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R Lamprecht

Publications and source records attributed to R Lamprecht.

10 recordsLinked to original sources
PubMed1999

CREB: a message to remember.

The prevailing hypothesis for the formation of long-term memory (LTM) is that introduction of a memory item alters the pattern of existing neuronal connectivity to form a neuronal network that will subserve the information for long-term storage. Modulation of synaptic efficacy is induced by changes in synaptic transmission within selected synapses or alteration in synaptic contacts. These changes are in turn supported by molecules that underlie transmission or synaptic remodeling. It is suggested that modulation of gene expression is needed for LTM formation to overcome the relative short lifetime of proteins in neurons (as compared with enduring memory). One of the most salient results consonant with this hypothesis is that the transcription factor cAMP response element binding (CREB) is involved in the formation of memory in organisms with diverse phylogenetic background from mollusks to mammals. CREB subserves the formation of memories of various types of tasks that utilize different brain structures. Circumstantial evidence is available suggesting that CREB regulates the transcription of genes that subserve LTM. The present review is focused on the CREB protein, its role in memory formation and considers mechanistic models pertaining to CREB action in modulating neuronal networks that underlie LTM.

Animals↗
PubMed1998

Fatal chloroquine intoxication.

A suicidal ingestion of an unknown quantity of Resochin (chloroquine) tablets is described. Although chloroquine is known since 1934, intoxications due to chloroquine overdose are rather rare in European countries. The authors report on a new and fast method of analysing and determining the chloroquine concentration in body fluids and postmortem specimens. The analytes were extracted from alkalinized samples into ethyl acetate before GC/MS analysis. The analyses of chloroquine were performed without any complex sample clean-up steps and, in addition, with little sample material. The proposed method resulted in a rapid procedure most useful in cases of deliberate poisoning with the anti-inflammatory and antimalarial drug chloroquine.

Adult↗
PubMed1997

cAMP response element-binding protein in the amygdala is required for long- but not short-term conditioned taste aversion memory.

In conditioned taste aversion (CTA) organisms learn to avoid a taste if the first encounter with that taste is followed by transient poisoning. The neural mechanisms that subserve this robust and long-lasting association of taste and malaise have not yet been elucidated, but several brain areas have been implicated in the process, including the amygdala. In this study we investigated the role of amygdala in general, and the cAMP response element-binding protein (CREB) in the amygdala in particular, in CTA learning and memory. Toward that end, we combined antisense technology in vivo with behavioral, molecular, and histochemical analysis. Local microinjection of phosphorothioate-modified oligodeoxynucleotides (ODNs) antisense to CREB into the rat amygdala several hours before CTA training transiently reduced the level of CREB protein during training and impaired CTA memory when tested 3-5 d later. In comparison, sense ODNs had no effect on memory. The effect of antisense was not attributable to differential tissue damage and was site-specific. CREB antisense in the amygdala had no effect on retrieval of CTA memory once it had been formed, and did not affect short-term CTA memory. We propose that the amygdala, specifically the central nucleus, is required for the establishment of long-term CTA memory in the behaving rat; that the process involves long-term changes, subserved by CRE-regulated gene expression, in amygdala neurons; and that the amygdala may retain some CTA-relevant information over time rather than merely modulating the gustatory trace during acquisition of CTA.

Amygdala↗
PubMed1997

NMDA receptor and the tyrosine phosphorylation of its 2B subunit in taste learning in the rat insular cortex.

We demonstrate that the NMDA receptor is involved in taste learning in the insular cortex of the behaving rat and describe two facets of this involvement. Blockage of the NMDA receptor in the insular cortex by the reversible antagonist APV during training in a conditioned taste aversion (CTA) paradigm impaired CTA memory, whereas blockage of the NMDA receptor in an adjacent cortex or before a retrieval test had no effect. When rats sampled an unfamiliar taste and hence learned about it, either incidentally or in the context of CTA training, the tyrosine phosphorylation of the NMDA receptor subunit 2B (NR2B) in the insular cortex was specifically increased. The level of tyrosine phosphorylation on NR2B was a function of the novelty of the taste stimulus and the quantity of the taste substance consumed, properties that also determined the efficacy of the taste stimulus as a conditioned stimulus in CTA; however, blockage of the NMDA receptor by APV during training did not prevent tyrosine phosphorylation of NR2B. We suggest that tyrosine phosphorylation of NR2B subserves encoding of saliency in the insular cortex during the first hours after an unfamiliar taste is sampled and that this encoding is independent of another, necessary role of NMDA receptors in triggering experience-dependent modifications in the insular cortex during taste learning. Because a substantial fraction of the NR2B protein in the insular cortex seems to be expressed in interneurons, saliency and the tyrosine phosphorylation of NR2B correlated with it may modulate inhibition in cortex.

Animals↗
PubMed1996

Population genetic study of the AmpFLP system APO B in an Austrian population sample.

Allele frequencies of the AmpFLP system APO B were determined in an Austrian population sample consisting of 210 unrelated Caucasian individuals living in the Salzburg region. A total of 25 different alleles could be observed. The allele distributions were in accordance with Hardy-Weinberg equilibrium. No new mutations were found in 184 meioses and seven "interalleles" and four alleles < 29 could be detected.

Alleles↗
PubMed1995

Differential modulation of brain immediate early genes by intraperitoneal LiCl.

We have used in situ hybridization to investigate the modulation of expression of the immediate early genes (IEGs) c-fos, fos-B, zif/268 and CREM in rat brain following oral administration of saccharin, i.p. injection of LiCl, and conditioned taste aversion (CTA) training in which these stimuli are used as the conditioned stimulus (CS) and the unconditioned stimulus (UCS), respectively. Modulation of c-fos, zif/268 and CREM was detected in the NTS, PBN, hypothalamic PVN and central nucleus of the amygdala after the administration of the UCS but not the CS. Our data are consonant with the hypothesis that differential and combinatorial expression of IEGs plays a role in encoding the representation of LiCl-induced malaise in the brain.

Animals↗
PubMed1992

Regulated coupling of the Neu receptor to phosphatidylinositol 3'-kinase and its release by oncogenic activation.

The neu protooncogene encodes a tyrosine kinase receptor that is involved in the regulation of normal growth and malignant transformation. To circumvent the use of the incompletely characterized ligand of Neu, we constructed a chimeric protein composed of the ligand-binding domain of the epidermal growth factor receptor and the transmembrane and cytoplasmic portions of Neu. By expressing this Neu-epidermal growth factor receptor chimera (termed NEC), we found that following stimulation by the heterologous ligand, the tyrosine kinase of Neu became associated with a phosphatidylinositol (PI) kinase activity. The association was dependent on the concentration of the ligand and was almost maximal within 30 s after ligand binding. The lipid kinase was identified as a type I PI 3'-kinase on the basis of its inhibition by Nonidet P-40 and high pressure liquid chromatography of the phosphorylated product. To confirm the identification of PI 3'-kinase as an effector of Neu, we raised antibodies to the alpha-isoform of the regulatory subunit of PI 3'-kinase (p85). Using these antibodies, it was possible to directly demonstrate ligand-dependent formation of a tyrosine-phosphorylated complex of NEC and PI 3'-kinase. Apparently, both PI 3'-kinase and phospholipase C gamma, another substrate of the Neu kinase, simultaneously associated with the same activated NEC molecule. Nevertheless, immunofluorescence localization of PI 3'-kinase revealed no significant cellular redistribution of the enzyme after activation of the Neu kinase. Interestingly, PI 3'-kinase was localized primarily to the cell nucleus and to confined regions of the plasma membrane. Analysis of mutants of the Neu protein indicated that the oncogenic point-mutated Neu (Glu664) was permanently coupled to PI 3'-kinase; but two nontransforming versions of the oncoprotein, a kinase-defective protein and a carboxyl-terminally deleted Neu, were devoid of the constitutive association with PI 3'-kinase. Hence, we concluded that phosphatidylinositol 3'-kinase is a physiological substrate of the Neu receptor, but the regulation of this coupling is released upon oncogenic activation.

1-Phosphatidylinositol 4-Kinase↗
PubMed1992

[Suspected SIDS diagnosis--van Praagh I truncus communis as a nonfatal incidental finding].

Autopsy of a baby suspicious to SIDS. Most interesting postmortem finding was a congenital malformation of the great vessels, a truncus arteriosus communis typus van Praagh A I. That one is very rare with a clinically frequency of only 1.7%. The malformation was not cause of death and was statistically survived for 2 months. The baby died of aspiration resultant from an incarcerated inguinal hernia.

Asphyxia↗
PubMedDate not supplied

Transient expression of c-Fos in rat amygdala during training is required for encoding conditioned taste aversion memory.

Local microinjection into rat amygdala of phosphorothioate modified oligodeoxynucleotides (ODNs) antisense to c-fos several hours before conditioned taste aversion (CTA) training impaired taste aversion memory tested 3-5 days after conditioning. In contrast, injection of the antisense ODNs several days before training, before testing, or into the basal ganglia, or injection of c-fos sense ODNs, had no effect on CTA memory. Inhibition of translation by local microinjection of anisomycin into the amygdala shortly before as well as during CTA training, but not several days before training or shortly before testing, also impaired CTA memory. We conclude that translation in general, and c-Fos translation in particular, in the amygdala during or immediately after CTA training is essential for encoding taste aversion memory.

Amygdala↗