Abstract
Both ethanol and neurotensin produce sedation and hypothermia. When administered in combination the behavioral effects of these two substances are potentiated. In order to better understand the biochemical nature of this interaction, the direct effects of ethanol on neurotensin receptors and an associated signal transduction process were determined in NIE-115 neuroblastoma cells. Ethanol in physiologically relevant concentrations (50mM) significantly reduced neurotensin stimulated [ 3H] inositol phosphate production while having no effect on the specific binding of [ 3H] neurotensin. In addition, ethanol up to 200 mM had no effect on GTPYS mediated [ 3H] inositol phosphate production. The results indicate that acute exposure to ethanol partially disrupts the normal coupling of activated neurotensin receptors to the guanine nucleotide binding protein associated with phospholipase C.
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