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C Wustmann

Publications and source records attributed to C Wustmann.

At least 19 recordsLinked to original sources
PubMed1992

Effects of postnatal ganglioside administration and hypoxia-exposure on the dopamine release from striatal slices, the behaviour and the ganglioside pattern of 2-3 months old rats.

Neonatal rats were injected with a mixture of bovine brain gangliosides (30 mg/kg body weight, s.c.) immediately before the exposure to hypoxia (pO2 = 10 kPa, 10 hrs daily) from the 2nd to the 11th day of life. At the age of 2-3 months the potential protective or restitutive effect of gangliosides on the radiolabelled dopamine release from striatal slices and on the conditioned avoidance learning was studied. No change in the content and the pattern of gangliosides of the rat striata was found after exposure to hypoxia and ganglioside administration, respectively. Both hypoxia exposure and ganglioside treatment of controls increased the dopamine release whereas hypoxic animals treated with gangliosides showed a diminished release. Hypoxia-induced impaired conditioned avoidance learning was improved by ganglioside treatment. The changed release of dopamine and the altered behavioural performance after ganglioside treatment alone indicate the necessity of a very cautious application of gangliosides to the developing brain.

Aging↗
PubMed1990

Effect of 2-mercapto-ethanol on some brain biochemical characteristics and behavioural changes in the ageing CBA/Ca mice.

Male CBA/Ca inbred mice were treated with a dose of 8 micrograms 2-mercapto-ethanol per animal per day in the drinking water from the age of 5 months onwards up to the age of 24 months. Dopamine release was greatly decreased in old animals in contrast to the elevation of dopamine release in the treated mice. Similarly, an elevated malondialdehyde content in brain homogenates was also observed in the aged treated animals compared with their controls. No essential differences were observed in locomotor activity and learning between treated an control mice.

Aging↗
PubMed1990

Effect of 2-mercaptoethanol on posthypoxic and age-related biochemical and behavioural changes in mice and rats.

2-Mercaptoethanol (2-ME) has a beneficial effect on the mean life span of laboratory rodents. This paper deals with the effects of 2-ME on changes of dopamine release from brain slices of old aged or hypoxia exposed mice and rats. The results were compared with data which reflect spontaneous peroxidation of brain lipid constituents. In addition, adequate behavioural properties were studied. Long-term 2-ME treatment for months abolishes the age-related decrease of transmitter release and prevents changes in malondialdehyde formation. If age-dependent release failure is already established, then neither single high doses of 2-ME nor repeated treatment for 3 weeks are effective. Posthypoxic release inhibition is prevented by a 2-ME pretreatment for 3 weeks but not by an acute single application even at high dosages. The preventive effect of 2-ME is a mediated one rather than an immediate direct action. Age-related behavioural deficits, such as locomotor activity, habituation performance and learning ability, do not reflect any effect of 2-ME long-term treatment.

Aging↗
PubMed1990

Influence of nootropic drugs on the age-dependent potassium-coupling of transmitter release.

The potassium-induced dopamine release from rat striatum slices shows an age-dependent decline comparable to observations after hypoxia. Pretreatment of aged animals with antihypoxically active nootropic drugs for three weeks results in an improvement of the impaired transmitter release. Simultaneously the slope of the stimulus-release relation is increased and an age-related 50% decrease of the high affinity Ca(++)-ATPase activity (brain P2 fraction) is partially compensated. Like the antihypoxic effect, the effectiveness of nootropic drugs regarding age-dependent changes of neuronal functions probably will consist, above all, in vascular influences of the microcirculation, repair of phospholipids damaged by free radical triggered peroxidation and improvement of stimulus-release coupling.

Aging↗
PubMed1989

The antihypoxic effect of ethymisole: a comparison with other nootropic drugs.

Ethymisole reveals a potent antihypoxic effect which is produced probably both by an acute free radical scavenging property and a persisting restitutive component of action. This is seen in its effect on posthypoxic inhibition of dopamine release from striatum slices of adult rats. Though ethymisole is considered a drug which increases brain adaptive potency, it does not modify the stimulus-response relation of potassium-evoked dopamine release in an adaptation-like manner, as it is seen after a long-lasting piracetam treatment.

Animals↗
PubMed1989

Influence of hypoxia on the age dependent stimulus-effect-relation of K+-induced dopamine release from rat brain structures.

There is a well defined correlation between stimulus intensity (potassium concentration) and the so-called fractional efflux rate of radio-labelled neurotransmitter from loaded brain structures. K+-induced dopamine release shows an age-dependent parallel shift of the stimulus-effect-relation which obviously reflects quantitative developmental changes during maturation (increasing release) and involution (restricted release) of neuronal structures and functions without modification of involved mechanisms in a qualitative manner. On the other side, mild hypoxia results in quite different, even opposite changes of the stimulus-effect-relation exhibiting the most diverse vulnerability and reactivity of neuronal stimulus-release-coupling at different age.

Aging↗
PubMed1989

Effect of pyritinol on the dopaminergic system and behavioural outcome in an animal model of mild chronic postnatal hypoxia.

Rats after mild chronic postnatal hypoxia always show late sequelae of behaviour and long-term alterations of neurotransmitter release from striatal slices. It was to test preventive or therapeutic actions of drugs using the model of mild chronic postnatal hypoxia of the rat. Pyritinol prevented the learning deficit due to hypoxia and decreases the potassium stimulated DA release from striatal slices. The experiments underline the high plasticity of the CNS during the neonatal period and stress the necessity of early therapy of perinatal brain damage.

Animals↗
PubMed1989

New aspects in mechanisms of antihypoxic piracetam action.

A long-term piracetam treatment leads to an improved stimulus-effect-coupling of potassium stimulated dopamine release: The maximum effect of the potassium stimulus is already obtained in presence of much lower Ca++-concentrations (Ca++-economizing effect) than normally. In consequence of the improved stimulus-effect-coupling by piracetam treatment the dose-dependent inhibitory effect of the calcium antagonist flunarizine on the fractional efflux rate of dopamine is decreased. The volume of vesicular structures is not involved in the piracetam effect.

Animals↗
PubMed1989

Antihypoxic effects of AWD 23-15 in mice and rats.

AWD 23-15 (6-Methyl-1,2,3,4-tetrahydro-pyrimidin-2,4 dion) which is known to improve learning and memory processes in laboratory animals, was investigated in several hypoxia models. The following results were obtained: 1. Increase of survival rate, 2. change in hypoxia-induced decrease of cerebral post-mortem adenylic energy charge and in concentrations of metabolic products in the brain and 3. antagonism of the hypoxia-induced decrease of dopamine release. However in the general behavioral test the drug was ineffective. These results support the idea that AWD 23-15 is a potential nootropic drug.

Adenine Nucleotides↗
PubMed1987

Respiratory function of rat brain mitochondria after hypobaric hypoxia and piracetam treatment.

After an acute hypobaric hypoxia the mitochondrial respiratory control index is reduced in consequence of a decreased active-state respiration. The finding is paralleled by decreased uncoupled respiration and a not significantly changed resting-state respiration. Long term hypoxic exposures show adaptive traits of this criterion of mitochondrial energy metabolism. The antihypoxic effect of piracetam may be reflected in a delayed normothermic in vitro aging of mitochondrial suspension.

Animals↗
PubMed1987

The influence of social isolation, hypoxia and immobilization on potassium-stimulated dopamine release from telencephalon slices of mice.

Dopamine release from mice telencephalon slices was investigated following immobilization or hypobaric hypoxia exposure during periods of social isolation of different length which itself affects dopamine release in a characteristic manner. Isolation initially results in a decreasing release, which is compensated at the end by adaptive processes. The decrease of dopamine release induced by immobilization is highly dependent on the foregoing isolation. On the other hand, a hypoxia-induced decrease of release always dominates the results. Adaptive processes in consequence of social isolation are supposed to be important in relation to immobilization effects but not to hypoxia-induced changes.

Adaptation, Physiological↗
PubMed1987

[ATP-metabolizing enzymes in suspensions of isolated coupled rat brain mitochondria].

An improved method for the isolation of rat brain mitochondria is described. The preparation exhibits a respiratory control index (RCI) of 6 or 7.3 in the presence of pyruvate and malate or glutamate and malate, respectively. RCI decreases to 2.5 in the presence of Mg++. When the phosphorylation of extramitochondrially added or formed ADP is suppressed by carboxyatractyloside (CAT) inhibition of the adenine nucleotide translocator, the remaining respiration amounts to 6 nmol O2/min X mg mitochondrial protein. These results and the ratio of 16 to 19 from the quotient of phosphorylating active-state respiration to CAT inhibited respiration refer to a high degree of mitochondrial coupling of respiration. Therefore the remaining respiration in the presence of Mg++ is due to a phosphokinase activity located outside the inner membrane of intact mitochondria or at nonphosphorylating mitochondrial fragments. The following activities were observed: Oligomycin sensitive ATPase, 47 mU/mg protein; hexokinase, 272 mU/mg protein; creatinphosphokinase, 116 mU/mg protein; and a surprisingly low activity of adenylatekinase, 57 mU/mg protein.

Adenosine Monophosphate↗
PubMed1987

Inhibition of stimulated dopamine release from striatum slices after hemorrhagic shock in the rat. Protective effect of piracetam.

The antihypoxic effect of piracetam was studied using a hemorrhagic shock model in the rat. Different shock severity was achieved by bleeding of 35% or 50% of estimated blood volume (EBV). Hemorrhagic shock caused an inhibition of K+ induced dopamine release from striatum slices in proportion to the magnitude of hemorrhage, reflecting the degree of membrane damage in dopaminergic transmission structures. Piracetam was effective in preventing the post-hemorrhagic changes in moderate shock and accelerated restitution of post-hemorrhagic release inhibition in severe shock.

Animals↗
PubMed1986

Postnatal administration of L-dopa normalizes hypoxia-induced long-term changes in dopamine release from striatum slices and in avoidance learning.

Newborn rats exposed to a mild chronic postnatal hypoxia always displayed at the age of 2-3 months an increased fractional efflux rate of dopamine (DA) from striatum slices combined with a decreased capacity for learning and retention. The protective effect of the administration of L-DOPA on these long-term changes was tested by the injection of L-DOPA 5-30 min prior to the beginning of daily exposure to hypoxia. L-DOPA administration during postnatal hypoxia prevents in a dose dependent manner the long-term effects of postnatal hypoxia as described. This finding supports the hypothesis that long-term changes in DA release and in behaviour due to early postnatal hypoxia may be brought about by changes in the DA-metabolism during a critical period of development.

Animals↗
PubMed1986

Protective and restitutive effects of antihypoxic drugs on posthypoxic dopamine release inhibition.

Exposure of rats to hypoxia results in a substantial decrease of dopamine release from striatum slices for several days. Nootropic drugs (piracetam, meclofenoxate hydrochloride, methylglucamine orotate, nicergoline) accelerate the restitution of posthypoxic release inhibition. In contrast, amphetamine is ineffective in this respect. The antihypoxic action of sedatives (diazepam, phenobarbital) prevents the decrease of dopamine release. Comparable results with free radical scavengers (cysteamine hydrochloride, sodium formiate, ouabain), ascorbic acid, natrii calcii edetas, selenium methionine and acetylsalicylic acid which protect dopamine release from hypoxically produced changes agree with and support the hypothesis of hypoxia induced free radical generation followed by phospholipid peroxidation altering particularly neuronal membrane function. On that account, dopamine release from rat striatum slices reflects not only the vulnerability of neuronal membrane function by hypoxia but also the preventive, protective and restitutive effects of antihypoxic drugs of different type and is able to contribute to discriminating drug investigation.

Amphetamine↗
PubMed1986

The vulnerable period of perinatal hypoxia with regard to dopamine release and behaviour in adult rats.

The relations between a perinatal exposure schedule and the outcome of dopamine (DA) release from striatum slices on the one hand and behaviour on the other, were studied in order to identify the vulnerable period. A mild chronic postnatal hypoxia (2nd-10th day of life) induces long-term effects on the DA release rate (FER) from striatum slices. A 10 h daily exposure to hypoxia for 5 days (2nd-6th day of life) induces the same long-term effects. Adult rats exposed to hypoxia (pO2 8.6 kPa) for 16 h respond with a drastic decrease of FER of DA. Exposure to early postnatal hypoxia prevented this drastic decrease of FER of DA when adult rats were again exposed to hypoxia. 3 ten h periods of hypoxia within the first 10 days of life were enough to the long lasting effects. Prenatal hypoxia as well as hypoxia during the adolescent period did not show any long-term effects on the dopaminergic system. Alterations in behaviour (decreased learning capacity as well as decreased reaction to stimuli after prolonged stress in adulthood) were found after 3-9 days of hypoxia between the 2nd and 10th day of life.

Aging↗
PubMed1986

Effects of nootropic drugs on some behavioural and biochemical changes after early postnatal hypoxia in the rat.

Piracetam (PIR) and dimethylaminoethanol (DMAE) were tested with respect to their ability to prevent changes of the locomotor behaviour and of the dopamine release from striatum slices after an intermittent postnatal hypoxia in the rat (2nd-10th day of postnatal life). The drugs given to pregnant rats (from 12th day of gestation) and continued after delivery to the newborns (till 10th day of postnatal life) displayed antihypoxic effects. Perinatal DMAE- but not PIR-treatment diminishes the consequences of postnatal oxygen deprivation regarding the motor activity as well as the dopamine release of adult animals. Hypoxia-caused open field hyperactivity of developing rats was found to be reduced to control values in PIR-treated rats. Only minor effects were seen after DMAE-treatment, but a marked depressant own effect on the explorative activity was detectable.

Animals↗