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B Tocque

Publications and source records attributed to B Tocque.

42 records · Page 3Linked to original sources
PubMed1984

Desipramine elicits the expression of opiate receptors and sulfogalactosylceramide synthesis in rat C6 glioma cells.

In the course of our studies on lipidoses induced by amphiphilic drugs, we have investigated the ef- of desipramine, a tricyclic antidepressant, on glial cells in culture. We noted that the addition of desipramine to the culture medium of C6 glioma cells resulted in the modification of the lipid profile of the cell membranes. Of particular interest was the presence, in the desipramine-treated cells, of an additional lipid comigrating on thin layer chromatography with sulfogalactosylceramide (S-GalCer). Addition of radiolabelled sulfuric acid in the culture medium of the desipramine-treated cells resulted in the incorporation of [35S]sulfate in the newly synthesized lipid. Furthermore, this lipid was localized selectively by indirect immunofluorescence using a specific rabbit anti-S-GalCer antibody on the cell surface of desipramine-treated, but not control, C6 cells. Desipramine also increased the activity of 3'-phosphoadenosine-5'-phosphosulfate sulfotransferase (the enzyme responsible for the synthesis of S-GalCer). Since it has been suggested that S-GalCer may be involved in opiate receptors, we looked for opiate binding sites on C6 glioma cells after exposure to desipramine. We found that dihydromorphine was able to bind to the desipramine-treated C6 cell membrane. The binding of [3H]dihydromorphine (180 fmol/mg protein) was stereospecific and had a KD of 30-60 nM. Furthermore, morphine reduced both the basal and isoproterenol-stimulated cyclic AMP levels of the desipramine-treated C6 cells. This effect was blocked by naloxone. In these respects, the opiate binding sites induced after treatment of C6 glioma cells with desipramine fulfill the requirements of a true opiate receptor.

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PubMedDate not supplied

The kinetics of cannabinoid distribution and storage with special reference to the brain and testis.

Male and female rats were given either single or repeated intramuscular injections of 2 microCi of 14C-delta 8-tetrahydrocannabinol. They were sacrificed by groups of three at regular intervals 2, 3, 4, 6, or 24 hours after the last injection. Samples of blood lung, brain and pituitary, spleen, liver, fat, testis, and ovary were removed. Some samples were pyrolysed in an automatic oxygen train system to measure 14C-CO2, which reflects total cannabinoid concentration; other samples were kept for measurements of individual cannabinoids after extraction. After a single administration of 14C-delta 8-THC, maximal concentration of total radioactivity was reached in the brain between 2 and 4 hours amounting to 6 ng/gm tissue, or 0.06 per cent of the administered dose. After two weeks of chronic administration, concentrations of radioactivity progressively increased in liver and neutral fat, while cannabinoid levels in brain and testis remained unchanged. These data illustrate the efficiency of the blood-brain and blood-testicular barrier in limiting the access and accumulation of cannabinoids in these tissues.

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