Morphine inhibits the thalamic component of the subcortical somatosensory evoked potentials in rats

Somatosensory evoked potentials (SEPs) were obtained by electrical stimulation of the volar surface of the rat forepaw. Subcortical evoked potentials were recorded from the skull overlying the contralateral somatosensory area of the cortex. Additionally, spinal evoked potentials were simultaneously recorded from the dura overlying the dorsal surface of the spinal cord at C3 level. The subcortical SEPs consisted of three peaks I, II, and III which arise from the spinal cord, the brain stem and the thalamus, respectively. The spinal evoked potentials consisted of a negative-positive wave. The latency of the negative peak of the spinal evoked potentials matched the peak latency of component I of the subcortical SEPs. Six doses of intravenous (i.v.) morphine were used: 0.5, 1.0, 2.5, 5.0, 10.0 and 20.0 mg/kg. The spinal evoked potentials and components I and II of the subcortical SEPs were not significantly affected by morphine whereas the amplitude of component III was inhibited (up to 50%) in a dose dependent manner. Optimal effect was achieved with the dose of 2.5 mg/kg. Microinjection of the optimal i.v. dose of morphine (25 micrograms/kg) into the thalamus showed a similar effect on wave III of subcortical SEPs. The effect of morphine was completely reversed by i.v. naloxone (0.25 mg/kg). In conclusion, these results indicate that the primary locus of morphine action on the subcortical SEPs could be at the thalamic level.