Effect of nociceptive stimulation of signal transmission from low-threshold cutaneous afferents in the somatosensory system

Abstract

Noxious heating of the chloralose-anesthetized cat foot skin to 44-60 degrees C caused a 2-4 fold increase in the amplitude of the primary cortical responses evoked by direct stimulation of the spinocervical tract neurons which receive messages from the heated skin area, but had no influence on the primary responses elicited by stimulation of these neuron axons in the dorsolateral funiculus and even suppressed the primary responses to stimulation of the nerve innervating the heated area. The suppression was accompanied by depolarization of the low threshold fibre central terminals of this nerve as evidenced by the fact that during the heating the amplitude of the antidromic action potentials evoked in the nerve by stimulation of its presynaptic terminals in the dorsal horn became 2-3 times greater than before heating. After abolition of presynaptic depolarization either by picrotoxin (0.2-0.7 mg/kg, i.v.) or as a result of acute asphyxia the heating began to facilitate also those primary responses which were evoked by stimulation of the nerve. In this case the amplitude of the primary responses increased 3-20 times. A conclusion is made that acute noxious stimulation brings about presynaptic inhibition which is strong enough to overcome the facilitatory action of nociceptive impulses on the spinal cord sensory neurons. This inhibitory mechanism is supposed to prevent development of hyperalgesia during acute noxious stimulations.