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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present investigation sought to determine whether the stimulus properties of morphine and lysergic acid diethylamide (LSD) would generalize to several narcotic analgesics which vary in their subjective effects. Morphine and saline served as discriminative stimuli for one group of rats in a 2-lever discrimination task. LSD and saline were discriminative stimuli for a second group. Depression of one lever in an operant chamber resulted in reinforcement following the administration of morphine or LSD and the opposite lever was reinforced after saline. After discriminated responding was stable, stimulus generalization tests with narcotic analgesics and antagonists showed that the stimulus properties of morphine generalized to methadone and meperidine, and partially to pentazocine, all of which produce morphine-like subjective effects in humans. Morphine stimulus properties did not generalize to nalorphine or cyclazocine, which produce dissimilar subjective effects. The stimulus properties of LSD generalized partially to cyclazocine, but not to nalorphine. In humans cyclazocine and nalorphine produce a high incidence of psychotomimetic effects, but the subjective effects of cyclazocine are differentiable from those of LSD.
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PMID:Generalization of morphine and lysergic acid diethylamide (LSD) stimulus properties to narcotic analgesics. 0 12

The nociceptive reflex activity and analgesic effect of morphine were studied in rats using the hind paw stimulation test. The stimulation threshold was significantly increased in animals with bilateral destruction of the locus coeruleus (LC), and was reduced after lesion of the dorsal raphe nucleus (DR). LC lesions produced a selective lowering of noradrenaline (NA) content in the forebrain, while DR lesions resulted in a reduction in serotonin levels. Lesioning both LC and DR significantly reduced both NA and serotonin contents even when the stimulation threshold was not altered. Morphine produced a significant and dose-dependent elevation of the stimulation threshold in sham-operated animals, while morphine analgesia was almost completely inhibited by destruction of LC, DR and both the nuclei. These results imply that a depression of LC-mediated noradrenergic tone results in a decreased sensitivity to painful stimuli, whereas a reduction of raphe-derived serotonergic tone produces the opposite effect against LC. It is suggested, however, that both of these monoamines from the LC and DR are necessary for the analgesic effect of morphine.
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PMID:Attenuation of morphine analgesia in rats with lesions of the locus coeruleus and dorsal raphe nucleus. 1 37

Lorazepam, a new benzodiazepine, was compared with morphine for premedication. Ten patients received morphine 10 mg/70 kg i.m. and 10 received lorazepam 4 mg/70 kg i.m. Respiratory effects were assessed from the change in slope (S) and intercept (B) of the carbon dioxide response line, using a development of Read's rebreathing method. Morphine depressed S by 47% (P less than 0.01), but after lorazepam S increased by 27% (P less than 0.05), neither drug altering B significantly. In two volunteers lorazepam was assessed by both the rebreathing and the steady-state methods; after lorazepam S was smaller by the steady-state than by the rebreathing technique. The findings for lorazepam are consistent with the known effects of sleep on carbon dioxide sensitivity. Amnesia lasting 4-8 h occurred in all patients who received lorazepam so that pain and nausea during this period were not recalled, but no patient who received morphine experienced amnesia. We conclude that lorazepam merits further study, particularly where sedation without respiratory depression is needed, as in obstetrics, and where amnesia for uncomfortable procedures is required.
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PMID:Respiratory effects and amnesia after premedication with morphine or lorazepam. 1 25

Morphine elicits dose-dependent tail erection in mice. Pretreatment of mice with atropine, phenoxybenzamine, propranolol, diphenhydramine, cyproheptadine or parachlorophenylalanine did not interfere with tail erection induced by morphone. Several neuroleptic drugs which are dopamine receptor blocking agents showed a clear antagonistic effect on morphine-induced tail erection (MITE). Haloperidol and penfluridol blocked MITE at doses which only produced a slight behavioral depression. Pimozide and chlorpromazine were less antagonistic than haloperidol and penfluridol and inhibited MITE only at doses which produced a marked behavioral depression. Results indicated that dopamine might be involved in tail erection induced by morphine. MITE in mice might be a useful model for the evaluation of neuroleptic drugs.
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PMID:Effects of neuroleptics on morphine-induced tail erection in mice. 2 20

Morphine, the principal alkaloid of "papaver somniferum" is the reference substance of central analgesics, the parmacodynamic constants of which are: analgesia and the possibility of addiction. Respiratory depression is, for many of them, a grave side-effect. At the present time, no substance in this category is fully satisfactory and all may result in dependence. Equi-analgesic doses of dextromoramide, phenoperidine and Fentanyl are less than those of morphine, whilst those of pethidine and pentazocine are higher. Study of the pharmacokinetics of these various substances indicates no common elements, and it is difficult to consider that the analgesic action is proportional to blood levels. Clinical assessment of the mean duration of action makes it possible to divide morphine derivatives into substances with a very short action (20 to 45 minutes) such as Febtanyl and phenoperidine, and those with a longer action (1 to 4 hours) which includes the majority of the other substances. The analgesic activity of Methoadone lasts for 4 to 6 hours. Morphine antagonists such as Methadone, nalophine, naloxone and naltrexone possess specific problems in terms of their utilization. Pharmacological data concerning theses substances are described.
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PMID:[Pharmacology of morphine and its derivatives (review)]. 2 28

The influences of the dopaminergic system on morphine-induced analgesia and respiratory depression were compared using modulators of dopaminergic activity. Blockade of dopaminergic receptors by haloperidol or pimozide produced a potentiation of morphine analgesia, while stimulation of dopaminergic activity by L-dopa methyl ester inhibited morphine analgesia. Morphine-induced depression of respiratory rate was potentiated by haloperidol and inhibited by pimozide or L-dopa methyl ester. These results suggest that the dopaminergic system plays a modulating role in morphine-induced analgesia, but not in morphine-induced respiratory depression.
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PMID:The effect of dopaminergic modifiers on morphine-induced analgesia and respiratory depression. 3 17

The effects of intracerebroventricular (i.c.v.) or systemic injections of Met- or Leu-enkephalin, beta-endorphin, FK 33.824 (D-Ala2, MePhe4, Met(O5)-ol-enkephalin) and of morphine and naloxone have been studied in baboons, Papio papio, which spontaneously show photically induced epileptic responses. Animals were chronically implanted with epidural or deep recording electrodes and a cannula in one lateral ventricle, and tested whilst seated in a primate chair. In some animals the natural syndrome was enhanced by the prior administration of DL-allylglycine, 100--200 mg/kg, i.v. Met- or Leu-enkephalin, 1--10 mg, i.c.v., did not lead to any manifest focal or generalized seizure discharges. Nor did it lead to any consistent enhancement or reduction of photically induced myoclonic responses (as tested 5--10 min after injection). beta-Endorphin, 0.1--0.5 mg, i.c.v., did not enhance or impair photically induced myoclonic responses. FK 33.824, 0.1--0.5 mg, i.c.v., depressed respiration and slowed EEG background rhythms for 9--15 h. This was associated with a loss of myoclonic responses to photic stimulation. These effects were reversed for 20--40 min following the injection of naloxone, 1 mg/kg i.m. A depression of respiration and a slowing of EEG rhythms was seen beginning 5--20 min after FK 33.824, 2 or 4 mg/kg, i.v. The higher dose also abolished photically induced myoclonic responses. Naloxone, 1 mg/kg, definitively reversed these effects. Morphine, 5--10 mg i.c.v., tended to increase the latency to onset of generalized myoclonus during photic stimulation. Myoclonic responses were delayed or diminished after morphine, 5 mg/kg, i.m. Naloxone, 1--2 mg/kg i.m., reversed this effect. Naloxone, 0.2--5.0 mg/kg i.m., alone, did not significantly modify photically induced myoclonus, either in animals of low or high initial responsiveness, or in those pretreated with allylglycine.
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PMID:Effects of opiate-like peptides, morphine, and naloxone in the photosensitive baboon, Papio papio. 22 24

1. Morphine inhibits the electrically evoked (0.1-0.15 Hz, 1 ms) contractions of the longitudinal muscle of the mouse vas deferens but not of the rabbit, guinea-pig, rat, cat, hamster or gerbil. This effect is stereospecific and is antagonized by naloxone or naltrexone. 2. Normorphine is equiactive with morphine but its effects are more rapid in onset and decline. 3. In the mouse vas deferens, the resting outflow of tritium-labelled catecholamines is unaffected by morphine. The electrically evoked outflow is depressed by morphine or normorphine in a dose-dependent manner. The ID50 for inhibition of contraction and for depression of outflow is 0.5 muM. 4. The relative agonist potencies of compounds without antagonist component (codeine, pethidine, morphine, normorphine, heroin, levorphanol, Ba-20227, etorphine) show good correlation with the relative agonist potencies determined in the guinea-pig ileum and for analgesia in man. 5. For compounds with dual agonist and antagonist properties, the dose-response curves for agonist activity are shallow. When the lowest concentrations giving a depression of the contraction of the mouse vas deferens are used, a good correlation is obtained with the guinea-pig ileum. 6. The relative antagonist potencies of naloxone, nalorphine, levallorphan, and cyclazocine agree well with those obtained in the guinea-pig ileum; these, in turn, correlate well with the values obtained in the morphine-dependent monkey. 7. The fact that the agonist effects of drugs with dual agonist and antagonist action show little or no dependence on concentration, makes the mouse vas deferens particularly suitable for the assay of assay of antagonist activity. 8. As an assay preparation, the mouse vas deferens is less robust and consistent in its responses than the guinea-pig ileum.
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PMID:Effect of morphine on adrenergic transmission in the mouse vas deferens. Assessment of agonist and antogonist potencies of narcotic analgesics. 23 96

Previous studies have indicated that morphine alters nerve impulse activity differently in various brain areas of intact animals. Because morphine has profound effects on visceral organs and on the spinal cord, cervically transected preparations, in which hypothermia was prevented, were used for recording spontaneous impulse activity before and for 30 min after morphine simultaneously from six regions of the brain: caudate (Cau), midbrain reticular formation (MBRF), central grey (CG), cingulate cortex (CC), hippocampus (Hip), and substantia nigra (SN). Morphine (5 and 15 mg/kg, i.p.) caused a naloxone-preventable depression of impulse activity in most brain areas. The depression was, however, especially pronounced in the CG, more so with the lower than the higher dose; naloxone completely blocked the low-dose effect. The MBRF responded with increased impulse activity after 5 mg/kg, but with depression after 15 mg/kg; naloxone blocked both responses. Activity in both the Hip and CC was depressed by the low dose of morphine, but not by the high dose; naloxone blocked the depression. Both doses of morphine generally depressed the variance in impulse activity, with a clear preferential depression of CG variance; naloxone blocked the CG variance effect, but not that of other brain areas.
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PMID:Morphine-induced regional and dose-response differences on unit impulse activity in decerebrate rats. 41 34

In chronic experiments on rats it was established that electric stimulation of certain areas of the midbrain depresses pain reactions of different genesis. Morphine in subanalgetic doses (2--2.5 mg/kg) reveals and potentiates the antinociceptive effect of central stimulation shown first of all by depression of the complex highly integrated components of an emotionally behavioral conductive reaction to pain.
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PMID:[Change in the antinociceptive effect occurring in stimulation of the rat midbrain under the influence of morphine]. 44 1


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