title: Calcium-activated cationic channel in rat sensory neurons.
abstract: Ion channels in sensory neurons are molecular sensors that detect external stimuli and transduce them to neuronal signals. Although Ca2+-activated nonselective cation (CAN) channels were found in many cell types, CAN channels in mammalian sensory neurons are not yet identified. In the present study, we describe an ion channel that is activated by intracellular Ca2+ in cultured rat sensory neurons. Half-maximal concentration of Ca2+ in activating the CAN channel was approximately 780 micro m. The current-voltage relationship of this channel was linear with a unit conductance of 28.8 +/- 0.4 pS at -60 mV in symmetrical 140 mm Na+ solution. The CAN channel was permeable to monovalent cations such as Na+, K+, Cs+, and Li+, but poorly permeable to Ca2+. The CAN channel in mammalian sensory neurons was reversibly blocked by intracellular adenine nucleotides, such as ATP, ADP, and AMP. Interestingly, single-channel currents activated by Ca2+ were blocked by fenamates, such as flufenamic acid, a class of nonsteroidal anti-inflammatory drugs. Thus, these results suggest that CAN channels in mammalian sensory neurons would participate in modulating nociceptive neural transmission in response to ever-changing intracellular Ca2+ in the local microenvironment.
authors.affiliation: The Sensory Research Center, Creative Research Initiatives, Seoul National University, College of Pharmacy, Kwanak, Shinlim 9-dong, Seoul 151-742, Korea.
authors.forename: Hawon
authors.initials: H
authors.lastname: Cho
authors.forename: Man Su
authors.initials: MS
authors.lastname: Kim
authors.forename: Won Sik
authors.initials: WS
authors.lastname: Shim
authors.forename: Young Duk
authors.initials: YD
authors.lastname: Yang
authors.forename: Jaeyeon
authors.initials: J
authors.lastname: Koo
authors.forename: Uhtaek
authors.initials: U
authors.lastname: Oh
mesh_terms: D000227:Adenine Nucleotides / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002211:Capsaicin / Q000494:pharmacology; D002478:Cells, Cultured; D002614:Chelating Agents / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D004533:Egtazic Acid / Q000494:pharmacology; D004553:Electric Conductivity; D005110:Extracellular Space / Q000378:metabolism; D005727:Ganglia, Spinal; D007052:Ibuprofen / Q000494:pharmacology; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials / Q000502:physiology; D009475:Neurons, Afferent / Q000187:drug effects / Q000502:physiology*; D018408:Patch-Clamp Techniques; D051381:Rats; D011955:Receptors, Drug / Q000502:physiology; D062367:ortho-Aminobenzoates / Q000494:pharmacology
chemical_list: D000227:Adenine Nucleotides; D000894:Anti-Inflammatory Agents, Non-Steroidal; D002121:Calcium Channel Blockers; D002614:Chelating Agents; D007473:Ion Channels; D011955:Receptors, Drug; D062367:ortho-Aminobenzoates; D004533:Egtazic Acid; C001209:fenamic acid; D002211:Capsaicin; D002118:Calcium; D007052:Ibuprofen