Premium
ω‐Agatoxin IVA, a P‐Type Calcium Channel Antagonist, Reduces Nociceptive Processing in Spinal Cord Neurons with Input From the Inflamed But Not From the Normal Knee Joint — An Electrophysiological Study in the Rat In Vivo
Author(s) -
Nebe J.,
Vanegas H.,
Neugebauer V.,
Schaible H.G.
Publication year - 1997
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.1997.tb01386.x
Subject(s) - nociception , spinal cord , noxious stimulus , ankle , anesthesia , calcium channel , electrophysiology , voltage dependent calcium channel , medicine , neuroscience , antagonist , calcium , chemistry , anatomy , receptor , psychology
High threshold voltage‐dependent P‐ and Q‐type calcium channels are involved in neurotransmitter release. In order to investigate the role of P‐ and Q‐type calcium channels in the mechanosensory (nociceptive) processing in the spinal cord, their participation in the responses of spinal wide‐dynamic‐range neurons to innocuous and noxious mechanical stimulation of the knee and ankle joints was studied in 30 anaesthetized rats. The knee was either normal or acutely inflamed by kaolin/carrageenan. During the topical application of ω‐agatoxin IVA (P‐type channel antagonist, 0.1 μM) onto the dorsal surface of the spinal cord, the responses to innocuous and noxious pressure applied to the normal knee were increased to respectively 124 ± 42% and 114 ± 23% of predrug values (mean ± SD, P < 0.05, 14 neurons). By contrast, in rats with an inflamed knee, the responses to innocuous and noxious pressure applied to the knee were reduced to respectively 72 ± 19 and 73 ± 22% of baseline (mean ± SD, P < 0.01, 13 neurons). In the same neurons, ω‐agatoxin IVA slightly increased the responses to pressure on the non‐inflamed ankle whether the knee was normal or inflamed. Thus P‐type calcium channels seem to acquire a predominant importance in the excitation of spinal cord neurons by mechanosensory input from inflamed tissue and hence in the generation of inflammatory pain. By contrast, the Q‐type channel antagonist, ω‐conotoxin MVllC (1 or 100 μM), had no significant effect upon responses to innocuous or noxious pressure applied to either normal or inflamed knees (25 neurons).