Abstract
Neuroblastoma x glioma hybrid NG108-15 cells have saturable, high affinity, sterospecific opiate receptors (KLEE & NIRENBERG, 1974; BLUME, et al., 1977). In viable cells, opiates lower the intracellular concentration of cAMP as well as prevent full elevation of cAMP by activa tors (i.e., PGE and adenosine) of adenylate cyclase. Inhibition of adenylate cyclase activity by opiates can be directly demonstrated in vitro with NG108-15 cell membranes. These actions of opiates appear to require agonist occupation of the opiate receptor and they are blocked by the specific opiate antagonist naloxone (SHARMA, NIRENBERG & KLEE, 1975; SHARMA, KLEE & NIRENBERG, 1975 & 1977). However, the affinities of agonists under adenylate cyclase assay conditions were generally 10-100 times poorer than those observed with viable intact cells suspended in an isotonic sucrose/Tris/HCl buffer. No such discrepancies were observed with the opiate antagonist naloxone. A priori, this specific alteration in opiate agonist affinity could be due either to (i) changes in the opiate receptor per se after cell homogenization or (ii) the presence of high concentrations of cations or nucleotide triphosphates in the adenylate cyclase assays.
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Blume, A.J., Boone, G., Lichtshtein, D. (1979). Regulation of the Neuroblastoma X Glioma Hybrid Opiate Receptors by Na+ and Guanine Nucleotides. In: Ehrlich, Y.H., Volavka, J., Davis, L.G., Brunngraber, E.G. (eds) Modulators, Mediators, and Specifiers in Brain Function. Advances in Experimental Medicine and Biology, vol 116. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-3503-0_9
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DOI: https://doi.org/10.1007/978-1-4684-3503-0_9
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