in painful diabetic neuropathy rats by decreasing excitability of nociceptive primary sensory neurons.NMP-7 inhibits chronic inflammatory and neuropathic pain via block of Cav3.2 T-type calcium channels and activation of CB2 receptors.Satellite glial cells in dorsal root ganglia are activated in streptozotocin-treated rodents.Small organic molecule disruptors of Cav3.2 - USP5 interactions reverse inflammatory and neuropathic pain.Mechanisms underlying purinergic P2X3 receptor-mediated mechanical allodynia induced in diabetic ratsERK, synaptic plasticity and acid-induced muscle pain.Diabetic neuropathy enhances voltage-activated Ca2+ channel activity and its control by M4 muscarinic receptors in primary sensory neurons.
P2860
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P2860
Cell-specific alterations of T-type calcium current in painful diabetic neuropathy enhance excitability of sensory neurons.
description
2007 nî lūn-bûn
@nan
2007 թուականի Մարտին հրատարակուած գիտական յօդուած
@hyw
2007 թվականի մարտին հրատարակված գիտական հոդված
@hy
2007年の論文
@ja
2007年論文
@yue
2007年論文
@zh-hant
2007年論文
@zh-hk
2007年論文
@zh-mo
2007年論文
@zh-tw
2007年论文
@wuu
name
Cell-specific alterations of T ...... citability of sensory neurons.
@ast
Cell-specific alterations of T ...... citability of sensory neurons.
@en
type
label
Cell-specific alterations of T ...... citability of sensory neurons.
@ast
Cell-specific alterations of T ...... citability of sensory neurons.
@en
prefLabel
Cell-specific alterations of T ...... citability of sensory neurons.
@ast
Cell-specific alterations of T ...... citability of sensory neurons.
@en
P2093
P1476
Cell-specific alterations of T ...... citability of sensory neurons.
@en
P2093
Douglas A Bayliss
Ethan R Rosenberg
Michael T Nelson
Miljen M Jagodic
Pavle M Joksovic
Slobodan M Todorovic
Sriyani Pathirathna
Stefani Mancuso
Vesna Jevtovic-Todorovic
P304
P356
10.1523/JNEUROSCI.4866-06.2007
P407
P577
2007-03-01T00:00:00Z