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B Zalc

Publications and source records attributed to B Zalc.

85 records · Page 5Linked to original sources
PubMed1981

Immunohistochemical localization of galactosyl and sulfogalactosyl ceramide in the brain of the 30-day-old mouse.

We have used purified antibodies against galactosylceramide (galCb) and sulfogalactosylceramide (sulf) to study the topographical distribution of these two lipid haptens in the brain of the 30-day-old mouse. This study has been conducted, using the indirect immunofluorescence method, on cerebellum, brain stem and hemispherical tissue sections. Both haptens are present in the myelin sheaths and in the oligodendrocytes within the myelinated bundles. Cortical oligodendrocytes as well as some of the subependymal cells are also galCb-positive but sulf-negative. On the contrary, ciliated ependymal cells and subpial astrocytic processes (especially the Bergmann glia fibers in the cerebellum) are sulf-positive and galCb-negative. Astrocyte cell bodies and other astrocytic cell processes are devoid of both haptens. Lastly, some-sulf positive galCb-negative processes, as yet unidentified, were also found in the periaqueductal gray matter and in the nucleus interpeduncularis.

Animals↗
PubMed1981

Regional distribution of myelin basic protein in the central nervous system of quaking, jimpy, and normal mice during development and aging.

Myelin basic protein (MBP) was quantified using a RIA technique in the spinal cord, cerebellum, diencephalon plus brainstem region and cerebral hemispheres of two dysmyelinating murine mutants, quaking (qk) and jimpy (jp) mice. Comparison was made with normal control values. The whole life-span has been investigated: ie, ages ranging from 0 to 26 days for the jp, O to one year for the qk, and prenatal stage to three years for the control animals. Assays in the mutants at early ages were rendered feasible by the use of marker genes, which has allowed the diagnosis of the mutation at birth, 12 days before the expression of their typical tremor phenotype. Special care was given to the period of early myelinogenesis in order to clarify the dysynchrony between the various parts of the central nervous system. In normal mice, MBP was already detected in the brain of 19-day-old embryos. During development, rapid accumulation of MBP first occurred in the spinal cord then in the diencephalon, the brainstem, the cerebellum, and finally in the cerebral hemispheres. In the 25-day-old jimpy mutant, levels of MBP were found dramatically decreased, never exceeding 6% of the normal controls in any of the areas investigated. The situation for the quaking mouse was quite different. This mutant could be investigated up to one year old. At that age, a high discrepancy was observed between the values found in the brain and in the spinal cord (respectively, 10% and 35%) compared to normal controls. In both mutants, not only were the levels of MBP decreased, but also its appearance during development was delayed. Nevertheless, in both mutants the caudo-rostral timing of myelination as assayed by MBP levels was maintained. Furthermore, the later myelination occurred, the stronger weas the deficit in MBP. Interestingly, in the quaking mutant, the specific plasticity of the spinal cord was exemplified by its ability to reduce constantly, even at an advanced age, its initial deficit of MBP.

Aging↗
PubMed1980

Antibodies to cerebroside sulfate inhibit the effects of morphine and beta-endorphin.

Morphine and beta-endorphin inhibit the shaking response of pentobarbital-anesthetized rats to ice water. Stereotaxically guided administration of antibodies to cerebroside sulfate into the periaqueductal gray region, the most sensitive brain region in which to demonstrate inhibition of this response, antagonizes the effect of morphine and beta-endorphin. These results suggest that cerebroside sulfate may be an integral component of an opiate receptor in rat brain.

Animals↗
PubMed1980

[Sulfatide: a multifunctional glycolipid constituent of biological membranes].

Sulfogalactosylceramide (or sulfatide) has been localized in the central nervous system by indirect immunofluorescence. This glycosphingolipid belongs essentially to the myelinated areas. Nevertheless, it has also been found in ependymal cells, subpial processes and, in the cerebellum, in the Bergmann fibers. In the brain areas, known to be enriched in opiate receptors, some cells and nerve terminals are also sulfatide positive. In this latter localization, opiates were shown to selectively inhibit binding of the antisulfatide antibodies. We have also shown that antisulfatide inhibited, in vitro, the stereo-specific binding of narcotic drugs and that they antagonized the in vivo effects of morphine and beta-endorphin.

Animals↗