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

Lesions of ventral tegmental area, localised in the region of A 10 group of dopaminergic mesolimbic neurons decreased the pain threshold in rats. The absolute threshold values in morphine treated animals with the above lesion were lower than in sham-operated controls, however, the thresholds expressed as percentage of predrug threshold values did not differ in both lesioned and sham-operated animals. It is thought, that lesions of ventral tegmental dopamine neurons decrease the pain threshold due to the increase of general excitability of animals, and that there is no direct involvement of the lesioned structure in the primary mechanism of morphine analgesia.
Pol J Pharmacol Pharm
PMID:The effects of lesion of mesolimbic dopamine neurons on pain threshold and morphine analgesia in rats. 2 47

The effect of clonidine, naphazoline and xylometazoline on analgesia induced by morphine, codeine, fentanyl and pentazocine, and on cataleptic effect of morphine, codine and fentanyl was studied in rats. The biochemical assays on the influence of four analgesics on the brain concentration and turnover of noradrenaline (NA) were also performed. It was found that three drugs stimulating central NA receptors failed to affect the analgesic ED50 of all antinociceptive agents and they enhanced catalepsy induced by morphine and fentanyl. Codeine catalepsy was increased by clonidine and decreased by naphazoline and xylometazoline. The brain concentration of NA was not changed by morphine and fentanyl, but one of the doses of codeine (45 mg/kg) slightly enhanced it. Pentazocine dose-dependently decreased the brain level of NA. The rate of NA turnover was not altered by analgesics except for the higher dose of fentanyl (0.2 mg/kg) following which the disappearance of NA from the brain was diminished. The results are discussed in the light of various and non-uniform data from the literature. It is suggested that in rats the brain NA plays a less important function than the other monoamines in the behavioural activity of potent analgesics.
Pol J Pharmacol Pharm
PMID:Central action of narcotic analgesics. Part IV. Noradrenergic influences on the activity of analgesics in rats. 3 81

Studies with azidomorphine derivatives have revealed that some of them, particularly N-cyclopropylmethylnorazidomorphine (CAM), stimulate some opiate receptors, while inhibit the others. The opiate receptors stimulated by CAM are called opiate A receptors, while those antagonized by CAM are called opiate B receptors. Opiate receptors are located at nerve terminals and upon stimulation decrease the release of a neurotransmitter. Opiate A receptors are most probably located at cholinergic nerve terminals, are present in the guinea pig ileum, mouse vas deferens and in the brain. Their stimulation leads to constipation and mental clouding. Opiate B receptors located on adrenergic nerve terminals are present in the cat nictitating membrane and in the brain. Their stimulation produces analgesia, depression of coughing and respiration, catalepsy, and mental clouding.
Pol J Pharmacol Pharm
PMID:Two kinds of opiate receptor. 19 68

In order to describe the interaction of morphine and 5-hydroxytryptamine (5-HT) in the raphe-hippocampus system we tested the influence on the antinocifensive effect of topic administrations of morphine and serotonergic substances into the dorsal hippocampus and the median raphe nucleus in rats. 5-HT administered into the dorsal hippocampus increased the morphine analgesia. Lysergic acid diethylamide injected into the raphe nucleus antagonized the morphine effect. Morphine given into the raphe nucleus was highly effective, while its injection into the striatum was ineffective. The effect of the intrahippocampal morphine was antagonized by methysergide. The results indicate the important role of the serotonergic raphe-hippocampus system in the mechanism of the morphine analgesia.
Pol J Pharmacol Pharm
PMID:Interaction of morphine and 5-hydroxytryptamine in the raphe-hippocampus system. 54 79

Noradnenaline-depleting lesions involving the locus coerulcus markedly reduced morphine analgesia. Rats were tested for analgesia using the tail-compression method. The results indicate that locus coeruleus plays an important role in analgesic action of morphine.
Pol J Pharmacol Pharm
PMID:Reduced analgesic effects of morphine after bilateral lesions of the locus coeruleus in rats. 64 40

Effects of electrolytic lesions of noradrenergic brain systems on clonidine-induced analgesia were tested in rats by tail-compression method. Bilateral lesions of the locus coereleus decreased clonidine analgesia whilst lesions involving the ventral noradrenergic bundle produced no significant effect. These data demonstrate that antinociceptive effect of clonidine is related to action upon the noradrenergic system of the locus coeruleus.
Pol J Pharmacol Pharm
PMID:Effects of lesions of the Locus coeruleus and the ventral noradrenergic bundle on the antinociceptive action of clonidine in rats. 75 Oct 6

A novel analog of dynorphin (1-13), D-Ala2,F5Phe4-dynorphin amide, was prepared and its pharmacological spectrum of activity was investigated. In a hot plate test on Swiss Webster and C57Bl mice, a 20 micrograms intracerebroventricular (icv) dose of the analog produced analgesia, which was greater in potency and duration than the parent dynorphin. This action of D-Ala2,F5Phe4-dynorphin amide was antagonized by the opiate receptor antagonist naloxone (2 mg/kg ip), administered either before or after the peptide. In addition to its analgesic action in mice, D-Ala2,F5Phe4-dynorphin amide produced a Straub tail and a catatonic-like state, both of which were also attenuated by naloxone. On the electrically-stimulated mouse vas deferens preparation, in vitro, D-Ala2,F5Phe4-dynorphin amide inhibited contractile activity and had an IC50 of 108.2 +/- 34.7 nM (SEM), about 4-fold weaker than that of dynorphin. This action was also attenuated by naloxone. An icv dose of 150 micrograms of D-Ala2,F5Phe4-dynorphin amide in mice, and a cumulative series of icv doses up to 2600 micrograms in anesthetized rats, failed to produce a lethal effect. No pathological changes were observed in mouse liver and kidney at 24 h after a 50 mg/kg dose of the peptide analog. In rats anesthetized with diallylbarbital (70 mg/kg ip) and urethane (280 mg/kg ip), D-Ala2,F5Phe4-dynorphin amide did not modify blood pressure, heart rate and respiratory rate. However, when mice were injected peripherally with single doses of D-Ala2,F5Phe4-dynorphin amide, convulsive episodes were produced, and lethal effects were observed with an LD50 of 60.0 mg/kg (95% confidence limits: 49.7-70.2 mg/kg) at 48 h. This action of D-Ala2,F5Phe4-dynorphin amide was not attenuated by naloxone (2.0 mg/kg, ip). Although analgesic and behavioral effects of D-Ala2,F5Phe4-dynorphin amide (e.g. Straub tail and catatonic-like state) are opiate-like, the lethal effect may be the consequence of actions of the peptide on non-opiate systems, Thus, the novel fluorinated dynorphin analog, D-Ala2,F5Phe4-dynorphin amide, may be a useful chemical tool for the study of opiate systems and their occasionally unanticipated biological or toxic actions.
Pol J Pharmacol Pharm
PMID:D-Ala2,F5Phe4-dynorphin amide, an opiate with analgesic and toxic properties. 135 36

The effect of selective adenosine receptor agonists on nociceptive responses of mice and rats and on morphine analgesia was investigated. All compounds used: phenylisopropyladenosine (R-PIA), adenosine ethylcarboxamide (NECA), cyclohexyladenosine (CHA) and 2-chloroadenosine (2-CADO) exhibited antinociceptive action in mice and rats in the hot-plate (56 degrees C) and tail-immersion (52 degrees C) tests. R-PIA, CHA and NECA potentiated the antinociceptive action of morphine in mice, and R-PIA and NECA--in rats. 2-CADO did not affect the morphine action in the tests.
Pol J Pharmacol Pharm
PMID:Interaction of adenosine analogs with morphine in analgesic tests. 140 13

The N-terminal tetrapeptide of substance P (SP1-4) was found to produce analgesia, after the icv injection to the rat brain, which is lower in its intensity than that produced by tuftsin (Thr-Lys-Pro-Arg tetrapeptide). Among investigated tuftsin analogues Thr-Lys-Pro-Thr and Thr-Lys-Pro-Thr-Asp (partial sequences of S-protein of HB virus) were weakly active, Thr-Arg-Pro-Arg was inactive, and Thr-Lys-Pro-Gly-Arg produced a weak hyperalgesia 30 min after the icv injection. The obtained results were compared with those obtained previously in the phagocytosis stimulation test. In the control experiments the effects of free amino acids of the tuftsin molecule (Thr, Lys, Pro, Arg) were also studied.
Pol J Pharmacol Pharm
PMID:Antinociceptive action of the SP1-4 tetrapeptide and of some tuftsin analogs. 171 Nov 98

Male Wistar rats were treated with morphine or pentazocine subcutaneously (sc) and then intrathecally (it) by methionine- or leucine-enkephalin, neurotensin, substance P or cholecystokinin octapeptide 26-33. Then antinociceptive effect was measured during 1 h using tail-immersion test. Leucine-enkephalin potentiated and methionine-enkephalin antagonized morphine or pentazocine analgesia. Neurotensin, substance P and cholecystokinin acted biphasically on morphine induced antinociception. After short elevation, the diminution of antinociceptive effect was seen. Neurotensin diminished but substance P and cholecystokinin elevated analgesic effect elicited by pentazocine. Experimental model employed by us may be useful for preliminary screening of pharmacological interactions between neuropeptides and opioid analgesics on the spinal level. Our data confirm the results of other authors that individual enkephalins have different pharmacological features.
Pol J Pharmacol Pharm
PMID:Pharmacological interaction between neuropeptides and morphine or pentazocine in rat spinal cord. 172 98


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