Abstract
The nervous system is able to synthesize prostaglandins (PG). The rate-limiting step of PG synthesis is the release of arachidonate from membrane glycerolipids by various phospholipases. These enzymes may be activated either punctually by neurotransmitters through receptor-mediated events or extensively by injuries and ischemia (for recent review see ref. 1). Consequently, newly-synthesized PGs would modulate either physiological or pathological processes via specific membrane receptors. Since PGE2 is one of the major prostanoids synthesized in chick spinal cord (2), the aim of the present work was to explore possible relationships between the variation of PGE2 synthesis and the saturation of PGE2 receptors.
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References
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Vesin, M.F., Billotte, C., Pralong, E. (1993). PGE2 Receptors: Involvement of EP2 and EP3 Subtypes in the Chick Spinal Cord. In: Nigam, S., Honn, K.V., Marnett, L.J., Walden, T.L. (eds) Eicosanoids and Other Bioactive Lipids in Cancer, Inflammation and Radiation Injury. Developments in Oncology, vol 71. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3520-1_32
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DOI: https://doi.org/10.1007/978-1-4615-3520-1_32
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