The effect of clonidine injection into the nucleus paragigantocellularis lateralis on nociception

University of Manchester (2003) J Physiol 552P, C80

Communications: The effect of clonidine injection into the nucleus paragigantocellularis lateralis on nociception

H. Fathi-Moghaddam†, M. Kesmati* and H. Mohammad Pour Kargar*

* Department of Biology, School of Sciences, Shahid Chamran University, Ahwaz, Iran and †Department of Physiology, School of Medicine, Ahwaz University of Medical Sciences, Ahwaz, Iran

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The paragigantocellularis lateralis (LPGi) is located in the rostroventrolateral medulla and involved in several functions such as cardiovascular regulation, sexual behavior, withdrawal syndrome, and especially nociception. α2-Adrenoceptor agonists such as clonidine have been used for induction of analgesia in clinics. This drug affects the CNS, especially the nucleus locus coeruleus and the spinal cord. There is no information about the role of LPGi in nociception.

In this study the effects of clonidine administration into LPGi on the response to nociception (hot plate, maximum time period, 45 s at 52 ± 0.5 °C) were investigated. Twenty-eight male N-MRI adult male rats (220 ± 20 g) were used. Animals were divided into control and experimental groups. Experimental groups contained three subgroups: sham group that received artificial cerebrospinal fluid (ACSF) and two other subgroups that received 1µg/0.5µl and 2µg/0.5µl clonidine into the paragigantocellularis nucleus. Rats were anaesthetized with an injection (I.P.) of a mixture of ketamine hydrochloride (110 mg kg-1) and Xylazine 2 % (5 mg kg-1) and LPGi cannulated bilaterally in experimental animals under surgical procedure using the atlas of Paxinos & Watson (1998) (AP = 5.74, L = ± 1.6, DP = 12.12). After a recovery period, ACSF or clonidine (dissolved in ACSF) was injected into LPGi bilaterally and the response to pain was evaluated with the hot plate apparatus. All data were analysed using one-way ANOVA. At the end of the experiments the animals were humanely killed.

The results showed the following: (1) no difference was found between control and sham groups; (2) there was no significant difference between sham and 1µg/0.5µl clonidine groups; and (3) there was a significant difference between sham and 2µg/0.5µl clonidine groups (P < 0.02).

The results showed that clonidine injection to LPGi increased response time to acute pain. It seems that α2-adrenoceptors in LPGi modulate the pathway of pain and that the analgesic effect of clonidine is induced by α2-adrenoceptors of the paragigantocellularis lateralis nucleus.

This project supported by Shahid Chamran University.



Where applicable, experiments conform with Society ethical requirements.

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