Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intrathecal (ITH) administration of 5 micrograms 6-hydroxydopamine (6-OHDA) in mice selectively lesioned descending catecholaminergic pathways. Uptake of 3H-noradrenaline (3H-NA) into synaptosomes from the lumbar spinal cord was reduced by 95%, without any change in the uptake of 14C-5-hydroxytryptamine (14C-5-HT). Synaptosomal uptake of 3H-NA and 14C-5-HT in the brain was not altered. The nociceptive sensitivity was evaluated using the tail-flick, hot plate and formalin tests 3 and 14 days after injection of 6-OHDA. At day 3 hyperalgesia was found in the hot-plate test, unchanged response latency in the tail-flick test and hypoalgesia in the formalin test. At day 14 there were no statistically significant differences from controls in any of the tests. The present findings support the contention that catecholaminergic pathways participate in the tonic regulation of nociception in the spinal cord. However, while supraspinally integrated responses to acute thermal pain, as measured with the hot-plate test, are inhibited by these pathways, responses to prolonged chemical pain are enhanced.
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PMID:Changes in nociception after 6-hydroxydopamine lesions of descending catecholaminergic pathways in mice. 308 10

The acute effects of the 5-hydroxytryptamine agonist, 5-Methoxy-N,N-dimethyltryptamine (5-MeO-DMT), upon pain sensitivity, using shock titration, tail-flick and hot-plate methods, in noradrenaline- and 5-hydroxytryptamine-depleted rats were examined. Noradrenaline depletion, following the systemic administration of N-2-chloroethyl-N-ethyl-2-bromobenzylamine hydrochloride (DSP4, 2 X 50 mg/kg, i.p.), caused a reversal of the analgesic effect of 5-MeO-DMT on shock-titration from hypo- to hypersensitivity, and a total blockade of the antinociceptive effect of 5-MeO-DMT upon pain responses in the hot-plate and tail-flick tests. Pretreatment with either p-chloroamphetamine (2 X 10 mg/kg) or p-chlorophenylalanine (200, 100, 100 mg/kg), that depletes central 5-hydroxytryptamine stores, failed to alter the analgesia caused by acute 5-MeO-DMT. Strong evidence is provided for the effect of central noradrenaline depletion upon the analgesic effect of the 5-HT agonist. These findings suggest an important tonic influence of the noradrenaline system upon the descending spinal 5-HT pathway in rats.
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PMID:Blockade and reversal of 5-methoxy-N,N-dimethyltryptamine-induced analgesia following noradrenaline depletion. 315 73

Self-reported levels of pain, anxiety, and depression, and plasma levels of beta-endorphin, epinephrine, norepinephrine, dopamine, and serotonin were measured in 19 arthritic pain patients before and after hypnosis designed to produce pain reduction. Correlations were found between levels of pain, anxiety, and depression. Anxiety and depression were negatively related to plasma norepinephrine levels. Dopamine levels were positively correlated with both depression and epinephrine levels and negatively correlated with levels of serotonin. Serotonin levels were positively correlated with levels of beta-endorphin and negatively correlated to epinephrine. Following hypnotherapy, there were clinically and statistically significant decreases in pain, anxiety, and depression and increases in beta-endorphin-like immunoreactive material.
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PMID:Biochemical correlates of hypnoanalgesia in arthritic pain patients. 315 43

The performance of strenuous physical exercise is associated with discomfort and pain, the tolerance for that being modulated by the activity of the endogenous opioid systems. As 5-hydroxy-tryptamine (5-HT) affects nociception through its effects on the enkephalin-endorphin system, we have analyzed the effects of a moderate supplementation with L-tryptophan, the immediate precursor of 5-HT, on endurance and sensation of effort. Twelve healthy sportsmen were subjected to a work load corresponding to 80% of their maximal oxygen uptake on two separate trials, after receiving a placebo and after receiving the same amount of L-tryptophan. The subjects ran on a treadmill until exhaustion. Total exercise time, perceived exertion rate, maximum heart rate, peak oxygen consumption, pulse recovery rate, and excess post-exercise oxygen consumption were determined during the two trials. The total exercise time was 49.4% greater after receiving L-tryptophan than after receiving the placebo. A lower rate of perceived exertion was exhibited by the group while on tryptophan although the differences from the control group were not statistically significant. No differences were observed in the other parameters between the two trials. The longer exercise time als well at the total work load performed could be due to an increased pain tolerance as a result of L-tryptophan ingestion.
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PMID:Effect of L-tryptophan supplementation on exercise performance. 324 61

Bilateral lower extremity vasospasm associated with severe pain and hyperesthesias in the legs, and digital gangrene in both feet developed in a 50-year-old man with carcinoid syndrome. Nifedipine and chemical lumbar sympathectomy were partially effective in relieving the vasospasm. Electromyographic findings were consistent with ischemic neuropathy. A skin biopsy specimen showed striking dermal fibrosis. Serotonin and other vasoconstrictor substances released from the tumor may be responsible for the vasospasm, the dermal sclerosis, and the ischemic neuropathy. The early use of lumbar sympathectomy in patients with lower extremity vasospasm may prevent these irreversible ischemic complications.
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PMID:Lower extremity vasospasm associated with ischemic neuropathy, dermal fibrosis, and digital gangrene in a patient with carcinoid syndrome. 340 64

The spinal trigeminal subnucleus caudalis processes nociceptive input from the head. However, physiological and behavioral studies in monkeys and humans indicate that painful stimuli from the central face and oral cavity also project through trigeminal nuclei rostral to the spinal subnucleus caudalis. Both enkephalin (ENK) and serotonin (5-HT) are present in rostral trigeminal nuclei and these regions receive inputs from the raphe complex. Thus, it appears that elements of pain-modulating circuitry proposed by Basbaum and Fields (Annu. Rev. Neurosci., 7:309-338, 1984) for the spinal and medullary dorsal horn may also exist in this region. In order to begin an exploration of this circuitry, the present study combines the techniques of retrograde transport of HRP from the ventral posteromedial thalamic nucleus (VPM) of the cat's thalamus to label trigeminothalamic relay cells. Secondarily, immunocytochemical techniques are employed to define the distribution patterns of ENK and 5-HT cells and terminals in relationship to both labeled and nonlabeled neurons in each of the subnuclei of the spinal trigeminal nucleus. Trigeminothalamic relay cells were observed in laminae I and II, the magnocellular region, and the interstitial nucleus (IN) of subnucleus caudalis (Vc). ENK was found in axodendritic and axosomatic terminals, together with a population of small fusiform neurons in all these same areas except the magnocellular region. ENK axosomatic contacts innervated approximately 30% of labeled relay cells, chiefly in lamina I and the IN, or small unlabeled neurons in the same area. Serotonin activity occurred principally in lamina I and the IN and was confined almost exclusively to axodendritic terminals. Examination of subnucleus interpolaris (Vi) revealed relay cells distributed throughout the length of the nucleus and increasing in numbers at rostral levels. A rostral extension of the IN was found just ventrolateral to the main body of Vi and contained numerous labeled cells. The distribution of ENK activity was restricted to the ventral part of Vi and the IN and occurred in axodendritic and axosomatic terminals. These latter elements innervated 30-40% of labeled relay cells in Vi, particularly those located in the IN. Cells containing ENK generally resembled the fusiform cells found in Vc and were distributed in ventral Vi and the IN. Some ENK cells were larger, displayed several dendrites, and occurred only in the ventral Vi. Serotonin within Vi and Vc was confined principally to axodendritic terminals.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunocytochemistry of enkephalin and serotonin distribution in restricted zones of the rostral trigeminal spinal subnuclei: comparisons with subnucleus caudalis. 345 61

The influence of the oral administration of different doses of citalopram (5, 15 and 45 mg/kg), imipramine (15, 30, 45 and 60 mg/kg), nortriptyline (15, 45 and 60 mg/kg) and amineptine (45 mg/kg) on stress-induced analgesia has been studied in anaesthetized rats. None of the administered antidepressants seem to have appreciable analgesic activity when analgesia is tested by the tail-immersion method. Citalopram, imipramine and nortriptyline, but not amineptine, increase the analgesia induced by inescapable footshock delivered continuously for 2 min to rats. Citalopram is the most potent drug. Our results support the suggested importance of 5-HT and noradrenaline terminals, but not those of dopamine, in the mediation of the stress-induced analgesia and seem to support the hypothesis that the analgesic activity of antidepressants is partially related to their modulating effects on the endogenously released opioid peptides involved in the endogenous pain inhibitory systems.
Pain 1987 May
PMID:Effect of citalopram, amineptine, imipramine and nortriptyline on stress-induced (footshock) analgesia in rats. 347 64

1. Ro 15-8081 (Hoffmann-La Roche, Basle, Switzerland) is a novel mixed 5-HT/noradrenaline uptake inhibitor producing potent antinociceptive effects in animal pain models. 2. In healthy man, two models with electrically and thermally induced pain, respectively, have been shown to reliably discriminate between the effects of opioid as well as of antipyretic analgesics and placebo. 3. This study investigated the effects of single oral doses of 10, 25, and 50 mg Ro 15-8081 in comparison with 60 mg codeine and placebo on threshold and tolerance to electrically induced pain and on threshold to thermally induced pain. Furthermore, the effects on psychomotor function, self-rated subjective feelings, and side effect profile were studied. 4. Twenty healthy males participated each in five experiments in which they received, in random double-blind fashion, each of the treatments. Every experiment comprised two series of measurements before and twelve after drug administration, carried out at 30 min intervals. 5. Ro 15-8081 produced marked elevations of threshold and tolerance to electrically and of threshold to thermally induced pain. The effects of all doses of Ro 15-8081 were significantly superior to those of placebo. Threshold and tolerance to electrically induced pain were not affected differently by the three doses of Ro 15-8081, whereas the threshold to thermally induced pain was elevated significantly more by 50 mg than by 10 and 25 mg Ro 15-8081. 6. Codeine 60 mg had a more rapid onset of action and greater maximal effects than Ro 15-8081.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of graded oral doses of a new 5-hydroxytryptamine/noradrenaline uptake inhibitor (Ro 15-8081) in comparison with 60 mg codeine and placebo on experimentally induced pain and side effect profile in healthy men. 350 28

In order to examine the sensitivity of the nociceptive system of birds to capsaicin, the algesic potency of the drug was compared with that of veratridine and mustard oil by instillation into the eye of conscious pigeons and guinea-pigs. In guinea-pigs, 10(-6) g/ml capsaicin provoked severe protective reactions, but even high concentrations of 10(-2) g/ml were insufficient in pigeons. Veratridine and mustard oil induced similar reactions in both species. Close arterial injections of algesic substances revealed that the threshold dose of capsaicin for cardiovascular and nocifensive reactions was 10,000-fold higher in pigeons (200 micrograms) than in guinea-pigs (0.02 micrograms). All other algesic substances tested (bradykinin, 5-HT, veratridine and KCl) had similar thresholds in both species. Slow infusion of a total dose of 600 mg/kg capsaicin into the radial artery of pigeons did not alter the sensitivity to any of the algesic substances tested, which demonstrates that even high concentrations of capsaicin have no desensitizing effect. The demonstrated insensitivity of pigeons to the algesic effect of capsaicin is discussed in the context of the inability of the drug to deplete substance P (SP) from afferent terminals in the spinal cord of the pigeon.
Pain 1986 Nov
PMID:Nociception in pigeons is not impaired by capsaicin. 379 18

The purpose of this study was to investigate modifications of 5-HT synthesis in a chronic pain model, the arthritic rat, at different times after the inoculation with Freund's adjuvant. This study confirms our previous findings that experimental induced polyarthritis is associated with a marked increase in free tryptophan levels in serum. During the acute phase of the disease (15-21 days after the adjuvant), the general increase in 5-HT synthesis observed in the CNS appeared to be related to an increase in tryptophan availability due to the elevation of free tryptophan in serum. During the post-acute phase of the disease (28-42 days after the adjuvant), the level of free tryptophan in the serum remained markedly increased but the levels in the CNS tended to return to normal values in all areas examined. At 42 days, 5-HT synthesis in the brain had also returned to normal values but was further increased at the spinal level. In addition, although 5-HT levels and 5-HT synthesis were increased in the dorsal as well as in the ventral part of the cord, an increase in the rate of disappearance of the amine after blockade of the decarboxylase (benserazide) was only observed in the dorsal part. This result tends to suggest that the descending serotonergic system projecting to the dorsal horn is preferentially activated during chronic pain.
Pain 1987 Feb
PMID:Complex temporal changes in 5-hydroxytryptamine synthesis in the central nervous system induced by experimental polyarthritis in the rat. 382 5


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