Glial pannexin1 contributes to tactile hypersensitivity in a mouse model of orofacial pain

Regina Hanstein, Menachem Hanani, Eliana Scemes, David C. Spray

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Drug studies in animal models have implicated pannexin1 (Panx1) in various types of pain, including trigeminal hypersensitivity, neuropathic pain and migraine. However, the tested drugs have limited specificity and efficacy so that direct evidence for Panx1 contribution to pain has been lacking. We here show that tactile hypersensitivity is markedly attenuated by deletion of Panx1 in a mouse model of chronic orofacial pain; in this model, trigeminal ganglion Panx1 expression and function are markedly enhanced. Targeted deletion of Panx1 in GFAP-positive glia or in neurons revealed distinct effects. Panx1 deletion in GFAP-positive glia cells prevented hypersensitivity completely, whereas deletion of neuronal Panx1 reduced baseline sensitivity and the duration of hypersensitivity. In trigeminal ganglia with genetically encoded Ca 2+ indicator in GFAP-positive glia or in neurons, both cell populations were found to be hyperactive and hyper-responsive to ATP. These novel findings reveal unique roles for GFAP-positive glial and neuronal Panx1 and describe new chronic pain targets for cell-Type specific intervention in this often intractable disease.

Original languageEnglish (US)
Article number38266
JournalScientific Reports
Volume6
DOIs
StatePublished - Dec 2 2016

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Facial Pain
Touch
Neuroglia
Hypersensitivity
Trigeminal Ganglion
Chronic Pain
Neurons
Pain
Neuralgia
Migraine Disorders
Pharmaceutical Preparations
Animal Models
Adenosine Triphosphate
Population

ASJC Scopus subject areas

  • General

Cite this

Glial pannexin1 contributes to tactile hypersensitivity in a mouse model of orofacial pain. / Hanstein, Regina; Hanani, Menachem; Scemes, Eliana; Spray, David C.

In: Scientific Reports, Vol. 6, 38266, 02.12.2016.

Research output: Contribution to journalArticle

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