PMID- 28647288
OWN - NLM
STAT- MEDLINE
DCOM- 20190905
LR  - 20200316
IS  - 1872-7972 (Electronic)
IS  - 0304-3940 (Print)
IS  - 0304-3940 (Linking)
VI  - 695
DP  - 2019 Mar 16
TI  - Gap junctions, pannexins and pain.
PG  - 46-52
LID - S0304-3940(17)30515-3 [pii]
LID - 10.1016/j.neulet.2017.06.035 [doi]
AB  - Enhanced expression and function of gap junctions and pannexin (Panx) channels 
      have been associated with both peripheral and central mechanisms of pain 
      sensitization. At the level of the sensory ganglia, evidence includes augmented 
      gap junction and pannexin1 expression in glial cells and neurons in inflammatory 
      and neuropathic pain models and increased synchrony and enhanced cross-excitation 
      among sensory neurons by gap junction-mediated coupling. In spinal cord and in 
      suprapinal areas, evidence is largely limited to increased expression of relevant 
      proteins, although in several rodent pain models, hypersensitivity is reduced by 
      treatment with gap junction/Panx1 channel blocking compounds. Moreover, targeted 
      modulation of Cx43 expression was shown to modulate pain thresholds, albeit in 
      somewhat contradictory ways, and mice lacking Panx1 expression globally or in 
      specific cell types show depressed hyperalgesia. We here review the evidence for 
      involvement of gap junctions and Panx channels in a variety of animal pain 
      studies and then discuss ways in which gap junctions and Panx channels may 
      mediate their action in pain processing. This discussion focusses on spread of 
      signals among satellite glial cells, in particular intercellular Ca(2+) waves, 
      which are propagated through both gap junction and Panx1-dependent routes and 
      have been associated with the phenomenon of spreading depression and the malady 
      of migraine headache with aura.
CI  - Copyright (c) 2018 Elsevier B.V. All rights reserved.
FAU - Spray, David C
AU  - Spray DC
AD  - Dominick Purpura Department of Neuroscience, Albert Einstein College of Medicine, 
      Bronx, NY, United States. Electronic address: david.spray@einstein.yu.edu.
FAU - Hanani, Menachem
AU  - Hanani M
AD  - Laboratory of Experimental Surgery, Hadassah-Hebrew University Medical Center, 
      Jerusalem, Israel.
LA  - eng
GR  - R01 NS041282/NS/NINDS NIH HHS/United States
GR  - R01 NS092466/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20170622
PL  - Ireland
TA  - Neurosci Lett
JT  - Neuroscience letters
JID - 7600130
RN  - 0 (Connexins)
SB  - IM
MH  - Animals
MH  - Connexins/*metabolism
MH  - Ganglia, Sensory/metabolism/pathology
MH  - Gap Junctions/*metabolism
MH  - Hyperalgesia/metabolism/pathology
MH  - Neuralgia/metabolism/pathology
MH  - Neuroglia/metabolism/pathology
MH  - Pain/*metabolism/pathology
MH  - Satellite Cells, Perineuronal/metabolism/pathology
MH  - Sensory Receptor Cells/metabolism/pathology
PMC - PMC6005766
MID - NIHMS973167
OTO - NOTNLM
OT  - Cx43
OT  - DRG
OT  - GJ: Panx1
OT  - Ganglia
OT  - Satellite glial cell
OT  - Sensory neuron
OT  - Spinal cord
OT  - TG
COIS- Conflict of interest statement The authors declare no conflicts of interest.
EDAT- 2017/06/26 06:00
MHDA- 2019/09/07 06:00
PMCR- 2020/03/16
CRDT- 2017/06/26 06:00
PHST- 2017/05/12 00:00 [received]
PHST- 2017/06/19 00:00 [revised]
PHST- 2017/06/20 00:00 [accepted]
PHST- 2017/06/26 06:00 [pubmed]
PHST- 2019/09/07 06:00 [medline]
PHST- 2017/06/26 06:00 [entrez]
PHST- 2020/03/16 00:00 [pmc-release]
AID - S0304-3940(17)30515-3 [pii]
AID - 10.1016/j.neulet.2017.06.035 [doi]
PST - ppublish
SO  - Neurosci Lett. 2019 Mar 16;695:46-52. doi: 10.1016/j.neulet.2017.06.035. Epub 
      2017 Jun 22.