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

Morphine analgesia measured by the tail withdrawal test was examined in rats that were either restrained or left free during testing. It was found that restraint potentiated morphine analgesia and decreased the latency of the peak analgesic effect. Methysergide, a serotonin antagonist, and valine, which prevents the increase in brain tryptophan induced by restraint, blocked the effect of restraint on morphine analgesia. Valine did not alter analgesia in unrestrained rats. An increase in brain tryptophan uptake induced by stress is suggested as a possible mechanism by which stress can interact with pain modulation systems.
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PMID:Evidence that stress augments morphine analgesia by increasing brain tryptophan. 672

We examined the behavioral effects of the dietary constituents tryptophan and tyrosine on human mood, sensorimotor performance and pain sensitivity. Tryptophan and tyrosine are neurotransmitter precursors present in varying amount in protein-containing foods. Tryptophan (50 mg/kg) increased subjective drowsiness and fatigue but unlike many hypnotics did not impair sensorimotor performance. Tryptophan also decreased human pain sensitivity in a manner that was more specific than certain analgesic drugs.
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PMID:Mood, performance, and pain sensitivity: changes induced by food constituents. 676 30

This study investigated the effects of daily administration of three grams of tryptophan in conjunction with a high carbohydrate, low fat, low protein diet on chronic maxillofacial pain, experimental pain thresholds, and anxiety and depression. In a double-blind study, 30 chronic pain patients were randomly assigned to a tryptophan or placebo group. At the initial appointment and 4 weeks later, the patients' subjective ratings of their pain were recorded, electrical tooth pulp stimulation was used to measure pain thresholds, and psychological tests of depression and anxiety were administered. Over the 4 weeks of the study, there was a greater reduction in reported clinical pain and a greater increase in pain tolerance threshold in the tryptophan group than in the placebo group. The group did not differ in anxiety and depression--for all subjects there was lowered depression and anxiety over the 4 weeks of study.
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PMID:The effects of dietary tryptophan on chronic maxillofacial pain and experimental pain tolerance. 676 35

5,7-Dihydroxytryptamine (5,7-DHT), median raphe nucleus (MRN)-lesioned and sham-lesioned rats were submitted to one-trial passive avoidance conditioning followed by electroconvulsive shock (ECS) or sham-ECS. On test session (24 h later) MRN-lesioned rats presented a longer conditioned response and, chiefly, a remarkable reduction of ECS-induced retrograde amnesia in comparison to sham-lesioned animals. This effect appeared unrelated to major changes in spontaneous behavior: on training session MRN-lesioned rats exhibited a faster stepping-down from the platform; their exploratory activity into a novel cage was characterized by a slightly higher initial response; moreover MRN lesion did not significantly effect pain threshold. A reduced brain 5-HT functional activity following MRN lesion was suggested by the study of the hyperactivity syndrome induced by tranylcypromine plus L-tryptophan. Lastly, MRN-lesioned rats showed a significantly lower brain 5-HT steady level without differing from the sham-lesioned ones with respect to turnover rate. The reduction of ECS-induced retrograde amnesia observed in 5,7-DHT, MRN-lesioned rats was considered as due to a lower synaptic availability of 5-HT at the time of ECS administration.
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PMID:Reduction of ECS-induced retrograde amnesia of passive avoidance conditioning after 5,7-dihydroxytryptamine median raphe nucleus lesion in the rat. 696 65

Pain perception and tolerance thresholds of 30 normal subjects were determined by electrical stimulation of dental pulps before and after dietary manipulation which included either tryptophan supplementation or placebo. Perception threshold levels were similar in tryptophan and placebo subjects; however, pain tolerance levels were significantly higher in the group receiving tryptophan. Side effects such as nausea, skin itching, weight loss and mood elevation were more common in the tryptophan group than in the placebo group.
Pain 1982 Aug
PMID:Alteration of human pain thresholds by nutritional manipulation and L-tryptophan supplementation. 713 33

The effects of dietary excesses of tryptophan, histidine, tyrosine or choline and of a tryptophan-free diet were examined on shock-induced fighting, muricide and jump-flinch thresholds. Following the tryptophan-free diet, shock-induced fighting and pain sensitivity were specifically increased. The increased incidence of muricide was not specific to the lack of tryptophan in the diet. Groups of rats which were pair fed chow or had 0.15% L-tryptophan added to the tryptophan-free diet increased muricide as well. Brain 5-HT levels were 41% depleted following the tryptophan-free diet and reduced 13% with the 0.15% tryptophan supplement. In addition body weights were reduced in the three groups compared to control. None of the excess diets affected shock-induced fighting, muricide and jump-flinch thresholds. Body weights were decreased in the excess tryptophan, histidine, tyrosine and choline groups. These data indicate that the expression of different forms of aggression appears to be influenced by a tryptophan deficiency in the diet, but not by excesses of tryptophan, tyrosine, histidine and choline.
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PMID:Effects of dietary supplements and a tryptophan-free diet on aggressive behavior in rats. 718 91

Five patients on chronic opiate medication to treat low-back and leg pain were determined to have developed opiate tolerance on the basis of their failure to obtain significant relief (rated on a subjective pain scale and by the degree of straight leg-raising they were able to endure) after receiving 30 mg of morphine administered i.v. in divided doses over 35 min. After these patients' diets had been supplemented with 4 g/day of L-tryptophan for 2-9 weeks, they achieved significant relief from pain when the opiate tolerance test was re-administered, and were able to lead more active lives while reducing their daily opiate intake. chronic opiate administration probably reduces the serotonin turnover rate in the central nervous system; it may be that this is reversed by loading with the serotonin precursor, L-tryptophan.
Pain 1980 Oct
PMID:Tryptophan loading may reverse tolerance to opiate analgesics in humans: a preliminary report. 745 82

(+/-)3,4-Methylenedioxymethamphetamine (MDMA; "Ecstasy"), an increasingly popular recreational drug, is known to damage brain serotonin 5-hydroxytryptamine (5-HT) neurons in experimental animals. Whether MDMA is neurotoxic in humans has not been established. Thirty MDMA users and 28 controls were admitted to a controlled inpatient setting for measurement of biologic and behavioral indexes of central 5-HT function. Outcome measures obtained after at least 2 weeks of drug abstinence included concentrations of monoamine metabolites in cerebrospinal fluid (CSF), prolactin responses to L-tryptophan, nociceptive responses to ischemic pain, and personality characteristics in which 5-HT has been implicated (i.e., impulsivity and aggression). Subjects with a history of MDMA exposure had lower levels of CSF 5-hydroxyindoleacetic acid (the major metabolite of 5-HT) than controls (p = .001). Although they resembled controls in their prolactin response to L-tryptophan and their response to ischemic pain, MDMA users had lower scores on personality measures of impulsivity (p = .004) and indirect hostility (p = .009). The CSF findings suggest that 5-HT neurotoxicity may be a potential complication of MDMA use. Further, differences in personality support the view that 5-HT systems are involved in modulating impulsive and aggressive personality traits. Additional studies of MDMA-exposed individuals are needed to confirm and extend the present findings. Such studies could help elucidate the role of 5-HT in normal brain function as well as in neuropsychiatric disease states.
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PMID:Serotonin neurotoxicity after (+/-)3,4-methylenedioxymethamphetamine (MDMA; "Ecstasy"): a controlled study in humans. 751 77

Since the first comprehensive description of the symptoms of FMS by Yunus et al (1981), numerous investigations have confirmed that FMS is a clinical entity. However, the aetiology of the syndrome is still not fully elucidated. It seems, however, logical to place the origin of the disorder in the muscle. Muscle pain, especially at the muscle-tendon junctions, fatigue and stiffness are the first symptoms. A malfunction of energy metabolism has been detected in part of the muscle fibres. However, it has to be considered that the muscle is not an isolated entity. Its activity is controlled by segmentally arranged motor units of the ventral horn of the spinal cord in response to proprioceptive afferent signals arising in the muscle spindles or in other sensory elements including nociceptors. Together with supraspinal descending inputs, the spinal motor neurone pool is the common final pathway for segmental and suprasegmental inputs, making the motor system extremely powerful for adaptive adjustments but also vulnerable if deficits occur in either of these input levels. A second, recently discovered abnormality seen in FMS is a lowered serotonin level in peripheral and most likely also central structures. The underlying mechanism seems to be defective absorption of the precursor amino acid tryptophan from the gut. Serotonin is involved centrally in the regulation of the sleep pattern, and at the spinal level it acts as a 'gain setter' of motoneurone excitability and suppresses signal transmission of noxious stimuli in dorsal horn neurones. Either of these two disturbances, muscle energy depletion or serotonin deficiency, could by itself evoke many of the symptoms of FMS, and their combined appearance will perpetuate the disease. Depressed levels of somatomedin C, caused by a deficit of stage 4 sleep-dependent release of GH, might represent an additional factor in preventing proper development or repair of myoskeletal structures. Malabsorption of certain amino acids, possibly due to a genetic disorder of gut transport mechanisms, may constitute an additional deleterious factor. The abnormalities found in the HPA and HPT axis may be seen as an attempt of the organism to restore homeostasis. The stimulus eliciting this counter-regulatory reaction may be pain or other afferent signals which normally do not reach the central nervous system. It is doubtful whether the unspecific activation of the HPA axis in a non-inflammatory disease is beneficial.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neuromediator and hormonal perturbations in fibromyalgia syndrome: results of chronic stress? 785 Aug 79

Because circulating melatonin levels are generally thought to be under the strict control of pineal N-acetyltransferase, little attention has been paid to the impact of an altered availability of serotonin (5-HT) on melatonin formation. In order to see whether melatonin synthesis is stimulated by an increased availability of free, cytosolic 5-HT, we studied the effects of 5-HT precursors, 5-HT releasers and reuptake inhibitors and of monoamine oxidase inhibitors, alone and in combination, on circulating melatonin levels in experimental animals. The administration of tryptophan and 5-HT-releasing drugs (fenfluramine, +/- 3,4-methylenedioxymethamphetamine) to rats caused a dose- and time-dependent elevation of circulating melatonin levels during the day and night. This increase in melatonin was further enhanced by inhibition of monoamine oxidase. The elevation of plasma melatonin caused by 5-HT-releasing drugs was prevented by prior administration of fluoxetine. Monoamine oxidase inhibitors and fluoxetine alone had no effect on circulating melatonin levels. These findings indicate that the administration of indirectly acting 5-HT receptor agonists which increase the free cytoplasmic pool of 5-HT may also elevate circulating melatonin levels. The results of this study suggest that the rate of pineal melatonin synthesis is dependent on the free cytoplasmic pool of 5-HT in pinealocytes and that the drug-induced elevation of this pool stimulates melatonin formation and increases circulating melatonin levels. At least some of the effects of indirectly acting 5-HT receptor agonists, e.g. on sleep, mood, food intake, pain perception, and neuroendocrine secretion, may therefore be mediated by the elevation of circulating melatonin and the subsequent activation of central melatonin receptors.
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PMID:Effects of indirectly acting 5-HT receptor agonists on circulating melatonin levels in rats. 840 95


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