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PubMedDate not supplied

Beta blockade and anticonvulsant activity of propranolol.

Racemic and dextro forms of propranolol were equipotent in their anticonvulsant activity in normal rats by the MES test. In an attempt to determine any difference in the anticonvulsant activity of the two forms a variety of adrenergic agents were used, viz. phenoxybenzamine, reserpine, alphamethyl dopa and acetazolamide. There was no difference between the two forms, in the absence or presence of several adrenergic drugs employed. However, racemic but not dextro propranolol reduced MET, in normal as well as in nialamide primed rats.

Acetazolamide↗

PubMed1981

DNA-damaging activity in vivo and bacterial mutagenicity of sixteen hydrazine derivatives as related quantitatively to their carcinogenicity.

Sixteen hydrazine derivatives (hydrazine, 1,1-dimethylhydrazine, 1,2-dimethylhydrazine, phenylhydrazine, procarbazine, isoniazid, isocarboxazid, nialamide, 2,4-dinitrophenylhydrazine, phenelzine, hydralazine, dihydralazine, carbamylhydrazine, mebanazine, iproniazid, and 1-carbamyl-2-phenylhydrazine) were tested for DNA-damaging activity by the alkaline elution technique and for mutagenic activity in the Salmonella-microsome (Ames) test. The first nine compounds listed (56%) were found to induce a significant DNA fragmentation in the liver and/or in the lung of i.p.-treated male Swiss mice. The DNA-damaging potency varied over an approximately 30-fold range. Thirteen of the first 14 compounds listed (81% of the total), isocarboxazid being inactive, were positive in the Ames test, with a broad range of activity towards the five bacterial strains of Salmonella typhimurium used (TA1535, TA100, TA1537. TA1538, and TA98) and of metabolic behavior in the presence of S-9 mix containing rat liver, mouse liver, or mouse lung postmitochondrial preparations from Aroclor-treated animals. The mutagenic potency varied over an almost 7000-fold range. For 11 of the 16 hydrazine derivatives tested, homogeneous carcinogenicity data (induction of pulmonary tumors in mice chronically treated p.o.) were available from literature. Elaboration of these data showed that carcinogenic potency varied over an approximately 1900-fold range. The five most potent carcinogens were all positive in the DNA damage test. Their carcinogenic potency varied over a 130-fold rage and their DNA-damaging potency varied over a 22-fold range. DNA-damaging potency seemed to vary on a more compressed scale, but regression analysis indicated the existence of a strong positive correlation between in vivo DNA-damaging and carcinogenic potencies, while a lack of correlation was found between mutagenic and carcinogenic potencies. There was no correlation between DNA-damaging and mutagenic potencies.

Animals↗

PubMedDate not supplied

[Comparative mydriatic effect of different groups of antidepressants].

Study of 16 antidepressants, (imipramine, amitryptyline, doxepin, dibenzepin, maprotilin, mianserin, nomifensin, trazodon, caroxazon, adepren, viloxazin, nialamid, asaphen, pyrazidol, inkasan, ftoracizin) in experiments on white mice have shown that the drugs tested may be arranged in the following way as regards the intensity of the mydriatic effect they produce: ftoracizin, amitryptyline, doxepin, imipramine, dibenzepin. Pyrazidol produces a very weak and short-lived mydriatic effect. Adepren, inkasan, caroxazon, adepren produce no mydriatic action.

Animals↗

PubMed1981

[The new versus the old antidepressant drugs: a comparative study of their psychopharmacological profiles (author's transl)].

We studied 13 known or potential antidepressants, choosen in different pharmacological classes: desipramine, imipramine, nialamide, dexamphetamine, AHR 1118, amineptine, iprindole, mianserine, nomifensine, salbutamol, TRH viloxazine, zimelidine. Each of these compounds was studied on 8 psychopharmacological tests: motor activity, reserpine induced hypothermia, reserpine induced ptosis, oxotremorine induced hypothermia, oxotremorine induced tremors, high doses apomorphine induced hypothermia, potentiation of toxic effects of yohimbine, behavioural despair. Clinical active compounds are efficient on yohimbine test and at least on one model of hypothermia; with a few exceptions, easy to explain, substances with a clearly demonstrated antidepressant activity in human have some common effects; these common effects can be used to predict, from animal experiments, an antidepressant effect in man.

Animals↗

PubMed1981

[Effect of antidepressants of different groups on the cholinergic structures of the brain].

In electroencephalographic experiments on cats and rabbits it was shown that antidepressants of different chemical classes exhibited different central anticholinergic activity. The antidepressants tested (there were 17 of them) acted differently on the EEG activation by galanthamine (an anticholinesterase drug). Pronouncingly antagonistic to the activating effect of galanthamine were doxepin, phthoracizin, aminotryptilin, imipramine. Next followed (in the regressing sequence) desipramine, lidiomil, mianserin, trazodon, viloxazin, noveril, nomifensin, adepren, caroxazon, nialamide, asaphin, pyrazidol and inkasan did not influence the synchronizing action of galanthamine. The substantial differences in the anticholinergic activity of the antidepressant show that the action upon the central cholinergic system is not an obligate component of the antidepressant effect.

Animals↗

PubMed1981

[Histochemical fluorescence study of aminergic cells throughout the central nervous system of the migratory locust (author's transl)].

We have investigated the aminergic neurosecretory cells in the brain and the ganglia of the ventral nerve cord of the adult female locust, by means of the Falck and Hillarp method, with or without a block of the degradation of amines by nialamide. In the brain, we have confirmed the presence of catecholamines and probably indolamines-containing cells and defined their positions in the protocerebrum and the lateral zones of the deutocerebrum and the tritocerebrum. In the ventral cord, we have found groups of catecholaminergic cell bodies in suboesophageal, thoracic and abdominal ganglia, and probably indolaminergic cell bodies in thoracic and some abdominal ganglia. Aminergic fibres are present in all the ventral cord. They are especially numerous in suboesophageal and thoracic ganglia. In these ganglia, some fibres enter the roots of some somatic nerves.

Animals↗

PubMedDate not supplied

The effect of drugs interfering with biogenic amines metabolism on gastric secretion and reserpine-ulcers development in rats.

The effect of drugs interfering with endogenous catecholamines metabolism on gastric secretion and gastric ulcers development 4 hr following reserpine administration was investigated in rats with chronic gastric fistulas. Drugs inhibiting catecholamine synthesis: alpha-methyl-p-tyrosine (alpha-MT) and sodium diethyldithiocarbamate (DDC) decreased substantially the reserpine-induced gastric acid and pepsin secretion, but only alpha-MT diminished the development of gastric ulcers. Pretreatment with nialamide (NLD) elicited in reserpinized rats a marked inhibition both of gastric secretion and of gastric ulcers development. Dopamine (DA), noradrenaline (NA) and adrenaline (A) decreased the secretion of hydrochloric acid but did not change the intensity of gastric ulcers caused by reserpine. Desipramine strongly inhibited reserpine-induced gastric acid secretion. Reserpine depleted DA, NA and 5-HT stores in the brain and decreased DA and 5-HT levels in the wall of the stomach in which the NA levels were increased. The changes in biogenic amines content induced by drugs in reserpinized rats did not correlate with their influence on gastric secretion and on the development of mucosal ulcers. The inhibitory effect of all of the drugs examined on gastric acid and pepsin secretion in reserpinized rats was accompanied by the inhibition of gastric ulcers formation following NLD and alpha-MT administration only, indicating that ulcer generation following reserpine depends more on changes in mucosal barrier resistance than on gastric acid secretion.

Animals↗

PubMed1996

Befloxatone, a new reversible and selective monoamine oxidase-A inhibitor. II. Pharmacological profile.

The pharmacological profile of befloxatone, a reversible, selective and competitive inhibitor of monoamine oxidase-A has been investigated in rodents. In mice, befloxatone was more active at potentiating generalized tremors induced by L-5-hydroxytryptophan (ED50, 0.21 mg/kg p.o.) than phenylethylamine-induced stereotypies (ED50, 58 mg/kg p.o.), indicating a very high in vivo selectivity for inhibition of the A form of monoamine oxidase. Befloxatone showed potent activity in behavioral models in rodents predictive of antidepressant activity (forced swimming test, learned helplessness and reserpine reversal) with minimal effective doses of 0.1 to 0.2 mg/kg p.o. In these tests, befloxatone was much more potent (10- to 500-fold) than reference antidepressant compounds (reversible and irreversible monoamine oxidase inhibitors and monoamine reuptake inhibitors). In rats, befloxatone increased rapid eye movement sleep latency and decreased rapid eye movement sleep duration, without rebound effects. Potential anxiolytic activity was observed in the elevated-plus maze test in rats (minimal effective dose, 1-2 mg/kg p.o.). Befloxatone had no effect on motor performance, did not induce sedative or stimulant activity up to doses of 200 mg/kg p.o. and was devoid of anticholinergic activity in mice. Interaction studies with p.o. dietary tyramine (12 mg/kg), carried out in freely moving rats, demonstrated that, in contrast to irreversible monoamine oxidase inhibitors, befloxatone did not potentiate the pressor effect of this amine in the range of doses which showed pharmacological activity in antidepressant behavioral models. Furthermore, of the compounds tested (moclobemide, brofaromine, nialamide and phenelzine), comparison of doses active in antidepressant models and doses potentiating the pressor effects of tyramine demonstrated that befloxatone had the best therapeutic index. The results suggest that befloxatone will show clinical antidepressant activity at low doses and will be devoid of the side effects associated with irreversible monoamine oxidase inhibitors.

Animals↗

PubMed1996

Modulation of [3H]quinpirole binding in brain by monoamine oxidase inhibitors: evidence for a potential novel binding site.

[3H]Quinpirole is a dopamine agonist with high affinity for the D2 and D3 dopamine receptor subtypes. A variety of drugs, most notably monoamine oxidase inhibitors (MAOls), inhibit the binding of [3H]quinpirole, but not [3H]spiperone or [3H](-)N-n-Propylnorapomorphine, in rat striatal membranes by a mechanism that does not appear to involve the enzymatic activity of MAO. This study extends the characterization of MAOI-displaceable [3H]quinpirole binding in rat brain. Clinically antidepressant MAOIs exhibited selectivity between sites labeled by [3H]quinpirole and [3H]spiperone as did a number of structurally related propargylamines and N-acylethylenediamine derivatives and other drugs such as debrisoquin and phenylbiguanide. The MAOIs clorgyline and Ro 41-1049 were the most potent. Anti-depressant MAOIs inhibited [3H]quinpirole binding with the following rank order of potency: phenelzine > pargyline > tranyl-cypromine > isocarboxazid > nialamide > moclobemide. In striatal membranes, MAOI Ro 41-1049 inhibited [3H]quinpirole binding with similar potency at a variety of incubation temperatures (4-37 degrees C), assay tissue concentrations (5-20 mg original wet weight/ml), and time points (2 min-4 hr) and in the presence or absence of K+, Mg2+, Ca2+ ions, ascorbate, EDTA and NaCl. The regional distribution of Ro 41-1049-displaceable [3H]quinpirole binding in brain paralleled that of D2-like receptors. These data suggest that MAOIs interact with a novel binding site that is labeled by [3H]quinpirole or that modulates [3H]quinpirole binding. This site may be associated with D2-like dopamine receptors.

Animals↗

PubMed1976

The effect of pargyline and other monoamine oxidase inhibitors on blood acetaldehyde levels in ethanol-intoxicated mice.

Pargyline (100 mg/kg i.p.) administered to Swiss-Webster mice prior to the injection of ethanol (4 g/kg i.p.) elevated blood acetaldehyde levels to a mean of 20 mug/ml, compared to less than 1 mug/ml in control mice treated with ethanol alone. Elevated blood acetaldehyde was observed when ethanol was given at 15 minutes, 2 or 5 hours after pargyline; the action of pargyline had largely disappeared after 18 hours. The magnitude of the increase in blood acetaldehyde levels was dependent upon the dose of pargyline between 20 and 100 mg/kg; however, the elevation was relatively independent of the ethanol dose between 1 and 6 g/kg. Of the other monoamine oxidase inhibitors tested, Lilly 51641 showed a strong elevation in acetaldehyde (mean 13.3 mug/ml), whereas deprenyl and clorgyline gave modest elevations (2.9 and 2.6 mug/ml, respectively), and nialamide and tranylcypromine were only weakly active (1.4 and 1.2 mug/ml, respectively). Blood acetaldehyde levels in mice treated with pargyline and ethanol were strongly depressed (85%) by pyrazole, an inhibitor of alcohol dehydrogenase, and moderately to strongly depressed (49-71%) by pretreatment with phenobarbital, an inducer of liver aldehyde dehydrogenase.

Acetaldehyde↗

PubMedDate not supplied

The influence of antidepressive drugs on the level of acetylcholine and on the acetylcholinesterase activity in the brain of rats.

Rats were treated ip with MAO inhibitos (MAO-I): nialamid (NL), pivalylbenzylhydrazine, tranylcypromine, pheniprazine (Ph) or pargyline, and the leve of total, free and bound acetylcholine (Ach) as well as the acetylcholinesterase (Ach-E) activity were estimated in four parts of rats brain 2 or 16 hr after the treatment. These parameters were estimated also after the treatment with tricyclic antidepressants: desmethylimipramine (DMI), amitriptyline, or protriptiline, and in the conditions of the reversal of reserpine-like syndrom. MAO-I, 2 hr after their application and the reversal of reserpine like-syndrom have not changed the level of measured fractions of Ach in parts of the brain. DMI increased the level of all Ach fractions in the striatum. NL caused the decrease of bound Ach level in all parts of the brain with no changes of free Ach level, 16 hr after the treatment. Ph, 16 hr after the treatment, decrease both fractions of ACh only in the cortex. All studied drugs affected evidently ACh-E activity in various parts of brain. It is concluded that:1) Cholinergic mechanisms in the rat brain are involved in the central action of DMI and of some MAO-I., 3) Cholinergic function of the brain may be modulated by the adrenergic activity, 2) Individual parts of the brain have different susceptibility to the influence of different MAO-I on the ACh-E activity.

Acetylcholine↗

PubMed1963