Presynaptic inhibition and spinal pain processing in mice: a possible role of the NKCC1 cation-chloride co-transporter in hyperalgesia
- PMID: 15135928
- DOI: 10.1016/j.neulet.2003.12.015
Presynaptic inhibition and spinal pain processing in mice: a possible role of the NKCC1 cation-chloride co-transporter in hyperalgesia
Abstract
We have examined the role of the NKCC1 sodium-potassium-chloride-cotransporter in the generation of touch-evoked pain. The pain behavior of NKCC1 knockout mice (KO) was studied and compared to that of heterozygous (HE) and wild-type (WT) littermates. NKCC1 KO mice showed an increase in tail flick latencies and a reduction of the duration of pain behavior induced by intradermal capsaicin compared to HE and WT mice. All three groups of animals expressed a normal level of plasma extravasation following capsaicin applications. NKCC1 KO mice showed a reduction in stroking hyperalgesia (touch-evoked pain) compared to WT and HE mice but no differences were detected between the three groups in the expression of punctate hyperalgesia. As the NKCC1 co-transporter is responsible for the generation of presynaptic inhibition between afferent terminals in the spinal cord, these results support the notion that presynaptic interactions between low and high threshold afferents can underlie touch-evoked pain.
Similar articles
-
Involvement of prostaglandin F 2 alpha receptor in ATP-induced mechanical allodynia.Neuroscience. 2009 Sep 29;163(1):362-71. doi: 10.1016/j.neuroscience.2009.05.069. Epub 2009 May 31. Neuroscience. 2009. PMID: 19490931
-
Increased nociceptive input rapidly modulates spinal GABAergic transmission through endogenously released glutamate.J Neurophysiol. 2007 Jan;97(1):871-82. doi: 10.1152/jn.00964.2006. Epub 2006 Nov 15. J Neurophysiol. 2007. PMID: 17108089
-
Stimulus-evoked release of neuropeptides is enhanced in sensory neurons from mice with a heterozygous mutation of the Nf1 gene.Neuroscience. 2006;137(2):637-45. doi: 10.1016/j.neuroscience.2005.09.030. Epub 2005 Nov 17. Neuroscience. 2006. PMID: 16298082
-
Feed-forward inhibition: a novel cellular mechanism for the analgesic effect of substance P.Mol Pain. 2005 Nov 18;1:34. doi: 10.1186/1744-8069-1-34. Mol Pain. 2005. PMID: 16297242 Free PMC article. Review.
-
Secondary hyperalgesia and presynaptic inhibition: an update.Eur J Pain. 2003;7(4):345-51. doi: 10.1016/s1090-3801(03)00047-8. Eur J Pain. 2003. PMID: 12821405 Review.
Cited by
-
NKCC1 in human diseases: is the SLC12A2 gene haploinsufficient?Am J Physiol Cell Physiol. 2023 Aug 1;325(2):C385-C390. doi: 10.1152/ajpcell.00238.2023. Epub 2023 Jul 3. Am J Physiol Cell Physiol. 2023. PMID: 37399495
-
Inhibition of NKCC1 in spinal dorsal horn and dorsal root ganglion results in alleviation of neuropathic pain in rats with spinal cord contusion.Mol Pain. 2023 Jan-Dec;19:17448069231159855. doi: 10.1177/17448069231159855. Mol Pain. 2023. PMID: 36760008 Free PMC article.
-
Pre-Synaptic GABAA in NaV1.8+ Primary Afferents Is Required for the Development of Punctate but Not Dynamic Mechanical Allodynia following CFA Inflammation.Cells. 2022 Aug 3;11(15):2390. doi: 10.3390/cells11152390. Cells. 2022. PMID: 35954234 Free PMC article.
-
NKCC1 Deficiency in Forming Hippocampal Circuits Triggers Neurodevelopmental Disorder: Role of BDNF-TrkB Signalling.Brain Sci. 2022 Apr 15;12(4):502. doi: 10.3390/brainsci12040502. Brain Sci. 2022. PMID: 35448033 Free PMC article. Review.
-
The structure of sensory afferent compartments in health and disease.J Anat. 2022 Nov;241(5):1186-1210. doi: 10.1111/joa.13544. Epub 2021 Sep 15. J Anat. 2022. PMID: 34528255 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical
Molecular Biology Databases
Research Materials