Morphine: Ability to block neuronal activity evoked by a nociceptive stimulus

Abstract

The effect of morphine on the neuronal activity evoked by a nociceptive stimulus, a foot pinch, was studied in the dorsal raphe nucleus (DR) and in the mesencephalic reticular formation (MRF) of the rat. In the MRF and adjacent areas, neuronal firing was accelerated by the nociceptive stimulus. Morphine blocked this acceleration when administered either microintophoretically or i.v. Three lines of evidence indicate that this is a specific narcotic effect. First, naloxone, a specific narcotic antagonist, antagonized the effect of morphine. Secondly, two morphine agonists, oxymorphone and methadone, blocked the evoked neuronal acceleration like morphine when administered either microiontophoretically or i.v.; naloxone also blocked the effects of the two agonists. Finally, two non-opioid CNS depressants did not block the acceleration in neuronal firing even though microintophoretic ejection currents 2–5 times greater than those for morphine were used. In contrast, neuronal firing in the DR was rarely altered by the nociceptive stimulus or by morphine, administered either microiontophoretically or i.v. Furthermore, morphine did not affect the inhibition produced by 5-HT on neurons in the DR. It is concluded from this study that the MRF is a possible site of action for the antinociceptive effects of morphine. It is also concluded that morphine does not affect the spontaneous neuronal firing rate in the DR and that the DR is not a site of action of the antinociceptive effects of morphine when a foot pinch is used as the nociceptive stimulus.