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Biomedical subjects

J Zabawska

Publications and source records attributed to J Zabawska.

9 recordsLinked to original sources
PubMed1979

Mediation of central prostaglandin effects by serotoninergic neurons.

Ten days after administration of 5,6-dihydroxytryptamine, which causes degeneration of central serotoninergic neurons, the depressive behavioral effects of PGF2 alpha and PGE2 were evidently inhibited. Central chemical serotoninectomy abolished the hyperthermic and hypertensive effects of PGF2 alpha, but only slightly affected those of PGE2. It is concluded that serotoninergic neurons mediate the depressive behavioral action of both PGF2 alpha and PGE2. They also mediate the hyperthermic and hypertensive action of PGF2 alpha but not of PGE2. This suggests that these prostaglandins have different central modes of action.

5,6-Dihydroxytryptamine↗
PubMed1979

Effect of prostaglandin F2 alpha on temperature and behaviour of centrally sympathectomized rats.

Prostaglandin F2 alpha (PG F2 alpha) in doses of 1 and 10 micrograms applied intraventricularly causes a rise in body temperature and exerts a sedative action on rat behaviour. Chemical sympathectomy of the central nervous system (CNS) induced by a twofold intraventricular administration of 250 micrograms of 6-hydroxydopamine reduces the influence of PG F2 alpha on the body temperature and behaviour. Reserpine administered to rats with chemical sympathectomy of the central nervous system reverses or prevents the PG F2 alpha action on body temperature of the animals. The results of the experiments seem to indicate that the central monoaminergic mechanisms play a role in the central action of PG F2 alpha on body temperature and behaviour.

Animals↗
PubMed1978

Influence of polyphloretin phosphate on the central effects of prostaglandin E2 and F2alpha in rats.

The possibility that polyphloretin phosphate (PPP) antagonizes the central effects elicited by prostaglandin (PG) E2 and F2alpha was investigated. PPP was administered i.c.v. to male Wistar rats (10 or 25 microgram) 10 or 30 min before i.c.v. injection of PGF2 or PGF2alpha (1 or 10 microgram). The duration of several component of behavior, the degree of irritability, and the rectal temperature of rats were measured; the levels of noradrenaline, dopamine, 5-hydroxytryptamine, and 5-hydroxyindoleacetic acid were measured spectrophoto-fluorometrically in discrete brain areas. PPP antagonized temperature and behaviroal changes induced in rats by PGF2alpha, but not those induced by PGE2. The magnitude of antagonism depended on the dose of PPP and on the time of the pretreatment before PGF2alpha administration. Changes in the level of biogenic amines in discrete brain areas evoked by PGs were not affected by PPP. We found that PPP antagonizes the central effects of PGF2alpha but not those of PGE2, and that changes of biogenic amines in discrete brain areas elicited by PGs are not specific.

Animals↗
PubMed1976

Central action of prostaglandin F2alpha on circulatory system in rats.

PGF2alpha administered into the lateral brain ventricle of anesthetized rats caused an increase of the blood pressure and heart rate. Reserpine, chemical sympathectomy of the CNS with 6-hydroxydopamine (6-OHDA), atropine, and vagotomy weakened the central action of PGF2alpha on the peripheral circulation. Propranolol and phenoxybenzamine exerted no influence. Neither reserpine nor 6-OHDA changed the influence of iv injected PGF2alpha on the circulation. The results of the experiments indicate to the participation of the central catecholamines in the mechanism of central action of the PGF2alpha on the circulatory system.

Animals↗
PubMed1976

The influence of central chemical sympathectomy and reserpine on peripheral effects of noradrenaline and cyclic AMP dibutyrate injected into the cerebral ventricles.

Chemical sympathectomy of the central nervous system by injection of 6-hydroxy-dopamine (2 X 250 mug) or 6-hydroxydopa (90 mug) intensified some of the peripheral effects of noradrenaline and cyclic AMP dibutyrate injected into the cerebral ventricles. Reserpine (5 mg/kg) injected intraperitoneally weakened the peripheral reactions to noradrenaline injected intraventricularly. The results of the experiments indicate that peripheral reactions to intraventricularly injected noradrenaline depend on changes in the content of endogenous narodrenaline in the brain and on the mechanisms leading to these changes.

Animals↗
PubMed1975

Action of biogenic amines injected intracerebrally on duration of hexobarbital-induced sleep in rats.

The influence of intracerebrally injected biogenic amines and cyclic AMP dibutyrate on duration of sleep induced with hexobarbital (50 mg/kg i.v.) in rats was studied. Duration of sleep was markedly prolonged by adrenaline, noradrenaline, dopamine, 5-hydroxydopamine and acetylcholine. Cyclic AMP dibutyrate injected 30 minutes before hexobarbital shortened time of sleep. The role of biogenic amines in hexobarbital-induced sleep is discussed.

Acetylcholine↗