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Review
, 28 (4), 231-5

Spinal Gap Junction Channels in Neuropathic Pain

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Review

Spinal Gap Junction Channels in Neuropathic Pain

Young Hoon Jeon et al. Korean J Pain.

Abstract

Damage to peripheral nerves or the spinal cord is often accompanied by neuropathic pain, which is a complex, chronic pain state. Increasing evidence indicates that alterations in the expression and activity of gap junction channels in the spinal cord are involved in the development of neuropathic pain. Thus, this review briefly summarizes evidence that regulation of the expression, coupling, and activity of spinal gap junction channels modulates pain signals in neuropathic pain states induced by peripheral nerve or spinal cord injury. We particularly focus on connexin 43 and pannexin 1 because their regulation vastly attenuates symptoms of neuropathic pain. We hope that the study of gap junction channels eventually leads to the development of a suitable treatment tool for patients with neuropathic pain.

Keywords: Connexin; Gap junction channel; Glial cell; Neuropathic pain; Pannexin 1; Spinal cord.

Figures

Fig. 1
Fig. 1. Diagram showing the topological structure of connexin and roles of gap junction channels and hemichannels. (A) A connexin (Cx) protein has one intracellular and two extracellular loops and intracellular N- and C-terminals, and six homomeric or heteromeric Cx proteins compose a functional gap junction channel. (B) Homotypic or heterotypic gap junction channels coupled between cells pass molecules less than 1 kD, such as Ca2+, IP3, cAMP, cGMP, glutamate, glucose, ATP, and ADP, but unopposed hemichannels, upon their activation, release those molecules, particularly, ATP, glutamate, and prostaglandins.

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