Abstract
This study was performed to examine the antinociceptive effect after microinjection of arginine vasopressin (AVP) into the central nucleus of amygdala. We recorded the jaw opening reflex in freely moving rats. After injection of 0.2 or 0.4 nM AVP into the central nucleus of amygdala, digastric electromyogram (dEMG) was suppressed to 55 ± 5% or 88 ± 3 of the control. Artificial cerebrospinal fluid had no effects on the basal dEMG activity. V 1 vasopressin receptor antagonist blocked the suppressive effect produced by microinjection of 0.4 nM AVP from 53 ± 3 to 81 ± 3% of the control. However, V 2 vasopressin receptor antagonist did not affect changes in dEMG. We observed dEMG activity after intracerebroventricular injection of naloxone, methysergide, or phentolamine. All drugs did not affect the basal dEMG activity at our dose. Naloxone blocked the suppressive effect of 0.4 nM AVP from 42 ± 4 to 79 ± 5% of the control. Methysergide also inhibited the suppression of dEMG from 44 ± 3 to 83 ± 6% of the control. However, phentolamine, an α-adrenergic receptor antagonist, did not affect the suppression of dEMG. These results indicate AVP in the central nucleus of amygdala has potent analgesic effects in the orofacial area. The antinociception of central AVP seems to be mediated by opioid and serotonergic pathways.
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