[The descending cortical control of nociceptive signals: the neurochemical mechanisms and pharmacological control].
The purpose of the present study was to determine whether electrical cortical stimulation (as a model of descending inhibitory control) could alter the electrophysiological and behavioral signs of a nociceptive response. The inhibitory cortical influence on the neuronal activity produced by nociceptive stimuli (the tooth pulp, C-fibers of afferent somatic nerves, cardiac afferents) was most marked during electrical stimulation the somatosensory (Sn and St) and fronto-orbital cortices. In chronic experiments, somatosensory cortical stimulation delayed the development of the deafferentation pain syndrome and reduced its intensity. The opioid mu-receptor agonists morphine and fentanyl potentiated the inhibitory action of the cortex on evoked neuronal activity. Pentazocine, a kappa-receptor agonist, was less effective. The opioid receptor blocker naloxone eliminated the effect of both cortical stimulation and opioid analgesics. The serotonin receptor blocker methisergide significantly decreased cortical action. Monoamine reuptake inhibitors (amitriptyline, imipramine, fluoxetine) potentiated the effect of cortical stimulation. Adrenergic, dopaminergic cholinergic, and GABA-ergic substances had a little effect. Among nonopioid analgesics, metamyzol and ketorolak only increased moderately descending cortical control.
Kharkevich
D A
DA
Churiukanov
V V
VV
D000818:Animals; D002415:Cats; D002540:Cerebral Cortex / Q000187:drug effects* / Q000502:physiology; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology; D009619:Nociceptors / Q000187:drug effects* / Q000502:physiology; D010146:Pain / Q000503:physiopathology; D051381:Rats; D011930:Reaction Time / Q000187:drug effects / Q000502:physiology; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology