Biomedical subjects

E Rudolph

Publications and source records attributed to E Rudolph.

17 recordsLinked to original sources

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↗

PubMed1990

[Characterization and pharmacological effect on brain damage as a result of cold injury].

Freezing lesion of brain damages the blood-brain-barrier and induces edema. Both injuries are partially separate processes with different progress and diverse response to pharmacological treatment. A very weak lesion fails in to induce edema despite of an enhanced permeation of Evans blue. The injured permeability responds to treatment with dexamethasone or piracetam whereas the edema does not.

Animals↗

PubMed1990

[Initial experiences with the Coping Questionnaire for measuring changes in adjustment within the scope of psychotherapy treatment].

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Adaptation, Psychological↗

PubMed1989

Adaptive changes in the central noradrenergic system in monocular deprived rats.

Noradrenaline and dopamine content, K+-stimulated release of 3H-noradrenaline, 3H-noradrenaline high-affinity uptake, 3H-prazosin and 3H-rauwolscine binding to alpha 1- and alpha 2-adrenoreceptors, respectively, were studied in isolated visual structures (visual cortex, superior colliculus, lateral geniculate nucleus) of three-month-old rats monocularly deprived by unilateral eyelid closure at postnatal day 11. Monocular deprivation resulted in a number of changes in comparison with normal littermates, mainly in the lateral geniculate nucleus, both ipsilateral and contralateral to the closed eye. K+-stimulated release of noradrenaline and high-affinity noradrenaline uptake were significantly increased, 3H-rauwolscine binding to alpha 2-adrenergic receptor sites was decreased in the contralateral and ipsilateral lateral geniculate nucleus. 3H-Prazosin binding to alpha 1-adrenergic receptors as well as the levels or noradrenaline and dopamine in the lateral geniculate nucleus were unaffected by monocular deprivation. The data support the suggestion that the lateral geniculate nucleus plays a key role in modulating visual information processing and that the lack of an adequate visual input within the first weeks of life interferes mainly with the development of the noradrenergic system at the level of the lateral geniculate nucleus.

Animals↗

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

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↗

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↗

PubMed1978

[Superfusion technique for studying the in vitro release of putative neurotransmitters from brain structures].

The superfusion technique described enables a stimulus synchronous observation of release mechanisms by reason of the size of the perfusion chamber and by the arrangement of the medium supply. The presentation of the results allows a quantitative comparison of releasing activity also in case of different chemical or electrical stimulation conditions.

Amphetamine↗

PubMed1976

Effect of arecoline on synaptosomal K+-phosphatase and (Na+ + K+)-ATPase.

Synaptosomal fractions and synaptosomal membranes from rat brain tissue were prepared and characterized enzymatically. Arecoline increased both the activity of K+-phosphatase in incubated synaptosomal fractions and the (Na+ + K+)-ATPase activity of synaptosomal membranes by 40% and 78%, respectively. This activation of ion transport processes is believed to be associated with increased ACh synthesis produced by arecoline.

Acetylcholine↗

PubMed1975