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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A single injection of phenelzine 100 mg kg-1 given 18 h before, decreased the analgesia and hypothermia induced by morphine, but potentiated the analgesic and hypothermic effects of pethidine, when the analgesics were administered either intraperitoneally, or intracerebroventricularly. The modification of pethidine analgesia and hypothermia, but not morphine analgesia, was antagonized by methysergide (10 mg lg-1, s.c.). The LD50 of pethidine, but not that of morphine, was 30-40% lower in mice treated with phenelzine tranylcypromine or iproniazid 6 h before the test. The increased lethality of a single dose of pethidine induced by phenelzine was also prevented by methysergide. Pretreatment of mice with 100 mg kg-1 phenelzine was followed by a significant rise in both brain tryptophan and 5-hydroxytryptamine (5-HT) concentrations which lasted for 24 h. Therefore, the changes in pethidine effects could have been due to raised brain tryptophan and 5-HT concentrations.
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PMID:Modification by monoamine oxidase inhibitors of the analgesic, hypothermic and toxic actions of morphine and pethidine in mice. 2 22

Single-dose tolerance to the antinociceptive effect of morphine can be demonstrated using an adequate initial priming dose of morphine and allowing an interval of 48 to 72 hours for its development. The threshold dose necessary to produce tolerance was found to be about 3 to 4 times greater than that for producing analgesia but higher doses of morphine did not enhance further tolerance development. Evidence of tolerance was indicated by the fact that when the antinociceptive response to morphine was assessed by the hot-plate and the tail-flick procedures, a shift in the dose-response curve of morphine to the right occurred after an adequate single priming dose of morphine. Cross-tolerance was evidenced by a decrease in analgetic response to methadone 3 days after a single priming dose of morphine and a decrease in morphine response after a single dose of methadone. The development of single-dose tolerance was inhibited by cycloheximide. Single-dose tolerance was also blocked by 5,6-dihydroxytryptamine and perhaps enhanced by L-tryptophan. Cyclic 3',5'-adensine monophosphate did not affect single-dose tolerance development significantly although the direction was in favor of augmentation. Morphine uptake by the brain was not modified by the development of single-dose tolerance. Physical dependence, as measured by naloxone-precipitated withdrawal jumping, was not observed when single-dose analgetic tolerance was maximal. The results suggest that single-dose tolerance to morphine involves the synthesis of some macromolecule and support previous findings in this laboratroy involving an association with serotonin.
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PMID:Studies on tolerance development to single doses of morphine in mice. 18 57

The latency to tail-flick response in the rat was significantly prolonged by cerebroventricular infusion of 1.0 microgram of somatostatin (SRIF) and more so with 10.0 microgram. The D-tryptophan analog was less effective than native SRIF. Pretreatment with naloxone eliminated analgesia but not seizures induced by SRIF. Recording of the EEG activity enabled determination of the specific state of the sleep-waking cycle in which the repeated tail-flick responses were tested: latency was generally longer in both control and test animals when tail immersion was performed during the state of sleep or drowsiness rather than during the awake state. Although animals receiving SRIF were less likely to fall asleep between subsequent test trails, the average latency was actually longer than after control saline infusion when the animals slept more. SRIF, unlike other releasing factors and peptides tested, showed significant activity in an opiate radioreceptor assay. The blockade of SRIF action by naloxone pretreatment, along with binding of SRIF to opiate receptors in vitro, suggest opiate receptors to be involved in the mediation of analgesia observed in present study.
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PMID:Opiate-like naloxone-reversible actions of somatostatin given intracerebrally. 63 75

Electrolytic raphe lesion was performed in 4-6-day-old rats and the resulting changes of 5HT metabolism within the central nervous system were analyzed up to 9 months later. As soon as the 2nd day following the selective destruction of B7 and B8 nuclei, forebrain 5HT levels were decreased by more than 75%. This reduction persisted for at least 9 months with no sign of recovery. The time course of 5-HIAA decrease was parallel to that of the indoleamine so that the ratio of 5-HIAA over 5-HT levels in the forebrain of lesioned rats was similar to that estimated in controls, whatever their age. This result would suggest that the remaining serotoninergic neurons in the lesioned rats did not develop a compensatory hyperactivity. The raphe lesion induced no change in MAO activity and synaptosomal tryptophan uptake but a pronounce decrease in the Vmax of synaptosomal KHT uptake process in various forebrain areas occurred. The serotonin sensitive adenylate cyclase activity in colliculi homogenate was not altered by the lesion suggesting that this enzyme was probably located in postsynaptic membranes. In addition, this observation would indicate that 5-HT receptors which are linked to this adenylate cyclase did not become supersensitive following the selective degeneration of serotoninergic neurons. Animals without forebrain serotoninergic innervation might be of great interest to analyse the role of serotoninergic neurons in various functions (sleep, analgesia, thermoregulation).
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PMID:Midbrain raphe lesion in the newborn rat: II. Biochemical alterations in serotoninergic innervation. 86 45

The administration to rats of tryptophan (CAS 73-22-3) in high dosage causes a significant increase in pain threshold values. The analgesic effects of tryptophan are potentiated by allopurinol (CAS 315-30-0). The analgesic effects shown by tryptophan injection are associated with increased levels of serotonin and 5-hydroxyindoleacetic acid in some areas of the brain. The combined allopurinol and tryptophan treatment elevates the serotonin levels furtherly when they are compared with the values observed in animals receiving tryptophan only. The analgesia caused by tryptophan administration has been attributed to an increased activity of the serotoninergic system involved in the control of pain transmission.
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PMID:Potentiation of the analgesic effects of tryptophan by allopurinol in rats. 172 97

The effectiveness of intravenous administration (i.v.) of L-tryptophan, which is the precursor of cerebral serotonin, was verified in the treatment of postoperative pain. The study was carried out on 45 female patients, aged between 34 and 61 years, undergoing cholecystectomy who were randomly divided into three groups. Group 1 (age: 50.33 +/- 8.64 years) received 100 ml of 5% mannitol solution i.v.; group 2 (age: 49.80 +/- 11.11 years) 100 ml of a mannitol solution containing 7.5 mg/kg L-tryptophan; and group 3 (age: 53.46 +/- 9.60 years) 100 ml of a mannitol solution containing 15 mg/kg L-tryptophan. Vital capacity (preoperative VC) was measured before surgery. Anesthesia used was isoflurane. Narcotics or neuroleptics were not used. Pain was assessed before treatment (T-0 min), at the end of administration (T-30) and at T-60, 120, 180, 240, 300 and 360 min by the following variables: respiratory rate (RR), heart rate (HR), mean arterial pressure (MAP), Scott-Huskisson test (VAS), pain vital capacity (PVC), analgesic vital capacity (AVC), and respiratory restoration factor (RRF) calculated from Bromage's formula (RRF = (AVC - PVC/preoperative VC - PVC) X 100). As regards variables RR, HR, MAP and VAS, differences between the values from T-30 to T-360 and the value at T-0 were calculated. Means and S.E.M. were calculated on the obtained values and on RRF values for each group. The significance of the differences between groups was calculated using Student's t test and Bonferroni's test. Results show a significant decrease of pain in groups 2 and 3 treated with L-tryptophan, in comparison with group 1 (controls). No significant difference was observed between the treated groups, although more lasting pain relief was observed in group 3 in comparison with group 2. Intravenous L-tryptophan showed its effectiveness in the treatment of postoperative pain even when used alone. Its use may be considered for patients with renal failure, in order to strengthen pharmacological analgesia or to prevent postoperative pain by its intraoperative administration.
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PMID:Postoperative pain treated by intravenous L-tryptophan: a double-blind study versus placebo in cholecystectomized patients. 176 11

The analgesic effects of low current transcranial electrostimulation are both naloxone and pCPA-reversible, suggesting that they may be mediated in part by endogenous opioid and serotonergic activity. The present experiments indicate that pretreatment with the serotonin precursor L-tryptophan results in an increased analgesic effect of electrostimulation as measured by the 50 degrees C wet tail flick test in the rat. Rats receiving both L-tryptophan and electrostimulation displayed significantly more analgesia than rats receiving electrostimulation and injection vehicle alone, rats receiving drug and sham stimulation or rats receiving vehicle and sham stimulation.
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PMID:Augmented analgesic effects of L-tryptophan combined with low current transcranial electrostimulation. 238 30

In the rat tail-flick test it was shown that ip lappaconitine (LA) 1-6 mg/kg, N-deacetyllappaconitine (DLA) 4-10 mg/kg or icv DLA 20-60 micrograms/rat exhibited a dose-dependent analgesic activity, but icv LA 20-40 micrograms/rat was inactive. The analgesic potency of ip LA was a little more potent than that of DLA and slightly weaker than that of morphine (P less than 0.05). Combined ip of subanalgesic doses of morphine and LA or DLA produced significant analgesic action. Analgesia mediated by LA was not antagonized by naloxone. The analgesic effect induced by LA or DLA was abolished and restored 3 and 120 h, respectively, after ip reserpine 3 mg/kg. Concomitant administration of 1-tryptophan or 5-HT as well as premedication of alpha-methyldopa prevented reserpine-induced decrease on LA or DLA analgesia. The elevation of brain 5-HT level by icv 5-HT significantly enhanced the analgesia of LA and DLA. LA- or DLA-induced analgesia was attenuated by pretreatment of p-chlorophenylalanine but this attenuation was reversed by icv 5-HT. p-Chloroamphetamine also markedly reduced LA- or DLA-induced analgesia. It is concluded that the central serotoninergic system is involved in the modulation of LA- or DLA-induced analgesia.
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PMID:[Effects of reserpine and 5-HT on analgesia induced by lappaconitine and N-deacetyllappaconitine]. 240 8

This chapter has reviewed biochemical and morphological studies of the human and monkey serotonergic system. In addition, the serotonin-producing neurons of M fascicularis were analyzed, using immunocytochemistry, radioautography, and measurements of synaptosomal serotonin reuptake and supernatant tryptophan hydroxylase activity. The major sections of the chapter covered cell bodies, pathways, subcortical distribution, and cortical distribution, and a gross brain dissection guide of M fascicularis is included. An atlas of the 5-HT-IR cell bodies was presented in Figures 7 to 33. Rostral and caudal groups of nuclei were discussed. The rostral group consists principally of the nuclei raphe dorsalis (B7 and B6), centralis superior (B8, B5, and part of B7), and prosupralemniscus (B9). These groups ascend mainly in tracts lying outside the medial forebrain bundle (MFB). In M fascicularis, 25% of the fibers within the MFB are myelinated. The caudal 5-HT-IR nuclei consist principally of the nuclei in a dorsal cluster (raphe obscurus, B2) and in a ventral cluster (pallidus, B1, and magnus B3). The dorsal 5-HT-IR cells in raphe obscurus are associated with the MLF, and cells extend into cervical spinal cord (lamina IX and X) with the descending MLF and the TTS. Fibers from the raphe obscurus innervate the motoneurons in both the cranial nuclei (X, XII) and the ventral horn. The ventral 5-HT-IR cells lie mainly medial to the medial leminiscal fibers. A large number of these cells extend laterally into paragigantocellularis lateralis and here extend caudally lying below the lateral reticular nuclei. Cells from this group are seen dorsally joining the internal arcuate fibers. The raphe magnus of the ventral cluster projects to the dorsal horn and is believed to mediate the serotonin-induced analgesia. The descending fibers from both of these clusters are occasionally myelinated. Also, in our tryptophan- and pargyline-pretreated monkeys, small 5 HT-IR cells were visible in the area postrema. Human and monkey biochemical data (detailed summary in Tables 1-6) provide evidence for the presence of serotonin fibers in all cortical and subcortical regions. In subcortical regions, the midbrain, medulla, amygdala, and substantia nigra have the highest, whereas the cerebellum, spinal cord, and ventral pons have the lowest amount of serotonin and its metabolite, 5-HIAA. In the basal ganglion, the globus pallidus has the highest rate of 5-HT synthesis. The temporal lobe receives the most serotonin of the major cortical lobes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The primate serotonergic system: a review of human and animal studies and a report on Macaca fascicularis. 241 48

Guanethidine treatment decreased morphine analgesia exhibited by restrained rats but had no effect on morphine analgesia exhibited by unrestrained rats or on baseline pain sensitivity. Guanethidine also prevented the rise in tryptophan uptake into the brain induced by the restraint stress. It is argued that the prevention of the stress-induced increase in brain tryptophan uptake is causal to guanethidine's attenuation of morphine analgesia exhibited by restrained rats, since the increase in brain tryptophan uptake has already been shown to be critical to this phenomenon. The blockade of the stress-induced increase in brain tryptophan uptake and morphine analgesia by guanethidine support the hypothesis that these effects depend upon sympathetic activity.
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PMID:Sympathetic control of tryptophan uptake and morphine analgesia in stressed rats. 242 29


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