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• W2072603669 endingPage "359" @default.
• W2072603669 startingPage "351" @default.
• W2072603669 abstract "In this study we show that the electrophysiological properties of a clonal line of prolactin secreting (PRL) rat pituitary cells (GH3/B6) are altered by local application of γ-aminobutyric acid (GABA). The effects of GABA on these cells are: 1) decrease in membrane conductance and 2) hyperpolarization of 5 to 10 mV. When the cells were spontaneously active, GABA reduced and usually arrested action potential firing. This effect was completely reversible. No desensitization of GABA effects was observed even after several applications. The reversal potential of the GABA induced responses was found to be near — 40 mV. Pharmacological studies were performed in order to assess the specificity of the response to GABA and to attempt to characterize the ionic mechanism involved. GABAergic receptor antagonists such as picrotoxin and bicuculline prevented the effect of GABA, whereas dopaminergic receptor antagonists, such as haloperidol or chlorpromazine had no effect. Furosemide, known as a blocker of chloride ion transport in a number of systems, competed with GABA. This substance induced a response similar to that observed with GABA and reduced the effect of GABA when administered before GABA. This study demonstrates a direct and specific effect of GABA on the electrical activity of a tumoral line of rat pituitary cells. Since this electrical activity has previously been shown to be calcium dependent and involved in the secretion of PRL by these cells, the data presented here suggest GABA as an inhibitory regulator of PRL secretion directly at the pituitary level." @default.
• W2072603669 created "2016-06-24" @default.
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• W2072603669 date "1981-07-01" @default.
• W2072603669 modified "2023-10-18" @default.
• W2072603669 title "Effects of GABA on electrical properties of cultured rat pituitary tumor cells: An intracellular recording study" @default.
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• W2072603669 doi "https://doi.org/10.1016/0024-3205(81)90328-3" @default.
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