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Trigeminal neuropathic pain is alleviated by inhibition of Cav3.3 T-type calcium channels in mice
M. Montera, A. Goins, L. Cmarko, N. Weiss, KN. Westlund, SRA. Alles
Jazyk angličtina Země Spojené státy americké
Typ dokumentu časopisecké články, Research Support, N.I.H., Extramural, práce podpořená grantem
Grantová podpora
R21 DE028096
NIDCR NIH HHS - United States
NLK
Directory of Open Access Journals
od 2018
Free Medical Journals
od 2008 do Před 1 rokem
PubMed Central
od 2007
Europe PubMed Central
od 2007 do Před 1 rokem
Taylor & Francis Open Access
od 2018-01-01
Medline Complete (EBSCOhost)
od 2011-01-01
ROAD: Directory of Open Access Scholarly Resources
od 2007
- MeSH
- hyperalgezie MeSH
- myši MeSH
- spinální ganglia MeSH
- upregulace MeSH
- vápníkové kanály - typ T * MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Research Support, N.I.H., Extramural MeSH
In this brief report, we demonstrate that the Cav3.3 T-type voltage-gated calcium channel subtype is involved in our FRICT-ION model of chronic trigeminal neuropathic pain. We first showed that the Cacna1i gene encoding Cav3.3 is significantly upregulated in whole trigeminal ganglia of FRICT-ION mice compared to controls at week 10 post-injury. We confirmed protein upregulation of Cav3.3 compared to controls using Western blot analysis of whole trigeminal ganglia tissues. Finally, we demonstrated that intraperitoneal injection of a selective TAT-based Cav3.3 blocking peptide in FRICT-ION mice significantly reduces Cav3.3 protein expression at the peak anti-allodynic effect (4 hrs post-injection) of the attenuated neuropathic pain behavior. We also suggest that blockade of Cav3.3 may be more effective in attenuating trigeminal neuropathic pain in female than male FRICT-ION mice. Therefore, blocking or attenuating Cav3.3 function may be an effective strategy for the treatment of trigeminal neuropathic pain.
Citace poskytuje Crossref.org
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