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Reciprocal Regulation of Fatty Acid Release In The Brain By Gaba and Glutamate

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Neurobiology of Essential Fatty Acids

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 318))

Abstract

Free fatty acids (FFA) and their metabolites have many effects on neurochemical processes, including altering receptor-effector coupling, modulating the activity of protein kinase C, and changing ion channel conductance in the cell membrane. However, the neurotransmitters and other factors that control the release of FFA in neurons in normal or pathological states are not well defined. The following studies investigate the regulation of FFA release in intact brain, synaptosomes, and isolated neurons in culture in response to drugs that interact at γ-aminobutyric acid (GABA) and glutamate receptors. The results suggest that neuronal excitation via stimulation of glutamate receptors or blockade of GABA receptors causes the activation of FFA release, and that phosphatidylcholine (PC) is a major source of FFA. Conversely, inhibition of neuronal activity reduces FFA release. FFA release occurs via activation of phospholipase A2 and possibly via activation of a PC-specific phospholipase C, followed by diacylglycerol (DG) lipase. The common pathway for these effects may be alterations in intracellular calcium.

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Birkle, D.L. (1992). Reciprocal Regulation of Fatty Acid Release In The Brain By Gaba and Glutamate. In: Bazan, N.G., Murphy, M.G., Toffano, G. (eds) Neurobiology of Essential Fatty Acids. Advances in Experimental Medicine and Biology, vol 318. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3426-6_6

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  • DOI: https://doi.org/10.1007/978-1-4615-3426-6_6

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-6515-0

  • Online ISBN: 978-1-4615-3426-6

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