Differential effects of morphine on corneal-responsive neurons in rostral versus caudal regions of spinal trigeminal nucleus in the rat.

Abstract

The initial processing of corneal sensory input in the rat occurs in two distinct regions of the spinal trigeminal nucleus, at the subnucleus interpolaris/caudalis transition (Vi/Vc) and in laminae I-II at the subnucleus caudalis/spinal cord transition (Vc/C1). Extracellular recording was used to compare the effects of morphine on the evoked activity of corneal-responsive neurons located in these two regions. Neurons also were characterized by cutaneous receptive field properties and parabrachial area (PBA) projection status. Electrical corneal stimulation-evoked activity of most (10/13) neurons at the Vi/Vc transition region was increased [146 +/- 16% (mean +/- SE) of control, P < 0.025] after systemic morphine and reduced after naloxone. None of the Vi/Vc corneal units were inhibited by morphine. By contrast, all corneal neurons recorded at the Vc/C1 transition region displayed a naloxone-reversible decrease (55 +/- 10% of control, P < 0.001) in evoked activity after morphine. None of 13 Vi/Vc corneal units and 7 of 8 Vc/C1 corneal units tested projected to the PBA. To determine if the Vc/C1 transition acted as a relay for the effect of intravenous morphine on corneal stimulation-evoked activity of Vi/Vc units, morphine was applied topically to the dorsal brain stem surface overlying the Vc/C1 transition. Local microinjection of morphine at the Vc/C1 transition increased the evoked activity of 4 Vi/Vc neurons, inhibited that of 2 neurons, and did not affect the remaining 12 corneal neurons tested. In conclusion, the distinctive effects of morphine on Vi/Vc and Vc/C1 neurons support the hypothesis that these two neuronal groups contribute to different aspects of corneal sensory processing such as pain sensation, autonomic reflex responses, and recruitment of descending controls.