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Neural KCNQ (Kv7) channels
KCNQ genes encode five Kv7 K+ channel subunits, which are the principal molecular components of the slow voltage‐gated M‐channel, which widely regulates neuronal excitability, although other subunits may contribute to M‐like currents in some locations.

KCNQ/M Currents in Sensory Neurons: Significance for Pain Therapy
It is suggested that IK(M) plays a key role in controlling the excitability of nociceptors and may represent a novel analgesic target.

Distinct Nav1.7-dependent pain sensations require different sets of sensory and sympathetic neurons
It is shown that Nav1.7 expression in different sets of mouse sensory and sympathetic neurons underlies distinct types of pain sensation, and possible insights into the mechanisms that underlie gain-of-function Nav 1.7-dependent pain conditions are provided.

Local Translation in Primary Afferent Fibers Regulates Nociception
It is found that rapamycin blunted the heightened response to mechanical stimulation that develops around a site of injury and reduced the long-term mechanical hypersensitivity that follows partial peripheral nerve damage - a widely used model of chronic pain.

Stoichiometry of Expressed KCNQ2/KCNQ3 Potassium Channels and Subunit Composition of Native Ganglionic M Channels Deduced from Block by Tetraethylammonium
It is concluded that coexpressed KCNZ2 plus KCNQ3 cDNAs generate channels with 1:1 (KCNQ2:KCNZ3) stoichiometry in CHO cells and that native M channels in SCG neurons adopt the same conformation during development, assisted by the increased expression of KCN Q3 mRNA and protein.

Functional significance of M-type potassium channels in nociceptive cutaneous sensory endings
An important physiological role of M-channels is demonstrated in controlling nociceptive Aδ-fiber responses and a rationale for the nocifensive behaviors that arise following intraplantar injection of the M-channel blocker XE991 is provided.

Oral Communications-Matching molecules to function : potassium channels in the brain 67 P C 103 Control of spike frequency adaptation in medial entorhinal cortex layer II stellate cells
It is found that whereas the mAHP of MEC layer II non-SCs could be inhibited by 300 nM apamin, that of M ECLayerIISCswas notaffected (300 nM; n = 9; p = 0.6982).
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