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Biomedical subjects

R Szkilnik

Publications and source records attributed to R Szkilnik.

8 recordsLinked to original sources

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

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

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

Influence of 6-hydroxydopamine on the behavioral effects induced by apomorphine or clonidine in rats.

The aim of this paper is to examine if central chemical sympathectomy induced by two injections of 6-hydroxydopamine (6-OHDA) in a dose of 250 mug intracerebroventricularly (i.c.v.) affects behavioral phenomena elicited by apomorphine (AP) (1 or 1.2 mg/kg i.p.) or clonidine (CL) (0.1 MG/KG, 5 Or 1 mug/kg i.p.). Experiments were carried out on male Wistar rats. The time of duration of several components of behavior and the degree of irritability of rats were measured. Moreover, open field and hole test were performed. The lower dose of AP did not affected behavior of rats. The higher dose increased the locomotor and exploratory activity of animals. 6-OHDA potentiated these effects of AP. CL (0.1 mg/kg) had a depressive effect on the rats' behavior, which was potentiated by 6-OHDA. CL (5 mug/kg) had no effect on the rats' behavior, but in a dose of 1 mug/kg caused excitatory behavior. This type of behavior was abolished by 6-OHDA. In conclusion, central chemical sympathectomy caused increased sensitivity of the central nervous system on AP. Excitatory behavioral effects of CL in low dosage may be connected with stimulation of central adrenergic receptors. Depressive behavioral effect of CL in high dosage is unspecific. Central chemical sympathectomy affects by different methods the reactivity of dopaminergic and noradrenergic neurons.

Animals

5-hydroxydopamine, unspecific centrally acting false neurotransmitter.

5-hydroxydopamine, unspecific centrally acting false neurotransmitter. Acta Physiol. Pol., 1977, 28 (1): 13-22. 3,4,5-trihydroxyphenetylamine-5-hydroxydopamine (5-OHDA) injected intracerebro-ventricularly decreases the level of noradrenaline, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in different parts of the rat brain. It does not affect acetylcholine level. 5-OHDA causes dose-dependent hypothermia, transient hypertension and depression of locomotor and exploratory activity in rats. This behavioral phenomena are reversed by central chemical sympathectomy elicited by 6-hydroxydopamine. It is concluded that 5-OHDA is an unspecific centrally acting false transmitter.

Animals