Central-amygdaloid carbachol suppressed nociceptive jaw opening reflex in freely moving rats

1. Experiments were carried out in rats with stimulating electrodes implanted in the dental pulp, recording electrodes inserted into the anterior digastric muscle, and indwelling cannula implanted in the central amygdaloid nucleus and the cisterna magna area. 2. Injection of 4.4 nM and 8.8 nM carbachol into the central amygdaloid nucleus suppressed digastric electromyogram (dEMG) to 81 +/- 8% and 47 +/- 9% of the control, respectively. 3. Atropine, a muscarinic receptor antagonist, blocked the suppression of dEMG in response to the administration of 8.8 nM carbachol into the amygdala. However, a mecamylamine, a nicotinic receptor antagonist, did not affect changes in dEMG. 4. Intracisternal naloxone, an opioid receptor antagonist, reduced the suppression of dEMG from 47 +/- 10 to 72 +/- 12% of the control. 5. Intracisternal methysergide, a serotonin receptor antagonist, also reduced the suppression of dEMG from 50 +/- 9 to 78 +/- 9% of the control. 6. The carbachol-induced antinociception from the central amygdaloid nucleus was attributed to opioid and serotonergic descending inhibitory influences on nociceptive pathways.