Location and Plasticity of the Sodium Spike Initiation Zone in Nociceptive Terminals In Vivo.

Abstract:

:Nociceptive 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.

journal_name

Neuron

journal_title

Neuron

authors

Goldstein RH,Barkai O,Íñigo-Portugués A,Katz B,Lev S,Binshtok AM

doi

10.1016/j.neuron.2019.03.005

subject

Has Abstract

pub_date

2019-05-22 00:00:00

pages

801-812.e5

issue

4

eissn

0896-6273

issn

1097-4199

pii

S0896-6273(19)30212-0

journal_volume

102

pub_type

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