Presence of benzodiazepine-like molecules in mammalian brain and milk.

From bovine cerebral cortex extracts, used to isolate n-butyl beta carboline-3-carboxylate (8), fractions active in displacing [3H] flunitrazepam binding were purified and shown to contain benzodiazepine-like molecules. These were recognized by UV spectra, retention time in HPLC, and interaction with a specific monoclonal antibody. Such molecules were localized in synaptic vesicles and cytosol of synaptosomes. Similar molecules were also found in cow milk. The possible dietary origin of these benzodiazepine-like molecules is discussed.

Different properties of two brain extracts separated in Sephadex G-50 that modify synaptosomal ATPase activities.

We have previously reported that Na+,K+-ATPase of nerve ending membranes is stimulated by catecholamines only in the presence of a brain soluble fraction. The filtration of this soluble fraction through Sephadex G-50 permitted the separation of two extracts of maximal UV absorbance (peaks I and II) which showed different effects on ATPases. Peak I stimulated both Na+, K+-ATPase and Mg2+-ATPase activities and peak II inhibited Na+, K+-ATPase activity. We have now studied the activity of ATPases in the presence of the whole eluate obtained from the Sephadex G-50 column. It was observed that maximal effects on ATPases were obtained with peaks I and II. Peak I and peak II fractions were unable to modify the activity of acetylcholinesterase or 5'-nucleotidase present in the synaptosomal membranes. The stimulatory effect of peak I on ATPases was concentration dependent (up to 1:100), it was stable at different pHs and it was reverted by catecholamines. The inhibitory effect of peak II on Na+,K+-ATPase was concentration dependent (up to 1:50,000), it was stable only at acid pH, and it was partially reverted by catecholamines. These findings indicate that the factors responsible for the effects of peaks I and II have different properties and that their actions on ATPases show enzyme specificity.

The urinary excretion of 5-hydroxyindoleacetic acid does not reflect brain levels of this metabolite of 5-hydroxytryptamine.

The present study was undertaken to determine if changes in the serotonergic central nervous system can be reflected by urinary 5-hydroxyindoleacetic acid (5-HIAA) levels. Cerebral, spinal and urinary levels of 5-HIAA were determined and compared in rats whose cerebral 5-HIAA concentration had been depleted by nucleus raphe dorsalis and medialis lesion or increased by L-tryptophan loading. Since no differences were observed in the urinary excretion of 5-HIAA we conclude that this parameter cannot be used to detect changes in the serotonergic central nervous system.

[Ferruginated neurons in cerebral infarcts]. / Incrustação ferruginosa de neuronios nos infartos cerebrais

The study of the ferruginated neurons in the analysis of 87 cases of cerebral infarcts is reported. The lesion found in 40,3% of the cases was demonstrared to contain iron and calcium. It was found to be more frequent in older patients and predominantly in the cortical necrotic areas. The minerals were also detected in basophilic granules found outside the cells in the necrotic tissue. There was no correlation with the basic disease, although in 17% of the cases there was an association with sickling of the red blood cells. The role of the mineral content of the nervous tissue in the pathogenesis of the incrustation is discussed. The demonstration of other minerals besides the iron in the cells makes the term "mineralization of neurons" more acceptable.

Brain tissue levels in a fatal case of neonatal mepivacaine (Carbocaine) poisoning.

A fatal case of mepivacaine poisoning in a newborn infant is reported. Regional brain tissue concentrations of mepivacaine were determined by a sensitive and specific gas chromatographic-mass spectrometric method. The brain tissue levels in this patient were higher than those previously reported, possibly due to alkalosis occurring several hours prior to the infant's death.