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Calcium‐activated cationic channel in rat sensory neurons
Author(s) -
Cho Hawon,
Kim Man Su,
Shim Won Sik,
Yang Young Duk,
Koo Jaeyeon,
Oh Uhtaek
Publication year - 2003
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.2003.02706.x
Subject(s) - chemistry , biophysics , intracellular , sensory system , ion channel , niflumic acid , reversal potential , neuroscience , electrophysiology , flufenamic acid , sensory neuron , nociceptor , membrane potential , microbiology and biotechnology , nociception , biochemistry , patch clamp , biology , receptor
Ion channels in sensory neurons are molecular sensors that detect external stimuli and transduce them to neuronal signals. Although Ca 2+ ‐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 Ca 2+ in cultured rat sensory neurons. Half‐maximal concentration of Ca 2+ in activating the CAN channel was approximately 780 µ 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 m m Na + solution. The CAN channel was permeable to monovalent cations such as Na + , K + , Cs + , and Li + , but poorly permeable to Ca 2+ . 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 Ca 2+ 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 Ca 2+ in the local microenvironment.