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At least 19 recordsLinked to original sources
PubMed1977

Harmine action in rats with lymphostatic encephalopathy.

In rats with lymphostatic encephalopathy the duration of harmine tremor was lengthened, and the brain concentrations of harmine decreased more slowly than in sham-operated controls. The tremor began simultaneously in both rat groups at coinciding brain concentrations of harmine. In rats with lymphostatic encephalopathy harmine concentrations in brain at the termination of tremor lay in the same range as in sham-operated controls. The plasma concentrations of harmine were not changed by the disease. It is concluded that during lymphostatic encephalopathy the lymphatic drug elimination from brain is impaired whereas--at least for harmine--the blood-brain barrier functions as normal.

Alkaloids↗
PubMedDate not supplied

The effect of aprotinin on the harmine-induced tremor in lymphostatic encephalopathic and normal rats.

In normal and lymphostatic encephalopathic rats, aprotinin pretreatment alters the duration of the harmine tremor and the cerebral concentration of the alkaloid; low doses shorten the tremor and decrease the concentration, a high dose causes the opposite. Aprotinin may decrease or increase the blood-brain barrier permeability of harmine. Because the findings are similar in both groups of rats the blood-brain barrier for harmine is assumed to be intact in lymphostatic encephalopathy. However, sick rats possibly suffer from an impaired cerebral elimination of harmine.

Alkaloids↗
PubMed1976

Effect of harmine and brain lesions on apomorphine induced motor activity.

Application of harmine (10 mg/kg IP) 30 min before apomorphine decreased the motoric effects of the latter. Following harmine an increase in 5-HT and a decrease in 5-HIAA in different brain regions have been found. Injection of 5,6-DHT into nucleus medianus raphe 7 days before the experiment caused a significant increase of the apomorphine effect. Harmine pretreatment reduced this escessive motility as well as additional lesion of the substantia nigra with 6-OH-DA. Lesion induced by 6-OH-DA alone was without significant effect on the hypermotility following apomorphine. Application of PCPA 3 days before testing elicited an increase of apomorphine-induced hypermotolity which could be abolished by preceding harmine application. The experiments demonstrate the inhibitory effect of the central serotoninergic system on the apomorphine syndrome as well as the serotoninergic-dopaminergic interaction in hypermotility.

5,6-Dihydroxytryptamine↗
PubMed1979

Modification by levo-propranolol of tremors induced by harmine in mice.

It has been recently reported that the levo isomer of propranolol possesses anti-serotonin properties in animals. Since harmine-induced behavioural changes in mice are reported to be mediated through central serotonergic receptors, an attempt was made to test whether 1-propranolol would also modify harmine-induced responses by virtue of its anti-serotonergic or anti-adrenergic property. The results indicated that l- and dl-propranolol inhibited central serotonin receptor mediated responses to harmine in mice, a finding that is analogous to other recent observations.

Animals↗
PubMed1975

Studies of the interaction of the fluorophores harmine and harmaline with calf thymus DNA.

The binding to calf thymus DNA of the hallucinogen harmine and one of its analogues harmaline was studied by absorption spectrophotometry and fluorescence quenching analysis. Viscosity measurements were also carried out. For both molecules, quenched and unquenched sites on DNA are present. For each type of binding site, the value of the product of the number of sites times the association constant was determined. Harmine is more strongly bound than harmaline. Viscosity measurements indicate intercalation in the case of harmine only.

Alkaloids↗
PubMed1979

The effect of harmine and other monoamine oxidase inhibitors on N-acetyltransferase activity.

Prior studies indicate that the monoamine oxidase inhibitors (MAOI) harmine and iproniazide inhibit N-acetyltransferase activity from liver. In this report we have demonstrated that harmine and harmaline are potent inhibitors of N-acetyltransferase, purified from hamster and rat liver. However, other MAOI such as deprenyl, clorgyline, methysergide, cyproheptadine, phenelzine, pargyline, methyltryptamine and tranylcypromine have either no effect, or only trivial effects on N-acetyltransferase. There is no correlation between a compound's properties as an MAO and N-acetyltransferase inhibitor. One must consider the inhibitory effect of harmine and harmaline on both MAO and N-acetyltransferase when evaluating the effects of these compounds on physiological processes.

Acetyltransferases↗
PubMed1977

Cardiovascular actions of three harmala alkaloids: harmine, harmaline, and harmalol.

Each of three harmala alkaloids, harmine, harmaline, and harmalol, decreased heart rate and increased pulse pressure, peak aortic flow, and myocardial contractile force in intact normotensive anesthetized dogs. Harmine reduced systemic arterial blood pressure and total peripheral vascular resistance; harmaline-evoked decreases were frequently followed by a secondary increase; and the effects of harmalol on these two parameters were inconsistent. A direct negative chronotropic effect of harmala alkaloids was suggested by observations of bradycardia in the isolated perfused rat heart and in the intact dog; neither vagotomy nor atropinization affected harmala alkaloid-induced bradycardia in the dog. Reduction in femoral vascular resistance by the alkaloids was not apparently due to activation of cholinergic, beta-adrenergic, or histamine (H1) receptors.

Alkaloids↗
PubMed1975

The importance of extrapyramidal function for the induction and antagonism of harmine tremor.

The brain lesion technique was used to investigate the role of the paleostriatum and the nigro-neostriatum in harmine-induced tremor and in its antagonism by dopaminergic agonists, apomorphine, 1-dopa, piribedil, d- and l-amphetamine. Bilateral lesions of the caudate--putamen or substantia nigra failed to modify the intensity of tremor or its antagonism by dopaminergic agonists. Bilateral lesions of the globus pallidus markedly reduced the intensity of tremor and the results indicated that such lesions were also able to reduce the effectiveness of dopaminergic agonists as tremor antagonists. The data suggest that the integrity of the paleostriatum is more important than that of the neostriatum for the mediation of harmine tremor and its antagonism by dopaminergic agonists. The results are discussed in relation to the proposed clinical relationship between paleostriatal dopamine dysfunction and tremor mechanisms.

Alkaloids↗
PubMed1976

Species and phenobarbitone-induced differences in the kinetic constants of liver microsomal harmine O-demethylation.

1. The apparent kinetic constants for the O-demethylation of harmine to harmol by 10 000 g supernatant fractions from livers of mice, rats, guinea-pigs, rabbits, cats and cows have been determined. The Km values were 10-39 muM and Vmax 0-25 and 1-65 nmol/mg protein/min. 2. Optimal conditions of incubation time and NADP requirements differed between species. In all species except cat and cow the rate of O-demethylation of harmine was linear for 5 min, but in the latter species was linear for 15 min. Maximum stimulation of O-demethylation occurred at NADP concn. of between 50 and 375 muM. 3. Phenobarbitone pre-treatment of weanling, young adult and mature adult mice increased the Vmax for O-demethylation by 2.9- to 4.6-fold but did not change Km. Increased Vmax values were greatest in young and least in old mice and these changes were directly correlated with a decrease of hexobarbitone sleeping time.

Animals↗
PubMed1975

Effect of antiphologistics on blood-brain barrier in lymphostatic encephalopathic and in normal rats.

Injection of the tremorigenic alkaloid harmine into lymphostatic encephalopathic rats leads to a longer duration of tremor and higher brain concentrations than in sham-operated controls. In lymphostatic encephalopathic as well as in normal rats different antiphlogistics shorten the tremor duration and decrease harmine concentration in brain. The antiphlogistics do not influence the plasma concentration of harmine, its protein binding and its tremorend concentration in brain. The effect of antiphlogistics in lymphostatic encephalopathic rats is considered as a consequence of the reduced blood-brain barrier permeability. Obviously in sick animals the blood-brain barrier permeability for harmine is not increased; the prolonged harmine tremor and the increased alkaloid concentration in the brain are consequences of the impaired cerebral lymphatic drainage only.

Alkaloids↗
PubMedDate not supplied

Intensification of central catecholaminergin and serotonergic processes by the hypothalamic factors MIF and TRF and by angiotensin II.

The present work deals with the action of MIF (melanocyte stimulating hormone release-inhibiting factor), TRF (thyrotropin releasing factor), and angiotensin II on the behavioral effects of L-DOPA and of D, L-5-hydroxytrytophan (5-HTP) in mice. The influence of MIF and TRF on the antagonistic effect of L-DOPA of harmine tremors in rabbits was also studied. MIF and TRF, injected i.p., intensify the effects of L-DOPA in mice. The minimal dose of MIF required to induce a +3 response is 0.1 microgram/kg; TRF is active at 500 micrograms/kg. When MIF or TRF are injected into the brain, potentiation of L-DOPA is obtained with exceedingly small quantities of MIF (0.1 pg); the effective dose of TRF is 1 microgram. The behavioral effects of 5-HTP are potentiated by TRF only, at doses of 0.1 microgram/kg, i.p. When TRF is administered intracerebrally, the active dose per mouse is 0.1 ng. Harmine (5 mg/kg i.v.) induced, in the rabbit, sustained whole body tremors; if L-DOPA (5 mg/kg) is administered i.v. at the peak of the harmine effect, tremors subside. When the rabbit is pretreated with MIF administered i.p. 1 -2 hr before harmine, in doses devoid of an antitumor effect per se (10 micrograms/kg), the L-DOPA antagonism appears at lower dose. Also dopamine (5-10 mg/kg i,v.) proved effective in abating harmine tremors; previous treatment with MIF (50 micrograms/kg) potentiated the antagonistic effect of dopamine. According to the prevailing theories on the mechanism of neurotransmission, some hypotheses will be discussed to explain the observed potentiation: impaired uptake, impaired degradation, interference with the turnover of the boiamines, supersensitivity of the receptors.

5-Hydroxytryptophan↗
PubMed1976

Effects of ATP and magnesium ions on the fluorescence of harmala alkaloids. Restrictions for the use of harmala alkaloids as fluorescent probes for (Na+ + K+)-ATPase.

1. Harmine and harmaline were investigated as potentially useful fluorescent inhibitors of (Na+ + K+) activated ATPase. 29 From spectroscopic measurements both compounds were shown to form 1 : 1 complexes with ATP, the dissociation constants being 0.65 mM and 1.83 mM for harmine and harmaline respectively. Addition of Mg2+ and enzyme further affected these equilibria. 3. Although it was possible to demonstrate a competitive effect of harmine at the sodium-loading site of the enzyme, other inhibitory effects, including inhibitions of ouabain binding and the ouabain-insensitive ATPase were found. 4. It was concluded that the harmala alkaloids can inhibit (Na+ + K+)-activated ATPase in a complex way involving both Na- and ATP-binding sites. This severely limits their usefulness as spectroscopic probes.

Adenosine Triphosphatases↗