EFFECTS OF MORPHINE ON UNIT DISCHARGES RECORDED FROM THE TRIGEMINAL NUCLEI IN CATS
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The primary relay nuclei of the afferent sensory pathway have been demonstrated by Fujita <I>et al</I>. (1, 2) as one of the sites of action of morphine in the central nervous system. They have shown that the evoked potentials in the spinal cord of the cat caused by afferent stimulation of the splanchnic, phrenic and inferior cardiac nerves are depressed by intravenous injection of morphine. However, Takagi <I>et al</I>. (3) have postulated that the inhibitory effect of morphine on the spinal cord derives from an activation of inhibitory mechanism in the midbrain reticular formation rather than from a direct action. The experiments of Mizoguchi (4) in the dog have demonstrated that morphine suppresses the evoked potentials in the Nucl. tractus spinalis n. trigemini but does not affect those in the Nucl. sensorius superior n. trigemini caused by electrical stimulation of the tooth pulp. The neurons in the former nucleus are known to receive pain and temperature impulses, while those in the latter nucleus to receive tactile impulses (5). Therefore, the experimental results presented by Mizoguchi (4) are well compatible with an explanation of the site of analgesic action of morphine.<BR> On the other hand, by using microelectrode technique Kruger and Michel (6) could not find any neuron activity uniquely sensitive to noxious stimuli in the Nucl. tractus spinalis n. trigemini, but they found that all tactile neurons in that nucleus responded well to painful stimuli.<BR> The present experiment is an attempt to elucidate the mode of action of morphine upon the unit discharges in the Nucl. sensorius superior and Nucl. tractus spinalis n. trigemini of the cat by means of microelectrode technique.
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