Effects of dopamine, gamma-aminobutyric acid and 5-hydroxytryptamine on incorporation of 32P into phosphatides in slices from the guinea pig brain.

Abstract

Abstract(1) Dopamine–In slices from guinea pig corpus striatum, dopamine significantly inhibited incorporation of 32P into phosphatidylethanolamine‐plus‐phosphatidylserine at a concentration of 0001 mM, and into phosphatidylinositol and phosphatidylcholine at 001 mM. In eight areas of the guinea pig brain in which the effects of 01 mM‐dopamine were studied, the only significant increase in incorporation of 32P into phosphatides was into phosphatidic acid in the hypothalamus; there was significant inhibition of incorporation of 32P into phosphatidylcholine in cerebellar cortex and thalamus, and into phosphatidylethanolamine‐plus‐phosphatidylserine in the olfactory bulbs.(2) Gamma‐aminobutyric acid—In slices of guinea pig cerebral cortex, GABA (1 mM) significantly inhibited incorporation of 32P into only phosphatidic acid, diphosphoinositide and phosphatidylinositol and did not significantly affect the level or the specific activity of the nucleotide ∼P. GABA (10 mM), significantly inhibited incorporation of 32P into diphosphoinositide, phosphatidylinositol and phosphatidylcholine, and significantly lowered the specific activity of the nucleotide ∼P.(3) 5‐Hydroxytryptamine—In slices of guinea pig cerebral cortex, 5HT, (1 mM) significantly increased incorporation of 32P into phosphatidic acid; in a concentration of 10 mM, 5HT increased incorporation of 32P into phosphatidic acid four‐fold and into both diphosphoinositide and phosphatidylinositol two‐fold; other phosphatides were not significantly affected and the specific activity of the nucleotide ∼P was not significantly different. In eight brain areas studied, 5HT (10 mM) significantly increased incorporation of 32P into phosphatidic acid in all areas; into phosphatidylinositol in six areas (excepting cerebellar cortex and hypothalamus); and into diphosphoinositide in the olfactory bulbs, cerebral cortex, hypothalamus and corpus striatum. Incorporation of 32P into triphosphoinositide was not significantly affected in any area. Incorporation of 32P into phospha‐tidylethanolamine‐plus‐phosphatidylserine was significantly greater than the control in the olfactory bulbs and incorporation of 32P into phosphatidylcholine was significantly less than the control in the cerebellar cortex, olfactory bulbs and hypothalamus.(4) The possibility is discussed that increased incorporation of 32P into phosphatidic acid and/or phosphatidylinositol in response to neurotransmitters might be associated with excitatory, but not inhibitory, neurotransmission; and that inhibition of incorporation of 32P into various phosphatides may be associated with inhibitory neurotransmission or neuromodulation.