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Biomedical subjects

B Siegfried

Publications and source records attributed to B Siegfried.

49 records · Page 3Linked to original sources
PubMed1977

Electrophysiological concomitants of eating induced from neocortex and hippocampus by electrical stimulation and injection of KC1 or norepinephrine.

EEG and DC activity were recorded from the hippocampus and neocortex in freely moving rats during consummatory behavior elicited by electrical stimulation and application of KC1 or norepinephrine to these structures. Eating induced by KC1 application or electrical stimulation of the neocortex or hippocampus was accompanied by single or multiple waves of spreading depression (SD), i.e., by traveling slow potential change. An analysis of single vs. multiple cortical SD waves indicated that when multiple waves occurred, feeding was elicited by the first wave. Injection of norepinephrine into the hippocampus resulted in a significantly larger and qualitatively different feeding response compared to KC1 injections. No apparent changes in the EEG or DC activity occurred upon norepinephrine injections.

Action Potentials↗
PubMed1975

Pavlovian conditioning of eating induced by spreading depression in cortex, striatum and hippocampus of rats.

A single wave of unilateral spreading depression in the cortex, hippocampus or caudate nucleus of rats elicits eating after 2-6 min. The present experiments provide evidence that such spreading depression-induced eating can be classically conditioned to a complex conditioned stimulus. A wave of spreading depression was triggered by injection of 0.5-2.0 mul of 25 percent KCl solution. In a first experiment successful conditioning was demonstrated in 20 rats, involving 7 cortical, 5 caudate and 8 hippocampal spreading depression sites. Four animals failed to show any conditioned eating. A control group of 8 animals, in which cortical spreading depression did not induce eating, showed no increase in eating in the presence of the CS after conditioning trials. A second experiment, which included pseudoconditioning and NaCl control groups, confirmed the results obtained in Experiment 1. Classical conditioning was successful in 11 animals, involving 6 cortical and 5 caudate spreading depression sites. Neither the pseudoconditioning (14 animals, involving 8 cortical and 6 caudate spreading depression sites) not the NaCl control group (8 animals, all with cortical sites), showed eating in the presence of the CS. In both experiments the conditioned eating underwent gradual extinction.

Animals↗
PubMedDate not supplied

Metabolism of difebarbamate in man.

The metabolism of 1,3-bis(3-butoxy-2-carbamoyloxypropyl)-5-ethyl-5-phenyl- (1H,3H,5H)-pyrimidine-2,4,6-trione (difebarbamate) in man was studied. Human volunteers received a single oral dose of 25 mg/kg difebarbamate. Urine was extracted with Amberlite XAD-2 resin and the extracts were separated by preparative HPLC after enzymatic hydrolysis. Four major metabolites were isolated and their structures were determined using NMR and mass spectrometry. The oxygen dealkylation led to the formation of two metabolites: 1-(3-butoxy-2-carbamoyloxypropyl)-3-(2-carbamoyloxy-3-hydrox ypropyl)-5-ethyl-5- phenyl-(1H, 3H, 5H)-pyrimidine-2,4,6,-trione and 1,3-bis(2-carbamoyloxy-3-hydroxypropyl)-5-ethyl-5-phenyl-(1H,3H,5H )- pyrimidine-2,4,6,-trione. The hydrolysis of the carbamoyloxy group with the oxygen dealkylation led to the formation of 1-(2-carbamoyloxy-3-hydroxypropyl)-3-(2,3-dihydroxypropyl)-5-ethyl - 5-phenyl-(1H,3H,5H)-pyrimidine-2,4,6,-tione, whereas the 4-hydroxylation of the benzene ring together with the oxygen dealkylation led to the formation of 1,3-bis(2-carbamoyloxy-3-hydroxypropyl)-5-ethyl-5-(4-hydroxyphenyl )-(1H,3H,5H)- pyrimidine-2,4,6,-trione. No traces of the parent drug were found.

Administration, Oral↗