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Biomedical subjects

E Mogilnicka

Publications and source records attributed to E Mogilnicka.

63 records · Page 4Linked to original sources
PubMedDate not supplied

The effect of alpha, alpha1-dipyridyl on noradrenaline, dopamine and 5-hydroxytryptamine levels and on dopamine-beta-hydroxylase activity in brain.

The effects of alpha, alpha1-dipyridyl (DP) on noradrenaline (NA), dopamine (DA) and 5-hydroxytryptamine (5-HT) levels in rat and mouse brain and on dopamine-beta-hydroxylase (DbetaH) activity in rat brain have been studied, DP decreases NA level and inhibits DbetaH activity in a dose dependent manner, without affecting DA or 5-HT levels.

2,2'-Dipyridyl↗
PubMedDate not supplied

The influence of dopamine-beta-hydroxylase inhibitors on avoidance reaction in rat.

Dopamine-beta-hydroxylase inhibitors sodium diethyldithiocarbamate (DEDTC), disulfiram (DS), sodium dimethyldithiocarbamate (DMDTC), tetramethylthiuram disulfide (T) and alpha,alpha'-dipyridyl (DP) were studied for their influence on avoidance reaction in rat. These compounds were given in the doses inhibiting noradrenaline synthesis (decreasing the level of this amine in brain). They all inhibit avoidance reaction although certain differences were stated in the values of effective doses and in the power of action. DEDTC, DMDTC and DS appeared to be most effective. The results of experiments suggest that noradrenaline in brain has significant importance for the avoidance reaction in rats, similarly as it is assumed for dopamine.

2,2'-Dipyridyl↗
PubMedDate not supplied

The influence of beta-agonists on normal and clonidine-decelerated noradrenaline turnover in the rat brain.

The effect of some beta-adrenoceptor agonists, such as clenbuterol, salbutamol, isoprenaline and formoterol on the NA turnover (estimated on the basis of NA disappearance after inhibition of its synthesis by FLA-63) in various regions of the rat brain was examined. All the used beta-agonists (given ip) accelerated the FLA-63 induced disappearance of NA in the cortex, limbic system and brain stem. That effect of the beta-agonists was antagonized by propranolol. The obtained results indicate that beta-adrenoceptors are involved in regulation of the NA turnover. After chronic treatment with salbutamol (5 mg/kg, twice a day for 10 days, the last dose--10 mg/kg), tolerance to acute affects of that substance developed. In turn, salbutamol given chronically prevented the clonidine-induced deceleration of NA disappearance. The effects observed after chronic salbutamol treatment may be due to developed adaptive changes in beta-, as well as in alpha 2-adrenoceptors.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Are beta- and alpha 2-adrenoceptors co-regulated during their stimulation? Behavioral studies.

The effects of beta-, and alpha 1-antagonists on the clenbuterol- and clonidine-induced depression of the exploratory activity was measured in rats in the open field test. The ability of clenbuterol (0.5 mg/kg) to reduce exploration was antagonized by 1-propranolol, significantly reduced by rauwolscine and unchanged by corynanthine and prazosin. Clonidine (0.2 mg/kg)-induced hypoactivity was significantly reduced by all the used adrenergic antagonists. A combined treatment with non-sedative doses of clenbuterol and clonidine significantly reduced exploration. Results suggest that both beta- and alpha 2-adrenoceptors are involved in clenbuterol- and clonidine-induced sedation. Moreover, they may indicate the existence of beta- and alpha 2-adrenoceptor interaction.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

Interaction between beta-adrenoceptor agonists and alpha 1-adrenergic system. A behavioral study with the clonidine-induced aggression test.

The effects of beta-adrenoceptor agonists on the clonidine-induced aggression in mice were studied. Clenbuterol (0.05-2 mg/kg ip), salbutamol (5-20 mg/kg ip) and terbutaline (10, 20 mg/kg ip) significantly potentiated the effect of clonidine. The enhancement of clonidine aggressiveness induced by clenbuterol (0.5 mg/kg) was prevented by propranolol (2.5, 5 mg/kg) and reduced by prazosin (1 mg/kg). The obtained results provide evidence that stimulation of beta-adrenoceptors facilitates the alpha 1-adrenoceptor-mediated behavior.

Adrenergic beta-Agonists↗
PubMedDate not supplied

The effect of L-DOPA and L-5-hydroxytryptophan on the pentetrazole seizures in rats after lesions of the median raphe nucleus and substantia nigra.

Electrolytic lesions of the median raphe nucleus and substantia nigra markedly increased susceptibility to pentetrazole seizures in rats. L-5-hydroxytryptophan, considerably increasing the serotonin (5-HT) level in the brain, markedly inhibited the seizures and abolished the seizure-enhanced effect of lesion of the substantia nigra. L-DOPA tended to potentiate the seizures-enhancing effect produced by lesions of the median raphe nucleus. The changes in the brain 5-HT level and the intensity of pentetrazole seizures were correlated. The results indicate that the balance between neurotransmitter systems in the brain is of importance to the susceptibility to pentetrazole convulsions.

5-Hydroxytryptophan↗
PubMedDate not supplied

Central action of Craviten (M-71).

Craviten (M-71) or 2S, 2'S) N, N'-dimethyl-N, N'-bis [1-(3', 4', 5' -trimethoxy-benzoyloxy)-butyl-2]-ethylenediamine dihydrochloride an agent with a strong antiarrhythmic action has practically no effect on the central nervous system of rats and mice. It exerts no effect on the spontaneous motor activity, on amphetamine-stimulated hyperactivity, on rota-red performance, it has no analgesic and anticonvulsant action and does not change the hexobarbital sleeping time. No effects of Craviten were observed on the body temperature in rats and mice. It decreased the arterial blood pressure in rats and stimulated slightly respiration. The hypotensive effect was dose-dependent. The LD50 of the preparation is: rats: 142 mg/kg ip, 15 x 8 mg/kg iv; mice: 550 mg/kg ip; rabbits: 5 x 1 mg/kg iv.

Amphetamine↗