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C Wustmann

Publications and source records attributed to C Wustmann.

29 records · Page 2Linked to original sources
PubMed1985

Posthypoxic transmitter release from brain slices and behavioural consequences of hypoxia in rats and mice.

Subsequent to a hypoxic exposure of adult rats and mice the stimulus induced release of dopamine from striatum slices is inhibited for several days. The posthypoxic release inhibition is not restricted to the striatal dopaminergic transmission system especially, but hypoxia causes comparable changes also in other brain regions regarding further transmitter systems. The transmitter release inhibition reflects a significant caudo-rostral gradient of increasing vulnerability of phylogenetically younger brain regions. The consequences of these biochemical changes in the brain following cessation of hypoxia are investigated with regard to behavioural manifestations. Corresponding in time with the inhibition of transmitter release and its restitution the seizure susceptibility is increased when pentetrazol is given in subconvulsive doses. On the other hand, the results of further tests (climbing behaviour, open field, rotarod test, forced-swimming test) do not point to behavioural changes induced particularly by a mild hypoxia.

Animals↗
PubMed1985

Characterization of the antihypoxic activity of tisochromid.

The antihypoxic activity of tisochromid is compared with the well-known restituting effect of piracetam on posthypoxic dopamine release inhibition. In addition to a distinct restituting effect which accelerates the normalization of dopamine release highly, tisochromid exhibits obviously an antioxidative potency which is responsible for a greater effectiveness of the drug when given prehypoxically. Therefore, tisochromid acts simultaneously as a protective and a restituting drug.

Animals↗
PubMed1984

On some mechanisms of antihypoxic actions of nootropic drugs.

The antihypoxic effect of meclofenoxate hydrochloride seen in the accelerated restitution of posthypoxic dopamine release inhibition originates in the alcoholic component of the drug. Via choline dimethylaminoethanol might run, like orotic acid, into a CDP-choline pool, the generation of which is able to be facilitated by piracetam which in turn increases the phosphorylation potential. All these nootropic drugs will in this way increase the biosynthesis of hypoxically vulnerable phospholipids by different mechanisms. Indeed, a combined treatment with piracetam, meclofenoxate hydrochloride and methylglucamineorotate leads to a more rapid restitution of posthypoxic dopamine release inhibition than the drugs are active when applied separately.

Animals↗
PubMed1984

Effects of piracetam on brain development in newborn rats exposed to hypoxia.

Perinatal hypoxia is one of the main causes of disturbances of the function of the CNS during childhood. In this study the protective effect of the nootropic drug piracetam (oxo-2-pyrrolidinyl-1)-2-acetamide was tested. One-day-old Wistar rats were exposed together with their mothers to hypoxia up to the 10th day of life (11 h daily, pO2 = 9.86 kPa). On the 11th day a 48% decrease of body weight and a 30% decrease of brain weight was found in the hypoxic animals. The protein/DNA ratio and the AChE activity in the brain cortex were decreased indicating retarded brain development. Piracetam (daily 100 mg/kg, s. c., before hypoxic exposure) did not affect the mortality rate, the somatic development of the animals, or the estimated basic neurochemical markers in the cortex of the brain. At the age of 3 months the fractional efflux rate (FER) of dopamine (DA) evoked chemically or electrically as a characteristic functional feature of chemical synaptic transmission, was examined. It was found that postnatal hypoxia induces a long lasting increase of FER of DA of striatum slices. Animals exposed postnatally to hypoxia and treated with piracetam showed an increased FER of DA (potassium as stimulus) by comparison with those animals also exposed postnatally to hypoxia but left untreated with piracetam.

Animals↗
PubMed1984

Ethanol preference behaviour and dopamine release in the rat.

The development of ethanol preference behaviour in rats is connected with a decrease of dopamine release from striatum slices seen after alcohol cessation. The inhibition of dopamine release vanishes spontaneously within a few days. Restitution is highly accelerated by piracetam, exhibiting similarities to posthypoxic membrane damages.

Alcohol Drinking↗
PubMed1983

Dopamine release from striatum slices of rats at different age: influence of hypoxia.

During the maturation and aging of rats the dopamine release from striatum slices shows different dynamics in dependence on the stimuli used. Electrically evoked release is very constant. Amphetamine induced release is fully developed at the age of day 14 and declines after 9 months. The K+ stimulated release develops to a maximum at 10 weeks and decreases thereafter. The stimulus and age dependent inhibition of dopamine release after an 18 h hypoxic exposure may be the result of peroxidative reactions of membranous phospholipid components induced by free radicals. Adult rats exposed to a 200 h hypoxia reveal no change in dopamine release after the last exposure probably in consequence of adaptive processes of physiological protection, among other things, by scavenging of free radicals. Adult rats exposed to long term hypoxia postnatally during the growth spurt period of neuronal structures show an increased dopamine release and no posthypoxic release inhibition. Our data indicate that different mechanisms are operative during hypoxia in animals of different age.

Aging↗
PubMed1982

[Effect of nootropic drugs on the dopamine release and dopamine uptake in structures of the rat striatum].

Nootropics increase the overflow of dopamine from rat striatum slices in a concentration dependent manner, but without relation to their clinical effectiveness. The influence of a nootropic drugs and of amphetamine on the stimulus induced dopamine release points to a relationship between nootropic and nooanaleptic activity, on the one hand, and transmitter release, on the other. Dopamine re-uptake is not altered by nootropics like piracetam.

Animals↗
PubMed1982

Inhibitory effects of hypoxia on dopamine release.

Behavioral and neurochemical results refer to an impairment of the dopaminergic system produced by hypoxia. On that account we determined the chemically (K+, amphetamine) and electrically stimulated release of dopamine from rat striatum slices which were preloaded with labeled dopamine following the animals' exposure to hypobaric hypoxia. The effect of hypoxia consists in a marked inhibition of dopamine release depending both on the degree of hypoxia and on the kind of stimuli used. Dopamine release inhibition reflects not only the direct effect of hypoxia, which seems to be connected especially with the vesicular compartment, but also adaption and restitution processes. Regarding the effects on rats at the age of two weeks the resistance of young animals against hypoxia may be founded also upon missing vesicular mechanisms of distinct vulnerability.

Animals↗
PubMed1982

The effect of piracetam on posthypoxic dopamine release inhibition.

Subsequently to a hypoxic exposure of adult rats the stimulus induced release of dopamine from striatum slices in inhibited for several days. Depending on the treatment with piracetam the restitution of this inhibition is accelerated manifold, though piracetam does not prevent the acute effect of hypoxia on dopamine release. The particular hypoxia related vulnerability of the potassium evoked dopamine release and the time course of piracetam effect obviously point to drug induced anabolic processes rebuilding vesicle storage sites.

Amphetamine↗
PubMedDate not supplied

The influence of social isolation on ethanol preference behavior and dopamine release in telencephalon slices in mice.

We examined the relation between the duration of social isolation and alterations in ethanol preference behavior and the dopamine release in telencephalon slices in mice. Ethanol preference developed only after an isolation period of 2 weeks and a further ethanol treatment of 2 weeks. It did not appear after an isolation period of 6 weeks, in mice without ethanol treatment, and in group-housed mice. The dopamine release was lowered in mice isolated for 2 weeks and is normalized in combination with ethanol treatment. The dopamine release inhibition evoked by social isolation of 2 weeks probably reflects a functional state with high sensitivity for induction of an ethanol preference behaviour.

Animals↗