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ATP-sensitive potassium currents reduce the PGE2-mediated enhancement of excitability in adult rat sensory neurons.

Abstract：

:Behavioral studies have shown that the hyperalgesia arising from inflammatory agents, such as prostaglandin E(2) (PGE(2)), can be antagonized by activators of the ATP-sensitive potassium current (K(ATP)). This observation raises questions as to whether this suppression results from a direct action on sensory neurons and what are the cellular mechanisms giving rise to this inhibition. We found that small to medium diameter sensory neurons isolated from the L4-6 DRGs expressed the mRNAs for Kir6.1, Kir6.2, and SUR1. In perforated-patch clamp recordings from acutely dissociated sensory neurons from the young adult rat, exposure to 300 microM diazoxide, a K(ATP) channel agonist, significantly hyperpolarized the resting membrane potential, reduced the number of action potentials evoked by a ramp of depolarizing current, and increased the amplitude of inward K(ATP) currents evoked by the voltage ramp. Similar results were obtained with the protonophore FCCP, which is known to reduce the levels of intracellular ATP and lead to the activation of K(ATP). Only a subpopulation of sensory neurons was sensitive to diazoxide whereas other neurons were unaffected. Treatment with 1 microM PGE(2) significantly enhanced the excitability of these small to medium diameter capsaicin-sensitive sensory neurons; this enhancement was reversed by subsequent exposure to diazoxide in a subpopulation of neurons. Similar to diazoxide, exposure to 8-Br-cyclic GMP antagonized the PGE(2)-induced increase in excitability. The effects of 8-Br-cyclic GMP could be reversed by exposure to glibenclamide, an antagonist of K(ATP) channels. As with diazoxide, only a subpopulation of sensory neurons were affected by 8-Br-cyclic GMP. These results demonstrate that activation of K(ATP) can reverse the sensitization produced by PGE(2) and may be an important means to modulate the enhanced excitability that results from inflammatory or injury conditions.

journal_name

Brain Res

journal_title

Brain research

authors

Chi XX,Jiang X,Nicol GD

doi

10.1016/j.brainres.2007.01.103

subject

Has Abstract

pub_date

2007-05-11 00:00:00

pages

28-40

eissn

0006-8993

issn

1872-6240

pii

S0006-8993(07)00266-1

journal_volume

1145

pub_type

杂志文章

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ATP-sensitive potassium currents reduce the PGE2-mediated enhancement of excitability in adult rat sensory neurons.