Lesions of the caudal ventrolateral medulla block the hypertension-induced inhibition of noxious-evoked c-fos expression in the rat spinal cord

• Type: Article in International Scientific Journal
• Date: 1997

Authors

Isaura Tavares (Author) FMUP; Almeida, A (Author) Other; Albino Teixeira, A (Author) FMUP; Deolinda Lima (Author) FMUP

Journal

Title: European Journal of Pain

Vol. 1

Pages: 149-160

ISSN: 1090-3801

Publisher: Wiley-Blackwell

Indexing

Scopus - 25 Citations

Other information

Authenticus ID: P-007-C36

DOI: 10.1016/s1090-3801(97)90073-2

Abstract (EN): The effect of lesioning the lateral portion of the caudal ventrolateral medullary reticular formation (VLMlat) on the noxious-evoked expression of the c-fos proto-oncogene in spinal neurons, was studied in short-term hypertensive rats. Occlusion of the renal artery for 96 h in unlesioned animals induced a 52% increase in blood pressure (BP) and a 66% decrease in the number of Fos-immunoreactive (Fos-IR) spinal cells following noxious cutaneous stimulation, as compared to values in normotensive controls. Lesioning the VLMlat in hypertensive rats by unilateral quinolinic acid (QA) injection (0.3 ¿l of a 180 nmol/¿l solution) 24 h before noxious stimulation, prevented the Fos-IR cell decrease. In normotensive rats, lesioning the VLMlat produced no changes in c-fos expression. To investigate the role played by the VLMlat in cardiovascular control, BP and heart rate (HR) were measured during local injections of QA or glutamate (0.5 ¿l of a 100nmol/¿l solution) to normotensive animals. Injections of QA produced an immediate rise in BP and HR which reached maximal values (18 and 14% increase, respectively) 5 min after the administration onset, then returning gradually to baseline levels. Glutamate injections resulted in an immediate decrease of the same values, which reached 29 and 39%, respectively, 4 min after the beginning of injection, after which they decreased to baseline levels. These results suggest that VLMlat neurons inhibit nociceptive spinal neurons in response to rises in blood pressure, while exerting negative control of cardiovascular parameters. It is suggested that the VLMlat is involved in the genesis of hypoalgesia during hypertension.

Language: English

Type (Professor's evaluation): Scientific