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Presynaptic inhibition and spinal pain processing in mice: a possible role of the NKCC1 cation-chloride co-transporter in hyperalgesia.
Neurosci Lett. 2004 May 06; 361(1-3):200-3.NL

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.

Authors+Show Affiliations

Department of Physiology, University of Alcalá, Madrid, Spain.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15135928

Citation

Laird, Jennifer M A., et al. "Presynaptic Inhibition and Spinal Pain Processing in Mice: a Possible Role of the NKCC1 Cation-chloride Co-transporter in Hyperalgesia." Neuroscience Letters, vol. 361, no. 1-3, 2004, pp. 200-3.
Laird JM, García-Nicas E, Delpire EJ, et al. Presynaptic inhibition and spinal pain processing in mice: a possible role of the NKCC1 cation-chloride co-transporter in hyperalgesia. Neurosci Lett. 2004;361(1-3):200-3.
Laird, J. M., García-Nicas, E., Delpire, E. J., & Cervero, F. (2004). Presynaptic inhibition and spinal pain processing in mice: a possible role of the NKCC1 cation-chloride co-transporter in hyperalgesia. Neuroscience Letters, 361(1-3), 200-3.
Laird JM, et al. Presynaptic Inhibition and Spinal Pain Processing in Mice: a Possible Role of the NKCC1 Cation-chloride Co-transporter in Hyperalgesia. Neurosci Lett. 2004 May 6;361(1-3):200-3. PubMed PMID: 15135928.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Presynaptic inhibition and spinal pain processing in mice: a possible role of the NKCC1 cation-chloride co-transporter in hyperalgesia. AU - Laird,Jennifer M A, AU - García-Nicas,Esther, AU - Delpire,Eric J, AU - Cervero,Fernando, PY - 2004/5/12/pubmed PY - 2004/8/31/medline PY - 2004/5/12/entrez SP - 200 EP - 3 JF - Neuroscience letters JO - Neurosci. Lett. VL - 361 IS - 1-3 N2 - 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. SN - 0304-3940 UR - https://www.unboundmedicine.com/medline/citation/15135928/Presynaptic_inhibition_and_spinal_pain_processing_in_mice:_a_possible_role_of_the_NKCC1_cation_chloride_co_transporter_in_hyperalgesia_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304394003013958 DB - PRIME DP - Unbound Medicine ER -