Contribution of guanine nucleotide regulatory proteins to prostaglandin hyperalgesia in the rat.

Abstract

The contribution of the stimulatory guanine nucleotide regulatory protein (Gs) to prostaglandin E2 (PGE2)-induced hyperalgesia was investigated in the hairy skin of the rat hindpaw using the Randall-Selitto paw-withdrawal test. Although without effect alone, guanosine-5'-[gamma-thio]triphosphate (GTP gamma S) and cholera toxin--which activate Gs--both increased, while guanosine-5'-[beta-thio] diphosphate (GDP beta S)--which prevents the activation of Gs--decreased the hyperalgesia induced by PGE2. These data support the hypothesis that the action of PGE2 on primary afferent nociceptors leading to decreases in paw-withdrawal threshold is Gs-mediated.

• Authors: Y O Taiwo, J D Levine
• Journal: Brain research (Brain Res) Vol. 492 Issue 1-2 Pg. 400-3 (Jul 17 1989) ISSN: 0006-8993 [Print] Netherlands
• PMID: 2502301 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Prostaglandins E
• Cholera Toxin
• GTP-Binding Proteins

Topics

• Animals
• Cholera Toxin (pharmacology)
• Drug Interactions
• GTP-Binding Proteins (pharmacology, physiology)
• Hyperalgesia (chemically induced, metabolism, physiopathology)
• Hyperesthesia (chemically induced)
• Male
• Neurons, Afferent (drug effects, metabolism, physiopathology)
• Pain (metabolism)
• Prostaglandins E (pharmacology)
• Rats
• Rats, Inbred Strains
• Sensory Thresholds (drug effects)