Halothane and γ-aminobutyric acid in cultured cells of nervous system origin

Abstract

C-1300 neuroblastoma and C-6 astrocytoma cells in culture were utilized as models of γ-aminobutyric acid (GABA) metabolism in neurons and glia, respectively. Both cell lines were exposed to 0, 0.7, 1.0, 1.7, or 3.0% halothane at 37C and pH 7.1 with glucose as substrate. Cellular viability was unaffected by the anesthetic in either cell line. Halothane did not alter cellular content of GABA in C-1300 neuroblastoma cells. However, 0.7 and 1.0% halothane lowered the levels of GABA in C-6 astrocytoma cells which had been provided with fresh medium 18–21 hr prior to anesthetic exposure (fed cells). This response was absent following treatment with 1.7 or 3.0% halothane. Efflux of GABA was decreased by 1% halothane in C-1300 neuroblastoma cells which had not received fresh medium for 48 to 72 hr (starved cells). This response was absent in fed cells. In contrast, starved C-6 astrocytoma cells exhibited an increase in GABA efflux following exposure to all concentrations of halothane. Similar results were observed in fed cells treated with 1% and 3% halothane. These data support the results of previous studies showing an increase in the GABA content of rat brain slices following exposure to halothane; however, they suggest that glia rather than neurons are the major source of the increased levels of GABA.