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The Journal of Neurophysiology Vol. 86 No. 6 December 2001, pp. 3061-3064
Copyright ©2001 by the American Physiological Society
RAPID COMMUNICATION
School of Biomedical Sciences, University of Nottingham Medical School, Queen's Medical Centre, Nottingham NG7 2UH, United Kingdom
Kelly, Sara and
Victoria Chapman.
Selective Cannabinoid CB1 Receptor Activation
Inhibits Spinal Nociceptive Transmission In Vivo. J. Neurophysiol. 86: 3061-3064, 2001. Cannabinoid1 (CB1)
receptors are located at CNS sites, including the spinal cord, involved
in somatosensory processing. Analgesia is one of the tetrad of
behaviors associated with cannabinoid agonists. Here, effects of a
potent cannabinoid CB1 receptor agonist arachidonyl-2-chloroethylamide (ACEA) on evoked responses of dorsal horn neurons in anesthetized rats were investigated. Extracellular recordings of convergent dorsal horn neurons were made in halothane anesthetized Sprague-Dawley rats (n = 16). Effects of
spinal application of ACEA on electrically evoked responses of dorsal
horn neurons were studied. Mean maximal effects of 0.5, 5, 50, and 500 ng/50 µl ACEA on the C-fiber-mediated postdischarge response were
79 ± 6, 62 ± 10, and 54 ± 7% (P < 0.01), 45 ± 6% (P < 0.01), of control, respectively.
ACEA (500 ng/50 µl) also reduced the C-fiber-evoked nonpotentiated
responses of neurons (59 ± 9% of control, P < 0.05) and A
-fiber-evoked responses of neurons (68 ± 10% of
control, P < 0.01). Minor effects of ACEA on
A
-fiber-evoked responses were observed. Spinal pre-administration of
the selective CB1 receptor antagonist SR141716A
(0.01 µg/50 µl) significantly reduced effects of ACEA (500 ng/50
µl) on postdischarge responses of dorsal horn neurons. This study
demonstrates that spinal CB1 receptors modulate
the transmission of C- and A-fiber-evoked responses in anesthetized
rats; this may reflect pre- and/or postsynaptic effects of cannabinoids
on nociceptive transmission. CB1 receptors inhibit synaptic release of glutamate in rat dorsolateral striatum, a
similar mechanism of action may underlie the effects of ACEA on noxious
evoked responses of spinal neurons reported here.
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