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At least 19 recordsLinked to original sources
PubMed1978

Cytological effects of phenothiazine tranquilizing agents on barley meristems.

A growth reduction of 30--40% was noted in barley plants grown in two phenothiazine tranquilizers. Similar reductions were noted in the number of mid-anaphase cells, indicating the reduced growth could have been the result of a reduced mitotic rate. Also observed were several types of chromosomal aberrations. Electron microscopy revealed less endoplasmic reticulum and cytoplasmic organelles in the treated cells than in untreated cells. Various sized discontinuities in the nuclear membrane was the most frequent abnormality observed in the electron micrographs. The abnormal nuclear membrane was possibly a result of enzyme degradation.

Antipsychotic Agents↗
PubMed1979

7-Bromo-5-(2'-chlorophenyl)-1,3-dihydro-2H-1,4-benzodiazepin-2-one (I), a new tranquillizing agent: metabolism in rats.

1. After intraperitoneal injection of rats with the new benzodiazepine (compound I), four metabolites (compounds II, III, IV and V) were found in the urine. 2. Compound II was identified as 7-bromo-5-(2'-chlorophenyl)-1,3-dihydro-3-hydroxy-2H-1,4-benzodiazepin-2-one by comparison of g.l.c. and mass spectral properties of the metabolite and synthetic compound. 3. Mass spectra of compound III and its acid hydrolysis products indicate that compound III contains a hydroxyl group in the C(5)-phenyl ring. 4. Compounds IV and V were identified by mass spectrometry as products of simultaneous aromatic hydroxylation and methoxylation of the diazepine I. 5. The major urinary excretion products are compounds III, IV and V. Only very small amounts of compounds I and II were detected.

Animals↗
PubMed1979

Pharmacological evidence on the specialization of CNS mechanisms responsible for motor act inhibition by aversive events.

Our use of selected pharmacological agents has now extended the range of treatment-behaviour interactions previously studied by other (e.g., lesion) approaches in the search for appropriate models of behaviour organization and underlying physiological mechanisms. The case of muscarinic blockers has special interest, because the drugs induce only one type of primary change. At present, it appears difficult to reconcile the evidence in favour of a motor (perseverative) deficit with other evidence favouring an impairment of sensory processes. However, critical experiments using several go-no go avoidance tasks show that the two deficits may be inseparable. The complex profile of cue-dependent disinhibitory effects of antimuscarinics suggests that separate sensori-motor mechanisms are employed for response suppression not simply as a function of cue type, response type, or response-reinforcement relation but as a joint function of all these factors. Sedative-tranquillizing agents with so-called anti-conflict properties add still another dimension to the problem of motor act inhibition. These agents are maximally effective in disrupting response withholding when both reward and punishment follow the emission of a particular response, less consistently effective in tests with CS paired with non-contingent shock (CER), and mostly ineffective in those go-no go avoidance tasks which show a very high sensitivity to muscarinic blockade.

Animals↗
PubMed1976

The action of psychotropic drugs on DOPA induced behavioural responses in mice.

The "DOPA potentiation" test in mice was investigated for its usefulness in the detection of compounds with antidepressant properties. It was found that the anti-depressant drugs imipramine, amitriptyline, 5-methylamino-acetyl-6-methyl-5,6-dihydro-phenanthridine-HCl (Org OI77) and 1,2,3,4,10,14b-hexahydro-2-methyl-dibenzo[c,f]pyrazino[1,2-a]azepine-HCl (mianserin, Org GB 94) potentiated the behavioural effect of DOPA in groups of mice which had been treated 17 h previously with the monoamine oxidase inhibitor (MAOI) iproniazid. However, the DOPA response was also potentiated by a variety of centrally acting drugs which do not have antidepressant properties (atropine, methysergide, chlordiazepoxide, apomorphine). The peptide hormones ACTH4-10 and desglycinamide lysine vasopressin had equivocal effects while melanocyte stimulating hormone release-inhibiting factor (MIF) had no effect on the DOPA response. The DOPA response was inhibited by the neuroleptics chlorpromazine and haloperidol. There appeared to be no correlation between the effects of the drugs on the behavioural responses elicited by DOPA and the changes found in the brain concentration of noradrenaline, dopamine, serotonin, gamma-aminobutyric acid, tryptophan and tyrosine. It is concluded that the "DOPA potentiation" test cannot be considered as a reliable test in the detection of anti-depressant compounds.

Animals↗
PubMed1976

[Neuroleptanalgesia as the anesthesia in pediatric surgery].

In work carried out over a period of two years in the department of anesthetics and intensive care of the Saint-Etienne University Hospital, the authors report their experience of neuroleptanalgesia using droperidol-dextromoramide in children in 104 cases. The observations may be divided up into 2 groups: - 1 group of children below the age of 2 years; - 1 group of children from 2 to 10 years. This study showed the side-effects and complications common to both groups, in particular, the extrapyramidal syndrome. Furthermore, the authors present their technique of administration.

Anesthesia↗
PubMed1976

Tardive dyskinesia.

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Antipsychotic Agents↗