Pages that link to "Q24814946"
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The following pages link to Neuropathic pain develops normally in mice lacking both Na(v)1.7 and Na(v)1.8. (Q24814946):
Displaying 50 items.
- Na(v) 1.8-null mice show stimulus-dependent deficits in spinal neuronal activity (Q21223666) (← links)
- Pain as a channelopathy (Q24622323) (← links)
- Structural determinants of drugs acting on the Nav1.8 channel (Q24644825) (← links)
- Conotoxins That Could Provide Analgesia through Voltage Gated Sodium Channel Inhibition (Q26774171) (← links)
- AMPK: An emerging target for modification of injury-induced pain plasticity (Q27021903) (← links)
- Food-Derived Natural Compounds for Pain Relief in Neuropathic Pain (Q28068743) (← links)
- Nav1.7 and other voltage-gated sodium channels as drug targets for pain relief (Q28273870) (← links)
- An SCN9A channelopathy causes congenital inability to experience pain (Q28278844) (← links)
- Targeting neuroprotection as an alternative approach to preventing and treating neuropathic pain (Q28820780) (← links)
- Cellular and Molecular Mechanisms of Pain (Q29011961) (← links)
- Voltage-gated Na+ channels in neuropathic pain (Q30443511) (← links)
- Nav1.7 expression is increased in painful human dental pulp (Q33329730) (← links)
- Identifying the Ion Channels Responsible for Signaling Gastro-Intestinal Based Pain (Q33664676) (← links)
- Contribution of primary afferent channels to neuropathic pain (Q33810382) (← links)
- Tetrodotoxin (TTX) as a therapeutic agent for pain. (Q34260913) (← links)
- A nonsense mutation in the SCN9A gene in congenital insensitivity to pain (Q34263684) (← links)
- Identification of molecular pathologies sufficient to cause neuropathic excitability in primary somatosensory afferents using dynamical systems theory (Q34288745) (← links)
- Two novel mutations of SCN9A (Nav1.7) are associated with partial congenital insensitivity to pain (Q34300278) (← links)
- Dysregulation of voltage-gated sodium channels by ubiquitin ligase NEDD4-2 in neuropathic pain. (Q34351740) (← links)
- Deletion of annexin 2 light chain p11 in nociceptors causes deficits in somatosensory coding and pain behavior. (Q34573436) (← links)
- Mutations in sodium-channel gene SCN9A cause a spectrum of human genetic pain disorders (Q34585790) (← links)
- Spider peptide toxins as leads for drug development (Q34620046) (← links)
- A-803467, a potent and selective Nav1.8 sodium channel blocker, attenuates neuropathic and inflammatory pain in the rat. (Q34625901) (← links)
- Are Voltage-Gated Sodium Channels on the Dorsal Root Ganglion Involved in the Development of Neuropathic Pain? (Q34639336) (← links)
- The roles of sodium channels in nociception: Implications for mechanisms of pain (Q34674268) (← links)
- Probing functional properties of nociceptive axons using a microfluidic culture system. (Q35053671) (← links)
- muO-conotoxin MrVIB selectively blocks Nav1.8 sensory neuron specific sodium channels and chronic pain behavior without motor deficits (Q35119068) (← links)
- Nerve injury induces robust allodynia and ectopic discharges in Nav1.3 null mutant mice. (Q35121209) (← links)
- Dorsal root ganglion myeloid zinc finger protein 1 contributes to neuropathic pain after peripheral nerve trauma (Q35196269) (← links)
- A novel selective and orally bioavailable Nav 1.8 channel blocker, PF-01247324, attenuates nociception and sensory neuron excitability (Q35538543) (← links)
- A 3.7 kb fragment of the mouse Scn10a gene promoter directs neural crest but not placodal lineage EGFP expression in a transgenic animal. (Q35625781) (← links)
- Sodium channels and mammalian sensory mechanotransduction. (Q36043204) (← links)
- The role of sodium channels in chronic pain (Q36103777) (← links)
- Colonic Hypersensitivity and Sensitization of Voltage-gated Sodium Channels in Primary Sensory Neurons in Rats with Diabetes (Q36426070) (← links)
- Conotoxins targeting neuronal voltage-gated sodium channel subtypes: potential analgesics? (Q36432810) (← links)
- Voltage-gated sodium channels: action players with many faces (Q36652537) (← links)
- Optogenetic Silencing of Nav1.8-Positive Afferents Alleviates Inflammatory and Neuropathic Pain (Q36693619) (← links)
- Differing alterations of sodium currents in small dorsal root ganglion neurons after ganglion compression and peripheral nerve injury (Q36718547) (← links)
- Blocking sodium channels to treat neuropathic pain (Q36734922) (← links)
- Electroacupuncture Reduces Carrageenan- and CFA-Induced Inflammatory Pain Accompanied by Changing the Expression of Nav1.7 and Nav1.8, rather than Nav1.9, in Mice Dorsal Root Ganglia (Q36737802) (← links)
- Identification of the sensory neuron specific regulatory region for the mouse gene encoding the voltage-gated sodium channel NaV1.8. (Q36925406) (← links)
- Development of a μO-Conotoxin Analogue with Improved Lipid Membrane Interactions and Potency for the Analgesic Sodium Channel NaV1.8. (Q36941125) (← links)
- Voltage-gated sodium channel blockers for the treatment of neuropathic pain (Q36998857) (← links)
- Genetics and molecular pathophysiology of Na(v)1.7-related pain syndromes (Q37382551) (← links)
- Neuropathic pain: a maladaptive response of the nervous system to damage (Q37401775) (← links)
- Sodium channel blockers for the treatment of neuropathic pain (Q37605350) (← links)
- Subtype-selective targeting of voltage-gated sodium channels (Q37618893) (← links)
- Electroacupuncture Attenuates CFA-induced Inflammatory Pain by suppressing Nav1.8 through S100B, TRPV1, Opioid, and Adenosine Pathways in Mice (Q37637997) (← links)
- Criticality and degeneracy in injury-induced changes in primary afferent excitability and the implications for neuropathic pain. (Q37675582) (← links)
- Nociceptors: the sensors of the pain pathway (Q37805996) (← links)