Biomedical subjects
Publications and source records attributed to A Hamberger.
During barbiturate sleep of rabbits, the succinoxidase activity in isolated neurons and glia from the caudal part of the reticular formation was lower than that during physiological sleep. No rhythmical, inverse enzyme changes were detected in barbiturate sleep in the neuron-glia unit, such as were found in physiological sleep.
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Neurochemical observations on cortical biopsies form 48 patients under surgical treatment for pharmacoresistant partial epilepsy showed a 70-80% increase in glutamate concentration when expressed in relation to neuron specific enolase. Intraperitoneal administration of one of its receptor agonists, kainic acid (KA), to the rat led to increased epileptogenic activity of the limbic type in a dose-dependent fashion. The KA injection also led to a neuronal cell death and a gliosis, closely correlated to the extent of seizure activity. In biopsies from human epileptogenic cortex, the concentration of neuron specific enolase correlated inversely to that of glial fibrillary acidic protein, a marker for astrocytic glial cells. Stimulation of the KA receptor decreased the extent of phosphorylation of the largest subunit of neurofilaments (NF-H) that have consequences for structural stability and axonal transport. Phosphorylated NF-H decreased also in human epileptic cortex, indicating either an overactivity of excitatory neurotransmitters or a loss of axonal compartments.
A simple mathematical description of mass transfer in brain dialysis devices is presented. The validity of this model is supported by results from both in vitro and in vivo dialysis experiments. Based on this description, an alternative approach for estimating the extracellular concentration of amino acids is outlined.
Extracellular fluid was topically sampled with a dialysis probe during electrocorticography from the exposed cerebral cortex in 23 patients undergoing epilepsy surgery. Sampling was done in parallel from epileptiform regions and from non-epileptic areas. The former were classified according to the histopathology, into neoplastic, non-tumoral or 'special cases'. The epileptiform regions had significantly higher extracellular concentrations of alanine, glycine and phosphoethanolamine in the majority of the cases. The excised epileptic lesions were analyzed to provide the corresponding intracellular concentrations of amino acids. Several of the non-tumoral group showed high concentrations of GABA, ethanolamine and alanine. The intra- to extracellular concentration ratio for amino acids was low for phosphoethanolamine, glycine, serine and glutamine in most of the samples of epileptiform cortex, while the intracellular accumulative ability for ethanolamine apparently was stronger in epileptiform than in normal cortex.
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