Short-echo proton spectroscopy allows the noninvasive study of metabolites, lipids, and macromolecules in stroke patients, but spectra are difficult to interpret and quantify because narrow metabolite peaks are added to a broad background of lipid and macromolecule peaks. "Metabolite nulling" was used to distinguish the lactate peak from underlying lipid and macromolecule peaks. Increases in the lipid and macromolecule peaks were initially observed within the region of infarction in all patients, and further increases in lipid peaks were seen in five of the six patients during the following 6 weeks. The initial high lactate concentration decreases during the first 2 weeks after stroke, whereas lipid and macromolecule signals show a persistent elevation during the same period. Differences in the time courses of the observed changes suggest that lipid, macromolecule, and lactate signals arise from more than one source.

Adult↗

PubMedDate not supplied

Alcohol inhibits neurite extension and increases N-myc and c-myc proteins.

Alcohol teratogenesis may be due, in part, to inhibition of neuronal differentiation by alcohol. Because decreases in the N-myc and c-myc proteins are believed to be linked causally to neuronal differentiation, we hypothesized that alcohol would increase N-myc and c-myc proteins in undifferentiated neuronal cells and would oppose the decreases in these two proteins that normally precede differentiation. In undifferentiated LA-N-5 cultured human neuroblastoma cells, alcohol increased N-myc protein levels (178% vs. control cells) and c-myc levels (222% of control). Retinoic acid decreased N-myc and c-myc and induced neurite outgrowth (a differentiation marker). Alcohol prevented retinoic acid-elicited decreases in both myc isoforms and prevented neurite outgrowth. A significant 100% increase in c-myc and an upward trend (48%) in N-myc were observed in CA1 pyramidal neurons of the dorsal hippocampus in mouse fetuses exposed prenatally to alcohol. These data suggest that increases in N-myc and c-myc protein levels are associated with inhibition of neurite extension by alcohol.

Animals↗

PubMedDate not supplied

Alcohol reduces neurofilament protein levels in primary cultured hippocampal neurons.

High concentrations of alcohol (> or = 1.8%) were shown previously to impair health and viability of cultured hippocampal neurons. Because neurofilament proteins are essential for neuronal process outgrowth and differentiation, the effects of alcohol on these proteins were determined in the neuronal processes of primary cultured gestational day 18 rat hippocampal neurons. At the relatively lower concentrations used in the present study, alcohol caused a concentration-dependent reduction (< or = 47%) in 68 and 200 kDa neurofilament proteins (p < 0.05). Alcohol caused a 32% downward trend in 160 kDa neurofilament protein levels. Alcohol up to 1% (72-h exposure) produced no obvious alterations in neurite extension or explant morphology, and there were no visual signs of cell death. The sensitive MTT dye reduction assay showed no biochemical evidence of decreased cell viability at < or = 0.5% alcohol. The 32-47% reductions in neurofilament protein levels in vitro may hold implications for later hippocampal neuronal differentiation events in animals prenatally exposed to alcohol.

Animals↗