Pharmacology, biochemistry, and behavior
-
Pharmacol. Biochem. Behav. · Dec 2011
Stimulation of the occipital or retrosplenial cortex reduces incision pain in rats.
The electrical stimulation of the occipital (OC) or retrosplenial (RSC) cortex produces antinociception in the rat tail-flick and formalin tests. This study examined the antinociceptive effects of stimulating the OC or RSC in a rat model of post-incision pain. The involvement of the anterior pretectal nucleus (APtN) as intermediary for the effect of OC or RSC stimulation was also evaluated because the OC and RSC send inputs to the APtN, which is implicated in antinociception and nociception. ⋯ The effects of stimulating the OC or RSC were not changed in rats treated with atropine. We conclude that stimulation-induced antinociception from the RSC or OC in rat post-incision pain activates distinct descending pain inhibitory pathways. The pathway activated from the RSC utilizes serotonergic and opioid mediation in the APtN, whereas stimulation of the OC utilizes a non-serotonergic, non-cholinergic and non-opioid mediation in the same nucleus.
-
Pharmacol. Biochem. Behav. · Dec 2011
Intra-accumbal NMDA but not AMPA/kainate receptor antagonist attenuates WIN55,212-2 cannabinoid receptor agonist-induced antinociception in the basolateral amygdala in a rat model of acute pain.
Previous studies showed the role of basolateral amygdala (BLA) in cannabinoid-induced antinociception. Several lines of evidence indicated that the nucleus accumbens (NAc) receives excitatory glutamatergic inputs primarily from limbic-related structures, including the hippocampus, BLA, and various thalamic nuclei. Additionally, it has been shown that the NAc plays an important role in mediating the suppression of animal models of pain. ⋯ Nonetheless, administration of AMPA/kainate receptor antagonist, CNQX, could not affect WIN-induced analgesia. Additionally, solely administration of intra-accumbal injection of CNQX (2.5 μg/0.5 μl DMSO), but not AP5 (5 μg/0.5 μl saline), could significantly change the baseline tail-flick latencies in the rats. It seems that NMDA receptors located in the NAc, in part, mediate the antinociceptive responses of cannabinoid within the BLA in acute model of pain.