Effects of Somatostatin on the Responses of Rostrally Projecting Spinal Dorsal Horn Neurons to Noxious Stimuli in Cats.
10.4196/kjpp.2008.12.5.253
- Author:
Sung Jun JUNG
1
;
Su Hyun JO
;
Sanghyuck LEE
;
Eunhui OH
;
Min Seok KIM
;
Woo Dong NAM
;
Seog Bae OH
Author Information
1. Department of Physiology, Kangwon National University College of Medicine, Chunchon, Korea. eurijj@naver.com
- Publication Type:Original Article
- Keywords:
Somatostain;
Spinal cord;
Dorsal horn;
Nociception;
A delta-fiber;
C-fiber;
Pain
- MeSH:
Animals;
Cats;
Central Nervous System;
Cold Temperature;
Hot Temperature;
Neurons;
Nociception;
Posterior Horn Cells;
Sciatic Nerve;
Somatostatin;
Spinal Cord
- From:The Korean Journal of Physiology and Pharmacology
2008;12(5):253-258
- CountryRepublic of Korea
- Language:English
-
Abstract:
Somatostatin (SOM) is a widely distributed peptide in the central nervous system and exerts a variety of hormonal and neural actions. Although SOM is assumed to play an important role in spinal nociceptive processing, its exact function remains unclear. In fact, earlier pharmacological studies have provided results that support either a facilitatory or inhibitory role for SOM in nociception. In the current study, the effects of SOM were investigated using anesthetized cats. Specifically, the responses of rostrally projecting spinal dorsal horn neurons (RPSDH neurons) to different kinds of noxious stimuli (i.e., heat, mechanical and cold stimuli) and to the A delta-and C-fiber activation of the sciatic nerve were studied. Iontophoretically applied SOM suppressed the responses of RPSDH neurons to noxious heat and mechanical stimuli as well as to C-fiber activation. Conversely, it enhanced these responses to noxious cold stimulus and A delta-fiber activation. In addition, SOM suppressed glutamate-evoked activities of RPSDH neurons. The effects of SOM were blocked by the SOM receptor antagonist cyclo-SOM. These findings suggest that SOM has a dual effect on the activities of RPSDH neurons; that is, facilitation and inhibition, depending on the modality of pain signaled through them and its action site.
