Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of serotonergic system on the changes in locomotor activity of mice and rats brought about by morphine, fentanyl, codeine and pentazocine and on morphine induced catalepsy in rats was studied. p-Chlorophenylalanine (pCPA) did not affect the behavioral changes produced in mice by morphine, fentanyl, codeine and pentazocine but reduced the behavioral depression produced by these drugs in rats. 5-Hydroxytryptophan (5-HTP) but not tryptophan (TP) reversed the action of pCPA on the effect of morphine and fentanyl. After reserpine the depression produced in rats by morphine and fentanyl was more pronounced. TP did not change the depression produced by combination of reserpine and morphine but counteracted the depression observed after combination of reserpine and fentanyl. In mice reserpine protected against hypermotility produced by morphine or fentanyl and TP potentiated the depression produced by the combination of reserpine and morphine or reserpine and fentanyl. Serotonin precursors, 5-HTP and TP evidently potentiated the morphine induced catalepsy. pCPA counteracted only the enhancement of the catalepsy observed after TP administration. Naloxone abolished the catalepsy after combined treatment with morphine and TP. Similarly but weaker acted cyproheptadine. The results suggest that the serotonin system plays a role in the effects of morphine and fentanyl on rat locomotor activity. An increase in the cerebral serotonin level increases the morphine catalepsy in rats.
Pol J Pharmacol Pharm
PMID:Central action of narcotic analgesics. V. Participation of serotonin in the mechanism of action of narcotic analgesics. 4 45

A mutant (nit8) with a lowered activity of glutamine synthetase (GS) was isolated in Aspergillus nidulans. The levels of GS and of an arginine catabolic enzyme, ornithine transaminase (OTA) were assayed under a variety of growth conditions leading to repression, depression and induction of OTA in the wild type, nit8 and several regulatory mutants. The results obtained appear to exclude the possibility of involvement of GS in the regulation of arginine catabolism in A. nidulans.
Acta Microbiol Pol 1978
PMID:Catabolite repression in Aspergillus nidulans; the role of glutamine synthetase. 8 77

Rats given quipazine (5 mg/kg) or LSD (0.05 mg/kg), were decapitated at the time of maximum of behavioral effect of drugs (head twitches), resp. 30 and 15 min, or when the behavioral effects disappeared (resp. 60 and 30 min), and concentrations of dopamine (DA), noradrenaline (NA), serotonin (5HT) and 5-hydroxyindole-3-acetic acid (5-HIAA) were assayed in the striatum. Quipazine significantly elevated the DA level at both periods tested. LSD at the peak of its action depressed the level of 5-HIAA, and in the next period produced a significant depression of striatal levels of NA, 5HT and 5-HIAA.
Pol J Pharmacol Pharm
PMID:The effect of quipazine and LSD on monoamines in the rat striatum. 9 44

The effect of nomifensine (NF) on the content of serotonin (5-HT) and catecholamines (CA) in discrete regions of rat brain was studied with the histofluorescence technique of Falck, NF, 20 and 40 mg/kg ip, produced, after 30 min, a depression of 5-HT content in the neurocytes of dorsal and median raphe nuclei (NDR and NMR). The blockade of dopamine receptors by spiperone did not abolish the action of NF in NDR, and inhibited the effect in NMR only in some animals. NF did not affect significantly the CA content in the striatum (caudate nucleus--putamen), hypothalamic paraventricular nucleus, and paraventricular rotundocellular nucleus. The results indicate, a direct action of NF on 5-HT neurons in the rat mesencephalon. In addition, the drug may also act indirectly on 5-HT neurons in NMR, via dopaminergic system.
Pol J Pharmacol Pharm
PMID:Nomifensine and central monoamine neurons: histofluorescence studies. 14 91

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

Hyperactivity produced in mice with morphine or fentanyl, and methylamphetamine was antagonized by naloxone. The depression of locomotor activity induced by codeine was practically unchanged by the opiate antagonist. L-DOPA did not restore the stimulatory action of morphine and fentanyl in reserpinized mice. The hyperactivity produced by morphine and fentanyl was abolished in mice treated with alpha-methyl-p-tyrosine, but this was restored by L-DOPA administration. Agents inhibiting the central noradrenaline receptors, phentolamine, phenoxybenzamine, and aceperone, prevented or even reversed the locomotor stimulatory action of morphine and fentanyl. Pimozide did not affect the increase of locomotor activity produced by morphine, but depressed that induced by fentanyl. Haloperidol, used in a dose which did not affect the locomotor activity of mice, completely blocked or even reversed the stimulatory action of morphine and fentanyl, and potentiated the depression of locomotor activity produced by pentazocine and codeine. Diethyldithiocarbamate significantly depressed, but did not inhibit completely the stimulatory action of morphine and fetanyl. The stimulatory action of methylamphetamine was also significantly depressed. It seems that the stimulatory effect of morphine and fentanyl depends on the release of endogenous noradrenaline.
Pol J Pharmacol Pharm
PMID:Central action of narcotic analgesics. Part III. The role of endogenous noradrenaline in hyperactivity induced by morphine or fentanyl in mice. 21 79

Chlorodiazepoxide (CDP) produces stimulation of the locomotor activity of CD-1 and DBA/2 mice. This effect is strongly pronounced at the commencement of the testing session, and it is followed by a decline of the locomotor activity. The drugs impairing noradrenergic transmission: reserpine, clonidine and alpha-methyltyrosine, depressed or abolished the stimulatory effect of CDP; clonidine, in addition antagonized the subsequent decline of the locomotor activity in CDP-treated mice. Mice receiving reserpine subchronically (in the dose of 0.5 mg/kg daily for 3 days) displayed either motor depression or hypermotility. In approx. 50% of subchronically reserpinized mice CDP produced a strong hypermotility, lasting for at least 1 hr. It can be concluded that a noradrenergic mechanism is involved in the stimulatory effect of CDP on exploratory locomotor activity in mice, and that there exist two distinct subpopulations within the CD-1 strain, reacting differently to chronic reserpine treatment.
Pol J Pharmacol Pharm
PMID:Stimulatory effect of chlordiazepoxide on locomotor activity in mice: importance of noradrenergic transmission. 22 33

In 22 children with lymphoblastic leukaemia peripheral blood lymphocytes were studied during 2.5 years of remission-maintaining treatment, and in 7 cases also after stopping treatment. Lymphocytes T and B were identified and lymphocyte surface receptors for complement and for the Fc fragment of IgF were determined. The immunological reactivity of lymphocytes was determined also using the test of PHA-induced blastic transformation. It was found that prolonged chemotherapy caused depression of lymphocytes B in the first place. A fall was observed also in the proportion of cells undergoing transformation. It was shown that after cessation of treatment PHA-reactivity and normal values of lymphocyte subpopulations returned.
Acta Haematol Pol
PMID:[Immunological characteristics of lymphocytes during intensive treatment maintaining remission of acute lymphoblastic leukemia in children and following withdrawal from chemotherapy]. 28 75

Quantitative determinations of lymphocytas were done in the active period of the disease, immediately after treatment by the COAP schedule and during remission. In 6 patients the determinations were done several times during 20 weeks of maintenance treatment. It was found that independently of the stage of the disease the absolute lymphocyte count and the counts of B and T populations were low, while that of lymphocyte O population was raised. It was observed that the reduced count concerned all 4 subclasses of lymphocytes B, that is those with surface receptors for IgA, IgM, IgG and IgE immunoglobulins. In remission the values of lymphocytes and their T and B subpopulations increased, failing, however, to reach the normal values. This rise was more pronounced in the case of lymphocytes T. Lymphocyte depression in these patients is explained by the authors as due mainly to intensive cytostatic treatment.
Acta Haematol Pol
PMID:[Changes in blood lymphocytes and their subpopulation in patients with myeloblastic leukemia treated with cytostatic agents]. 31 15

Electrolytical lesions of the dorsal raphe nucleus in the rat did not change frequency of head twitches produced by codeine and apocodeine. The action of serotonergic drugs was affected differently: the lesion depressed the frequency of head twitch episodes produced by 5-hydroxytryptophan (5-HTP), LSD and quipazine, but did not change the frequency of head twitches produced by 5-methoxytryptamine. On the other hand, the lesions protected against high mortality produced by combined treatment with tranylcypromine and 5-methoxytryptamine. There was a good correlation between the extent of lesion, measured by the depression of the level of prosencephalic serotonin, and the depression of head twitch frequency produced by 5-hydroxytryptophan and quipazine, while the correlation was not significant for the action of LSD. It is concluded that presynaptic serotonergic structures belonging to the mesostriatal serotonergic system are necessary for appearing of head twitches after treatment with 5-HTP, LSD and quipazine, and therefore these compounds have a presynaptic action in this test.
Pol J Pharmacol Pharm
PMID:Head twitches produced by serotonergic drugs and opiates after lesion of the mesostriatal serotonergic system of the rat. 31 25


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