Abstract
The contribution of the stimulatory guanine nucleotide regulatory protein (G s) to prostaglandin E 2 (PGE 2)-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′-[γ-thio]triphosphate (GTPγS) and cholera toxin — which activate G s — both increased, while guanosine-5′-[β-thio] diphosphate (GDPßS) — which prevents the activation of G s — decresed the hyperalgesia induced by PGE 2. These data support the hypothesis that the action of PGE 2 on primary afferent nociceptors leading to decreases in paw-withdrawal threshold is G s-mediated.
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