Operant conditioning of somatosensory evoked potential (SEP) amplitude in rats. I. Specific changes in SEP amplitude and a naloxone-reversible somatotopically specific change in facial nociception.

The aim of this experiment was to investigate possible endogenous opioid modulation of innocuous somatosensory activity. Somatosensory activity was measured by recording cortical somatosensory evoked potential (SEP) and reflex movement amplitude evoked by innocuous electrical stimulation of the spinal trigeminal tract in awake rats. Putative endogenous opioid activity was blocked using the opiate antagonist naloxone (1 mg/kg). The amplitude of midlatency SEP components (14-50 ms latency) increased following administration of naloxone and repeated stimulus presentations. The amplitude of these components decreased following administration of the opiate agonist morphine (3 mg/kg). An early cortical component (10 ms latency) habituated following the administration of saline but did not habituate following naloxone. Naloxone also enhanced habituation of the late SEP components (60-120 ms latency) and reflex movement evoked at higher stimulus intensities. Morphine decreased the amplitude of the early cortical component but had no consistent effect on the amplitude of the late SEP components.