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Biomedical subjects

A Hamberger

Publications and source records attributed to A Hamberger.

At least 73 records · Page 4Linked to original sources
PubMed1991

Neuronal and glial marker proteins in the evaluation of the protective action of MK 801.

A quantitative dot immunobinding procedure was used to quantify glial [the S-100 protein and the glial fibrillary acidic (GFA) protein] and neuronal (the 68- and 200-kDa neurofilament polypeptides, neuron-specific enolase, and neuronal cell adhesion molecule) markers. A single intraperitoneal administration of 10 mg/kg of MK 801 blocked the increase of glial parameters and the decrease in content of neuronal marker proteins that occurred as the response to an N-methyl-D-aspartate (NMDA) lesion in the rat hippocampus. The degradation products of GFA protein and the 68-kDa neurofilament polypeptide that were induced by the NMDA lesion did not appear after MK 801 treatment. This study shows that brain-specific proteins are a set of precise tools for the evaluation of neuroprotective effects of antagonists to excitatory amino acids.

Animals↗
PubMed1990

The neurotoxicity of zinc in the rat hippocampus.

Intrahippocampal injections of zinc chloride (5-10 nmol) caused a discrete lesion in the rat hippocampus, involving all neuronal perikarya. In addition to the necrosis, the lesion was also characterized by a decrease in staining of the neuropil, the presence of pyknotic neurons, and occasionally infarction. Pathological changes occurred within 8 h of an injection, and neuronal loss, as judged by the loss of Nissl staining, was complete within 24 h. On the other hand, the loss of acidophilic staining of the neurons was more gradual, as acid fuchsin staining was still present in neurons in the periphery of the damaged area 4 days later. In comparison with an excitotoxic lesion, glial infiltration into the damaged area was minimal, even up to 3 weeks later, suggesting that some glial cell toxicity also occurred.

Animals↗
PubMed1990

The neurotoxicity of ouabain, a sodium-potassium ATPase inhibitor, in the rat hippocampus.

Intrahippocampal injection of 1 nmol ouabain, a sodium/potassium (Na+,K(+)-)ATPase inhibitor, produced a necrotic lesion within 4 days, characterised by a massive invasion by foaming macrophages. A lower dose of ouabain (0.1 nmol) produced a more discrete lesion of all groups of neuronal perikarya in the hippocampus, with only a minimal degree of glial infiltration. The neuronal perikaryal death produced in the subicular, CA1 and CA2 regions was only partially decreased by intraperitoneal injections of the anticonvulsants diazepam and MK-801; these drugs were without effect in the CA3 or hilar interneuronal regions. At neither dose of ouabain was there any indication of neuronal loss in brain regions outside the hippocampus, typically produced by prolonged seizure activity. It is suggested that ouabain has a two-fold action, a release of toxic acidic amino acids and a prolonged depolarization of neurons leading to osmolysis or calcium necrosis.

Animals↗
PubMed1990

Ketamine and MK801 attenuate paired pulse inhibition in the olfactory bulb of the rat.

We have investigated the effects of the phencyclidine like-compounds ketamine and MK801 on the evoked field potentials of rat olfactory bulb. Low doses of ketamine (3-6 mg/kg) blocked the inhibition of mitral cells by granule cells evoked by stimulation of lateral olfactory tract fibres or by stimulation of olfactory nerve. This blockade was not accompanied by a decrease in granule cell excitation as revealed by field potential recording. MK801 had a similar effect on the inhibition of mitral cells evoked by stimulation of the lateral olfactory tract. As ketamine does not influence the inhibitory action of GABA (Anis et al. 1983) these results suggest that both ketamine and MK801 block inhibition by an action on intrinsic excitatory feed-back circuits in the olfactory bulb.

Action Potentials↗
PubMed1990

The contribution from the choroid plexus and the periventricular CNS to amino acids and proteins in the human CSF.

During neurosurgery the freshly secreted extracellular fluid (ECF) from the choroid plexus was sampled with small pieces of application paper in three patients with intractable epilepsy. The samples were analyzed for free amino acids and for soluble proteins. The results were compared with corresponding data on extracellular fluid from the brain surface obtained with dialysis-perfusion as well as with the cerebrospinal fluid (CSF) acquired by lumbar punction. The dialysis data were calibrated against the paper results. The choroid plexus secretion had a high concentration of transthyretin as well as of an unidentified protein with an isoelectric point of 7.4. The cortical ECF exhibited high concentrations of tau-globulin and gamma-trace protein. Among the amino acids, glutamine had lower concentration in the choroid plexus secretion and higher concentrations in the ECF of the brain compared to the CSF. The amino acid derivative ethanolamine exhibited a similar pattern. This was interpreted to demonstrate that these compounds enter the CSF from the brain tissue. In contrast, alanine, serine, and taurine had a lower concentration in the CSF than in the plexus secretion which suggests that they are removed from the CSF by brain tissue.

Adolescent↗
PubMed1989

Liquid chromatographic separation of cerebrospinal fluid amino acids after precolumn fluorescence derivatization.

Sampling and HPLC analysis procedures for CSF amino acid determination were evaluated. It is recommended to analyse native CSF. The sample should be taken from the first 12 ml obtained by lumbar puncture. Amino acid concentrations are stable for short periods over a wide range of temperature however, storage at -70 degrees to -80 degrees C is recommended. With the precolumn derivatization and a 30 cm reverse-phase column, the separation and reproducibility are reliable for analyses in the daily hospital routine.

Adult↗
PubMed1988

Secretion of newly synthesized proteins into the extracellular fluid of the rabbit hippocampus.

Extracellular proteins were collected continuously from the hippocampus of the rabbit by slow perfusion of a protein-permeable thin tubing. After pulse labelling with radioactive amino acids via the tubing a rapid appearance of labelled proteins was seen in the extracellular fluid. The half-life of the proteins in the extracellular space varied between 15 min and 2 h. Protein fractions were separated with gel electrophoresis or HPLC. The extracellular fraction differed distinctly from intracellular proteins with respect to the labelling pattern.

Animals↗
PubMed1988

Changes in brain temperature and free amino acids in normal and protein deprived suckling rats exposed to room temperature.

Previous reports on early-induced protein-calorie malnutrition (PCM) in rats have indicated alterations in the concentration of free amino acids and of protein synthesis in the brain. Recently it was shown that early-induced protein deprivation (PD) retards the development of thermoregulation. This resulted in a failure to maintain a normal rectal temperature after short exposure to room temperature (+22 degrees C) still at the age of 20-25 days corresponding to changes seen in normal rats at an age of 10-15 days. In the present study, 20-day old PD and normal rats where examined with regard to the effect of exposure to room temperature on brain temperature and on brain free amino acids. The results show a similar reduction in brain and rectal temperature of the PD rats occurring within 30 minutes after exposure to room temperature. The reduction was in the range of 5 degrees C. PD rats kept in room temperature for 5 hours and then allowed to recover at 32.5 degrees C showed a slow increase in brain and rectal temperature but normal temperatures were not reached even after 1 hour. The concentration of free amino acids in the brain was examined in rats kept for 1 hour at room temperature or at 32.5 degrees C. In the PD rats kept at 32.5 degrees C, free aspartate and glutamate were reduced whereas taurine, GABA and glycine were increased as compared to their corresponding control rats. As a result of the reduced brain temperature in PD rats exposed to room temperature there was a reduction in free asparagine.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acids↗
PubMed1988

On the epileptogenic effects of kainic acid and dihydrokainic acid in the dentate gyrus of the rat.

The in vivo effects of the acidic amino receptor agonist, kainic acid and the inhibitors of the uptake of glutamate, dihydrokainic acid and threo-3-hydroxyaspartate, on spontaneous activity and perforant path evoked field potentials were examined in the dentate gyrus of the rat. The effect of these compounds on extracellular levels of endogenous amino acids in the hippocampus was assessed simultaneously using in vivo microdialysis. Kainic acid (10-100 microM) and dihydrokainic acid (1-10 mM) both evoked epileptiform activity and an apparent loss of recurrent inhibition (as assessed using the paired-pulse technique). Extracellular increases in taurine, alanine and phosphoethanolamine were noted following administration of kainate (100 microM) and dihydrokainate (1-10 mM). An increase in extracellular glutamate and aspartate was also noted in rats treated with dihydrokainate (100 microM-10 mM). In contrast, threo-3-hydroxyaspartate did not induce epileptiform activity, suggesting that the epileptogenic effects of dihydrokainate and kainate are not mediated by inhibition of uptake. The effect of the N-methyl-D-aspartate receptor antagonist, D-2-amino-5-phosphonovalerate on these responses was studied. This compound attenuated the epileptiform activity and reversed the apparent loss of recurrent inhibition in response to both kainic acid and dihydrokainic acid. These data suggest that activation of N-methyl-D-aspartate receptors underlies the epileptogenic effects of both compounds, and the possible mechanisms which might be involved in this response are discussed.

Amino Acids↗
PubMed1987

Analysis of amino acids: neurochemical application.

For high sensitivity analysis of neuroactive amino acids, liquid chromatography employing precolumn derivatisation with o-phthalaldehyde (OPA) is suitable for several reasons. The OPA reagent is non-fluorescent per se, the reaction occurs rapidly in alkaline aqueous solutions and forms highly fluorescent derivatives with primary amines.

Amino Acids↗
PubMed1987

2-Amino-5-phosphonovalerate attenuates the severe hypoglycemia-induced loss of perforant path-evoked field potentials in the rat hippocampus.

The effects of severe hypoglycemia on perforant path-evoked field potentials were examined in the rat hippocampus. Although a complete loss of this response was noted when blood glucose concentration fell below 1 mM, this occurred before cessation of electroencephalogram (EEG) activity. Both spontaneous and evoked responses recovered partially following glucose readministration. D-2-Amino-5-phosphonovalerate, an NMDA-sensitive acidic amino acid receptor antagonist, facilitated this recovery from the hypoglycemic challenge when administered via a dialysis probe.

2-Amino-5-phosphonovalerate↗
PubMed1987

Effects of Ca2+ entry blockers on kainate-induced changes in extracellular amino acids and Ca2+ in vivo.

The effect of organic Ca2+ channel blockers and Co2+ on kainate-induced changes in 45Ca2+ efflux and amino acid release was studied in the rabbit hippocampus with the dialysis-perfusion technique. Administration of 1 mM kainate caused a transient, 50% drop of extracellular Ca2+. This effect was insensitive to 100 microM flunarizine or verapamil, 10 microM nimodipine, and 6 mM CoCl2. The organic Ca2+ entry blockers did not significantly influence kainate-induced changes in extracellular amino acids, whereas Co2+ affected both basal and kainic acid stimulated release of amino acids. These results indicate that kainate-regulated Ca2+ ionophores differ from Ca2+ channels in peripheral tissues in terms of sensitivity to Ca2+ entry inhibitors.

Amino Acids↗