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Biomedical subjects

J Knauber

Publications and source records attributed to J Knauber.

6 recordsLinked to original sources
PubMed2003

Anseculin improves passive avoidance learning of aged mice.

Anseculin is a new coumarine derivative with promising cognition improving properties. We investigated its possible effects on passive avoidance learning in young and aged mice and the possible relationship to its alpha(1)-antagonistic properties.A single dose of anseculin did not affect long-term memory of young and aged mice. Moreover, in young mice, subchronic treatment with anseculin had no effect on cognitive functions, whereas aged, cognitively impaired mice clearly showed improved long-term memory with no effects on short-term memory. Further biochemical studies of aged control mice showed in comparison to the young mice a significant decrease of central alpha(1)-adrenoceptors density, but unchanged alpha(1)-adrenoceptor-mediated IP hydrolysis. Subchronic treatment with anseculin had no effect on the density of central alpha(1)-adrenoceptors in young adult mice and only a small although not significant effect on the density of cognitively-impaired aged mice. Furthermore, anseculin has no effects on alpha(1)-adrenoceptor-mediated IP hydrolysis.

Aging↗
PubMed2000

Subchronic treatment with prazosin improves passive avoidance learning in aged mice: possible relationships to alpha1-receptor up-regulation.

While many evidences indicate that deficits of central noradrenergic neurotransmission are involved in the age-related decline of cognitive functions in animals and man, very little is known about the specific role of central alpha1-adrenergic receptors. Therefore, this problem was specifically addressed in the present communication using the alpha1-adrenoceptor antagonist prazosin as pharmacological tool. While the acute administration of prazosin did not affect passive avoidance learning of young or aged mice, an improvement of learning capabilities was seen after subchronic treatment, but for the aged animals only. An U-shaped dose response curve was seen. 0.3 mg/kg prazosin was most effective. Very interestingly, only for this dose a significant up-regulation of the density of alpha1-adrenoceptors in the mouse brain was found in the aged animals only. The data suggest a possible causal relationship between effects of prazosin on passive avoidance learning and central alpha1-receptor density.

Adrenergic alpha-Antagonists↗
PubMed2000

Decreased exploratory activity and impaired passive avoidance behaviour in mice deficient for the alpha(1b)-adrenoceptor.

There is growing evidence that a dysfunction of central noradrenergic neurotransmission is involved in age-related impairments of cognitive performance and the pathophysiology of Alzheimer's disease (AD). A reduction of density of central alpha(1)-adrenergic receptors (alpha(1)-AR) has been shown in aging and AD brains. Three alpha(1)-AR subtypes (alpha(1a), alpha(1b) and alpha(1d)) have been identified by molecular cloning. However, very little is known about the functional role of distinct alpha(1)-AR subtypes in the brain. This problem was specifically addressed using a model of knockout mouse deficient in alpha(1b)-AR (alpha(1B)-/-) because these animals show a 40% reduction of alpha(1)-AR density in the brain as already reported. In comparison to the wild-type mice (alpha(1B)+/+), alpha(1B)-/- mice showed significantly reduced square entries and a reduced rearing behaviour was observed over all sessions in the open field. In passive avoidance procedures, alpha(1B)-/- mice showed a tendency towards decreased short-term-latency and a significant decline in long-term-latency. The present results indicate that mutation of a single member of the alpha(1)-AR gene family creates a distinct phenotype and provide evidence that alpha(1B)-AR is possibly involved in modulation of memory consolidation and fear-motivated exploratory activity. Furthermore, this model of knockout mice may be useful in elucidating the role of alpha(1B)-AR in dementias involving deficits of the noradrenergic system.

Animals↗
PubMed1999

Modulation of striatal acetylcholine concentrations by NMDA and the competitive NMDA receptor-antagonist AP-5: an in vivo microdialysis study.

The effects of local perfusion with the competitive NMDA receptor antagonist 2-amino-5-phosphonovalerate (AP-5) and the glutamate receptor agonist N-methyl-D-aspartate (NMDA) on release of extracellular acetylcholine (ACh) and choline (Ch) in the dorsolateral striatum were studied using in vivo microdialysis in freely moving rats. AP-5 caused a dose-dependent decrease in ACh release that was counteracted by the addition of NMDA. Perfusion with AP-5 also decreased Ch levels. Local perfusion with NMDA induced an elevation of ACh release in low (10(-5) M), but not high (10(-2) M and 10(-3) M) concentrations, that were associated with massive cellular death. These inhibitory effects of AP-5 and the stimulatory effect of NMDA in non-neurotoxic dosages on ACh release provide further evidence for a tonic stimulation of striatal cholinergic interneurons by glutamatergic neurons via NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1992

A new case of Zimmermann-Laband syndrome with atypical retinitis pigmentosa.

This paper reports a case study of a 10-year-old girl exhibiting symptoms of a Zimmermann-Laband syndrome (ZLS), including an ocular involvement not previously observed. In addition to the case reported, we have also discovered 21 patients described in the literature. Major clinical findings, defined as being present in more than 75% of the cases under discussion, are presented.

Child↗