Evidence that diffuse noxious inhibitory controls (DNIC) are medicated by a final post-synaptic inhibitory mechanism

Nineteen convergent neurones, 19 'non-noxious only' neurones and 13 'proprioceptive' neurones all with peripheral excitatory receptive fields on the ipsilateral hindpaw, were recorded in the lumbar dorsal horn of non-spinalized, anaesthetized rats. These neurones were all excited by the electrophoretic application of glutamate; using 20 s applications of appropriate electrophoretic currents, almost identical levels of activity (around 30 spikes/s) were produced for each of the 3 types of neurones. The application of heterotopic noxious stimuli resulted in strong inhibitions of the glutamate-evoked activity of the convergent neurones. During the application of noxious heat (52 degrees C) to the tail and noxious pinches to the tail, contralateral hindpaw and muzzle, the glutamate-evoked activity was depressed by 78%, 84%, 63% and 59%, respectively. It was also found that these inhibitions outlasted the period of conditioning stimulation by several minutes (post-effects). Twenty seconds after i.p. injection of bradykinin (20 micrograms) the glutamate-evoked activity was depressed by 56% and this effect also lasted for several minutes. The application of identical heterotopic noxious stimuli did not affect the glutamate-evoked activity of the 'non-noxious only' neurones or the 'proprioceptive' neurones. The application to convergent neurones, of doses of glutamate, which were very much larger than the threshold for firing, produced an intense discharge followed by a progressive decrease in spike amplitude and finally a blocking of the spike discharge. During such sequences, which are typical of excessive depolarization, the application of noxious conditioning stimuli (e.g pinch of the contralateral hindpaw or muzzle) resulted in recovery of the spike discharge. In several cases, this recovery long outlasted the period of conditioning noxious stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)