Nav1.9 Channel Contributes to Mechanical and Heat Pain Hypersensitivity Induced by Subacute and Chronic Inflammation

Sodium-Calcium Exchanger and Multiple Sodium Channel Isoforms in Intra-Epidermal Nerve Terminals

(2016) Anna-Karin Persson et al.   Molecular Pain

Aldosterone and vasopressin affect  - and  -ENaC mRNA translation

(2010) A. Perlewitz et al.   NUCLEIC ACIDS RESEARCH

Exploring the role of nociceptor-specific sodium channels in pain transmission using Nav1.8 and Nav1.9 knockout mice

(2009) Sandra Leo et al.   BEHAVIOURAL BRAIN RESEARCH

Role of Acid-Sensing Ion Channel 3 in Sub-Acute-Phase Inflammation

(2009) Yi-Tin Yen et al.   Molecular Pain

Trinitrobenzenesulphonic acid colitis alters Nav1.8 channel expression in mouse dorsal root ganglia neurons

(2009) d. e. king et al.   NEUROGASTROENTEROLOGY AND MOTILITY

Lack of colonic inflammation-induced acute visceral hypersensitivity to colorectal distension in Nav1.9 knockout mice

(2008) V. Martinez et al.   EUROPEAN JOURNAL OF PAIN

Inflammatory Mediators Increase Nav1.9 Current and Excitability in Nociceptors through a Coincident Detection Mechanism

(2008) François Maingret et al.   JOURNAL OF GENERAL PHYSIOLOGY

Changes in the expression of NaV1.7, NaV1.8 and NaV1.9 in a distinct population of dorsal root ganglia innervating the rat knee joint in a model of chronic inflammatory joint pain

(2007) Iain T. Strickland et al.   EUROPEAN JOURNAL OF PAIN

GTP up-regulated persistent Na+current and enhanced nociceptor excitability require NaV1.9

(2007) Johan A. R. Östman et al.   JOURNAL OF PHYSIOLOGY-LONDON