Inhibition of nociceptive responses of spinal cord neurones during hypertension involves the spinal GABAergic system and a pain modulatory center located at the caudal ventrolateral medulla

• Type: Article in International Scientific Journal
• Date: 2006

Authors

Morato, M (Author) FFUP; Pinho, D (Author) Other; Sousa, T (Author) FFUP; Tavares, I (Author) FMUP; Albino Teixeira, A (Author) FMUP

Journal

Title: Journal of Neuroscience Research

Vol. 83

Pages: 647-655

ISSN: 0360-4012

Publisher: Wiley-Blackwell

Indexing

ISI Web of Knowledge - 8 Citations

ISI Web of Science

Scopus - 9 Citations

Scientific classification

FOS: Medical and Health sciences > Basic medicine

CORDIS: Health sciences

Other information

Authenticus ID: P-004-N1P

DOI: 10.1002/jnr.20770

Resumo (PT): The mechanisms of hypertension-induced hypoalgesia were studied in a model of hypertension induced by adenosine receptors blockade with the non-selective antagonist 1,3-dipropyl-8-sulfophenylxanthine (DPSPX) during 7 days. Based on the positive correlation between pain thresholds and noxious-evoked expression of the c-fos protooncogene in spinal cord neurones, we used this marker of nociceptive activation of spinal neurones to evaluate the involvement of the spinal GABAergic system and the caudal ventrolateral medulla (VLM), an important inhibitory component of the supraspinal endogenous pain modulatory system. In DPSPX-treated animals, a 20% increase in blood pressure was achieved along with a decrease in Fos expression in the superficial (laminae I–II) and deep (laminae III–VII) dorsal horn. In these animals, lower percentages of neurones labeled for GABAB receptors that expressed Fos were obtained in the superficial dorsal horn. Lesioning the VLMlat with quinolinic acid prevented the decrease in Fos expression at the spinal cord of DPSPX-hypertensive rats whereas in normotensive animals, no changes in Fos expression were detected. The present results support previous findings that hypertension is associated with a decrease of nociceptive activation of spinal cord neurones, through descending inhibition exerted by the VLMlat. This study further shows that during hypertension a decrease in the expression of GABAB receptors in nociceptive spinal neurones occurs, probably due to changes in the local GABAergic inhibitory system <br> <br> Keywords:c-fos;descending modulation;1,3-dipropyl-8-sulfophenylxanthine;GABAB receptors;rat <br> <a target="_blank" href="http://onlinelibrary.wiley.com/doi/10.1002/jnr.20770/abstract"> Texto integral</a> <br> <br>

Abstract (EN): The mechanisms of hypertension-induced hypoalgesia were studied in a model of hypertension induced by adenosine receptors blockade with the non-selective antagonist 1,3-dipropyl-8-sulfophenylxanthine (DPSPX) during 7 days. Based on the positive correlation between pain thresholds and noxious-evoked expression of the c-fos protooncogene in spinal cord neurones, we used this marker of nociceptive activation of spinal neurones to evaluate the involvement of the spinal GABAergic system and the caudal ventrolateral medulla (VLM), an important inhibitory component of the supraspinal endogenous pain modulatory system. In DPSPX-treated animals, a 20% increase in blood pressure was achieved along with a decrease in Fos expression in the superficial (laminae I-II) and deep (laminae III-VII) dorsal horn. In these animals, lower percentages of neurones labeled for GABA(B) receptors that expressed Fos were obtained in the superficial dorsal horn. Lesioning the VLMIat with quinolinic acid prevented the decrease in Fos expression at the spinal cord of DPSPX-hypertensive rats whereas in normotensive animals, no changes in Fos expression were detected. The present results support previous findings that hypertension is associated with a decrease of nociceptive activation of spinal cord neurones, through descending inhibition exerted by the VLMIat. This study further shows that during hypertension a decrease in the expression of GABAB receptors in nociceptive spinal neurones occurs, probably due to changes in the local GABAergic inhibitory system. (C) 2006 Wiley-Liss, Inc.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 9