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Location and plasticity of the sodium spike initiation zone in nociceptive terminals in vivo

AuthorsGoldstein, Robert H.; Barkai, Omer; Íñigo-Portugués, Almudena; Katz, Ben; Lev, Shaya; Binshtok, Alexander M.
Nociceptor terminal
Sodium channels
Proinflammatory cytokines
Issue Date2019
CitationNeuron 102(4): 801-812.e5 (2019)
AbstractNociceptive terminals possess the elements for detecting, transmitting, and modulating noxious signals, thus being pivotal for pain sensation. Despite this, a functional description of the transduction process by the terminals, in physiological conditions, has not been fully achieved. Here, we studied how nociceptive terminals in vivo convert noxious stimuli into propagating signals. By monitoring noxious-stimulus-induced Ca2+ dynamics from mouse corneal terminals, we found that initiation of Na+ channel (Nav)-dependent propagating signals takes place away from the terminal and that the starting point for Nav-mediated propagation depends on Nav functional availability. Acute treatment with the proinflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) resulted in a shift of the location of Nav involvement toward the terminal, thus increasing nociceptive excitability. Moreover, a shift of Nav involvement toward the terminal occurs in corneal hyperalgesia resulting from acute photokeratitis. This dynamic change in the location of Nav-mediated propagation initiation could underlie pathological pain hypersensitivity.
DescriptionReferred to by: Sharon R. Ha, Matthew N. Rasband. The SIZ of Pain. Neuron, Volume 102, Issue 4, 22 May 2019, Pages 709-711
Publisher version (URL)https://doi.org/10.1016/j.neuron.2019.03.005
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