α1‐Adrenergic Receptor Mediates Arachidonic Acid Release in Spinal Cord Neurons Independent of Inositol Phospholipid Turnover

• DOI: 10.1111/j.1471-4159.1990.tb01952.x
• Publication Date: 2006-10-05T23:55:33Z
• Authors: Robert Y. Kanterman; Christian C. Felder; Douglas E. Brenneman; Alice L. Ma; Sandra Fitzgerald; Julius Axelrod
• Keywords: Inositol trisphosphate

The alpha 1-adrenergic receptor has been shown to mediate the release of arachidonic acid in FRTL5 thyroid cells and MDCK kidney cells. In primary cultures spinal cord cells, norepinephrine stimulated (from neurons only) turnover inositol phospholipids glia) via receptors. These two responses were dissociated by treatment with phorbol ester pertussis toxin, which inhibited production phosphates no appreciable effect on acid. Extracellular calcium was required for acid, but not phosphates. channel blockers nifedipine verapamil only. However, 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8), a compound that blocks intracellular release, diminished phosphates, had little results suggest receptors couple mechanism independent activation phospholipase C, possibly A2.