-
Something wrong with this record ?
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
Language English Country United States
Document type Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't
Grant support
R21 DE028096
NIDCR NIH HHS - United States
NLK
Directory of Open Access Journals
from 2018
Free Medical Journals
from 2008 to 1 year ago
PubMed Central
from 2007
Europe PubMed Central
from 2007 to 1 year ago
Taylor & Francis Open Access
from 2018-01-01
Medline Complete (EBSCOhost)
from 2011-01-01
ROAD: Directory of Open Access Scholarly Resources
from 2007
- MeSH
- Hyperalgesia MeSH
- Mice MeSH
- Ganglia, Spinal MeSH
- Up-Regulation MeSH
- Calcium Channels, T-Type * MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't 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.
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc22003063
- 003
- CZ-PrNML
- 005
- 20220127150710.0
- 007
- ta
- 008
- 220113s2021 xxu f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1080/19336950.2020.1859248 $2 doi
- 035 __
- $a (PubMed)33283622
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xxu
- 100 1_
- $a Montera, Marena $u Department of Anesthesiology and Critical Care Medicine, University of New Mexico School of Medicine , Albuquerque, NM, USA
- 245 10
- $a Trigeminal neuropathic pain is alleviated by inhibition of Cav3.3 T-type calcium channels in mice / $c M. Montera, A. Goins, L. Cmarko, N. Weiss, KN. Westlund, SRA. Alles
- 520 9_
- $a 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.
- 650 _2
- $a zvířata $7 D000818
- 650 12
- $a vápníkové kanály - typ T $7 D020747
- 650 _2
- $a spinální ganglia $7 D005727
- 650 _2
- $a hyperalgezie $7 D006930
- 650 _2
- $a myši $7 D051379
- 650 _2
- $a upregulace $7 D015854
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a Research Support, N.I.H., Extramural $7 D052061
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Goins, Aleyah $u Department of Anesthesiology and Critical Care Medicine, University of New Mexico School of Medicine , Albuquerque, NM, USA
- 700 1_
- $a Cmarko, Leos $u Institute of Biology and Medical Genetics, First Faculty of Medicine, Charles University , Prague, Czech Republic $u Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences , Prague, Czech Republic
- 700 1_
- $a Weiss, Norbert $u Institute of Biology and Medical Genetics, First Faculty of Medicine, Charles University , Prague, Czech Republic $u Institute of Organic Chemistry and Biochemistry, Czech Academy of Sciences , Prague, Czech Republic
- 700 1_
- $a Westlund, Karin N $u Department of Anesthesiology and Critical Care Medicine, University of New Mexico School of Medicine , Albuquerque, NM, USA
- 700 1_
- $a Alles, Sascha R A $u Department of Anesthesiology and Critical Care Medicine, University of New Mexico School of Medicine , Albuquerque, NM, USA
- 773 0_
- $w MED00182173 $t Channels (Austin, Tex.) $x 1933-6969 $g Roč. 15, č. 1 (2021), s. 31-37
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/33283622 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y p $z 0
- 990 __
- $a 20220113 $b ABA008
- 991 __
- $a 20220127150706 $b ABA008
- 999 __
- $a ok $b bmc $g 1750744 $s 1154212
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2021 $b 15 $c 1 $d 31-37 $e - $i 1933-6969 $m Channels $n Channels $x MED00182173
- GRA __
- $a R21 DE028096 $p NIDCR NIH HHS $2 United States
- LZP __
- $a Pubmed-20220113
