The effects of strychnine, bicuculline, and ketamine on 'immersion-inhibited' dorsal horn convergent neurons in intact and spinalized rats.
In both intact and spinalized rats, this study examined the effects of strychnine (a glycine antagonist), bicuculline (a GABAA antagonist), and ketamine (a non-competitive NMDA receptor antagonist) on one particular class of lumbar dorsal horn convergent neurons. This group of convergent neurons are inhibited when a rat's entire ipsilateral hindpaw is immersed in 50 degrees C water and has a strong afterdischarge as soon as the paw is removed from the water. Strychnine (2 mg/kg, iv) increased ongoing activity and blocked the 'inhibition phase' in both intact and spinalized rats demonstrating that a spinal-related glycine mechanism was involved in the inhibition. However, only in intact rats did the firing rate of the 'afterdischarge phase' increase significantly from pre-drug levels, suggesting that supraspinal sites may be involved in modulating this phase. Ketamine (15 mg/kg, iv) depressed ongoing activity and the firing rate in the afterdischarge phase of these neurons. Additionally, ketamine reversed the strychnine-induced increase in ongoing activity. Bicuculline (2 mg/kg, iv) had no effect on the activity of this cell class. As shown previously, and replicated here, these 'immersion-inhibited' neurons invariably have both inhibitory and excitatory mechano-receptive fields on the ipsilateral hindpaw. Thus, the response of this class of convergent neurons to noxious stimulation may be a function of relative inputs of glycine and EAA's, each possibly triggered by the stimulation of different receptive fields/regions on the same paw. Furthermore, when both fields are co-stimulated during noxious immersion of the entire paw, glycine has a stronger influence on activity than does the EAA's.
McGaraughty
S
S
Departments of Physiology and Psychiatry, McGill University, 3655 Drummond St., Montreal, Que., Canada.
Henry
J L
JL
D000818:Animals; D001640:Bicuculline / Q000494:pharmacology*; D003655:Decerebrate State / Q000473:pathology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology*; D005110:Extracellular Space / Q000502:physiology; D018756:GABA Antagonists / Q000494:pharmacology*; D058787:GABA-A Receptor Antagonists; D018684:Glycine Agents / Q000494:pharmacology*; D007649:Ketamine / Q000494:pharmacology*; D008297:Male; D009474:Neurons / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors; D013331:Strychnine / Q000494:pharmacology*
D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D058787:GABA-A Receptor Antagonists; D018684:Glycine Agents; D016194:Receptors, N-Methyl-D-Aspartate; D007649:Ketamine; D013331:Strychnine; D001640:Bicuculline