Abstract

The actions of morphine and nalorphine antagonism on tooth pulp primary and secondary afferent systems were determined in acute dogs. Morphine usually was given intravenously in doses of 2 mg/kg or 10 mg/kg. Nalorphine usually was given intravenously in doses of 1 mg/kg or 2.5 mg/kg.

Drug effects on the potentials in the primary afferent pathway were determined cortically in the contralateral coronal gyrus and in the brainstem in the contralateral nucleus ventralis posteromedialis and the medial lemniscus. In general, morphine did not depress the amplitude or the latency of the responses in this system.

The actions of morphine and nalorphine on the secondary tooth pulp afferent potentials were complex. The potentials evoked from the tooth were usually enhanced in the areas surrounding central grey, some of the diencephalic nuclei (nucleus centralis medialis, nucleus medialis dorsalis, nucleus lateralis posterior, and nucleus subparafascicularis), and in some of the medullary reticular areas, but occasionally were depressed, or in other animals were unaffected. The latencies of evoked responses in nucleus medialis dorsalis were prolonged in spite of an enhancement in amplitude. Frequently an early depression in amplitude of evoked potentials from the tooth within the first few minutes after intravenous administration of morphine was associated with a marked fall in arterial blood pressure. Upon return of the blood pressure toward normal within 25 minutes after morphine administration, a subsequent enhancement of the amplitude of the potential occurred. In general, nalorphine partially antagonized these effects of morphine.

In human subjects it was shown that single shock electrical stimulation above threshold intensity of the central incisors produced a transient painful sensation.

The actions of morphine on cortical primary responses evoked by stimulation of the sciatic nerve were inconsistent. In the majority of the animals morphine had no effect.

Morphine in doses of 0.2 to 2 mg/kg given intravenously produced a definite enhancement of cortical recruiting responses following electrical stimulation of various thalamic areas. Nalorphine partially antagonized these effects.

Nalorphine in doses of 0.25 to 2.5 mg/kg given intravenously ½ to 1 hour following morphine produced a statistically significant increase in the mean arterial blood pressure above control values.

It is concluded that the neural mechanisms of morphine analgesia of tooth pulp pain are complex. It does not appear that a simple depression or blockade of single afferent impulses arising from the peripheral tooth pain receptors can explain the analgesic action of morphine. Its effects on the secondary pathways from the tooth pulp are variable. Either an occasional depression, no effect, or a definite enhancement of potentials was observed. It is of considerable theoretical interest that an enhancement of the evoked afferent responses was the predominant action of morphine.