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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical and experimental data indicate that the cerebral cortex plays an important role in pain perception and endogenous antinociceptive system function. Moreover, the enhancement of descending inhibitory cortical control may be involved in the mechanisms of analgetic effect of some agents. The present study was designed to investigate the effect of cortical electrical stimulation (as a model of descending inhibitory control) on the behavioral and electrophysiological signs of nociceptive response, decipher the mechanisms involved therein and evaluate the action of central analgesics (both opioid and non-opioid) on descending cortical control. In acute experiments in cats the inhibitory cortical influence on neuronal activity produced by nociceptive stimuli (electrical stimulation of tooth pulp, C-fibers of afferent somatic nerves, afferent cardiac structures) was most marked after stimulation of the first and second sensory and fronto-orbital areas. In chronic experiments on rats cortical stimulation reduced behavioral signs of visceral pain (writhing test) and also delayed the development of neuropathic pain syndrome along with lowering its intensity. Mu-opioid receptor agonists (morphine, fentanyl) potentiated the inhibitory cortical effect on the evoked neuronal activity. Pentazocine, which has pronounced kappa-receptor agonistic activity, was less effective. Naloxone eliminated the effects of both cortical stimulation and opioid analgesics. Serotonin receptor antagonist methysergide as well as p-chlorophenylalanine significantly decreased inhibitory cortical control and opioids effect. Monoamine re-uptake inhibitors with analgetic properties (imipramine, fluoxetine) potentiated the inhibitory effect of cortical stimulation. Adrenoceptor, dopamine, acetylcholine, GABA-receptor agents and antagonists of NMDA receptors had minor or no effect. Among non-narcotic analgesics, inhibitors of cyclooxygenase, metamysole and ketorolak increased only moderately the descending cortical control of nociception. Thus, the cerebral cortex is able to control the nociceptive processing in different pain syndromes (somatic, visceral or neuropathic pain). Opioidergic and serotonergic systems play the key role in this control. The effect over the cortical descending control is likely to be one of the components of the analgetic effect exerted by opioids and some other central analgesics.
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PMID:Pharmacological regulation of descending cortical control of the nociceptive processing. 1044 70

Serotonin (5HT1A) is a chemical mediator of inflammation and the largest single neurotransmitter system of the brain. Its secretion and physiological actions mediate stress and pain, affecting both immune and nervous system functions through the hypothalamic-pituitary-adrenal axis. Serotonin receptor dysfunction is well-characterized in mental disturbances like depression and anxiety. Transcranial magnetic stimulation has been used therapeutically to treat refractory disorders like non-responsive depression and may act in part through its effect on 5HT1A receptors. Previously we have shown that in vitro, 5HT1A receptor binding to a radioactive agonist can be modulated by specific intensity and frequency electromagnetic fields (EMFs). In the present report we have used quantitative receptor autoradiography to evaluate 5HT1A receptor density in rat brain and the impact of pulsed EMF exposure on receptor binding in key brain regions. Rats used in this study had whole body exposures to either a geofield control or to pulsed EMFs to evaluate the treatment for chemically-induced tendinitis. Since the brains were exposed coincidentally as a consequence of the main experiment, we investigated the potential for EMF-induced changes in areas such as the hippocampus. This pilot study should provide a detailed understanding of magnetic field effects on stress-responsive brain regions and will lead to a more coordinated approach to the use of such modalities for therapeutic intervention in humans.
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PMID:Autoradiographic evaluation of electromagnetic field effects on serotonin (5HT1A) receptors in rat brain. 1272 37

Experimental and clinical data indicate that the cerebral cortex plays an important role in pain perception and endogenous antinociceptive system function. Moreover, the enhancement of descending inhibitory cortical control may be involved in the mechanisms of analgesic effect of some agents. The present study was designed to investigate the effect of cortical electrical stimulation (as a model of descending inhibitory control) on the behavioral and electrophysiological signs of nociceptive response, elucidate the mechanisms involved therein and evaluate the action of central analgesics (both opioid and non-opioid) on descending cortical control. In acute experiments on cats, the inhibitor y cortical influence upon neuronal activity produced by nociceptive stimuli (electrical stimulation of tooth pulp, C-fibers of afferent somatic nerves, afferent cardiac structures) was most marked after stimulation of the first and second sensory and fron-to-orbital areas. In chronic experiments on rats, cortical stimulation reduced behavioral signs of visceral pain (writhing test) and also delayed the development of neuropathic pain syndrome along with lowering its intensity. mu-Opioid receptor agonists (morphine, fentanyl) potentiated the inhibitory cortical effect on the evoked neuronal activity. Pentazocine, which has pronounced kappa-receptor agonist activity, was less effective. Naloxone eliminated the effects of both cortical stimulation and opioid analgesics. Serotonin receptor antagonist methysergide, as well as p-chlorophenylalanine significantly decreased inhibitory cortical control and the effect of opioids. Monoamine re-uptake inhibitors with analgesic properties (imipramine, fluoxetine) potentiated the inhibitory effect of cortical stimulation. Adreno-, dopamine-, acetylcholine-, GABA-receptor agents and antagonists of NMDA receptors had minor or no effect. Among non-narcotic analgesics, the cyclooxygenase inhibitors metamysole and ketorolak increased only moderately the descending cortical control of nociception. Thus, the cerebral cortex is able to control the nociceptive processing in different pain syndromes (somatic, visceral or neuropathic pain). Opioidergic and serotonergic systems play the key role in this control. Action through the cortical descending control is likely to be one of the components of the analgesic effect exerted by opioids and some other central analgesics.
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PMID:[Neurochemical analysis and pharmacological regulation of the corticofugal control of the nociceptive signals in the afferent pathways]. 1296 44

Serotonin receptor (5-HTR) agonists that target 5-HT(4(a))R and 5-HT(1A)R can reverse mu-opioid receptor (mu-OR)-evoked respiratory depression. Here, we have tested whether such rescuing by serotonin agonists also applies to the cardiovascular system. In working heart-brainstem preparations in situ, we have recorded phrenic nerve activity, thoracic sympathetic chain activity (SCA), vascular resistance and heart rate (HR) and in conscious rats, diaphragmatic electromyogram, arterial blood pressure (BP) and HR via radio-telemetry. In addition, the distribution of 5-HT(4(a))R and 5-HT(1A)R in ponto-medullary cardiorespiratory networks was identified using histochemistry. Systemic administration of the mu-OR agonist fentanyl in situ decreased HR, vascular resistance, SCA and phrenic nerve activity. Subsequent application of the 5-HT(1A)R agonist 8-OH-DPAT further enhanced bradycardia, but partially compensated the decrease in vascular resistance, sympathetic activity and restored breathing. By contrast, the 5-HT(4(a))R agonist RS67333 further decreased vascular resistance, HR and sympathetic activity, but partially rescued breathing. In conscious rats, administration of remifentanyl caused severe respiratory depression, a decrease in mean BP accompanied by pronounced bradyarrhythmia. 8-OH-DPAT restored breathing and prevented the bradyarrhythmia; however, BP and HR remained below baseline. In contrast, RS67333 further suppressed cardiovascular functions in vivo and only partially recovered breathing in some cases. The better recovery of mu-OR cardiorespiratory disturbance by 5-HT(1A)R than 5-HT(4(a))R is supported by the finding that 5-HT(1A)R was more densely expressed in key brainstem nuclei for cardiorespiratory control compared with 5-HT(4(a))R. We conclude that during treatment of severe pain, 5-HT(1A)R agonists may provide a useful tool to counteract opioid-mediated cardiorespiratory disturbances.
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PMID:The potency of different serotonergic agonists in counteracting opioid evoked cardiorespiratory disturbances. 1965 61