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Acetylcholine Releases Prostaglandins from Brain Slices Incubated In Vitro
Author(s) -
Reichman Melvin,
Nen Wu,
Hokin Lowell E.
Publication year - 1987
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1987.tb10013.x
Subject(s) - acetylcholine , muscarinic acetylcholine receptor , medicine , endocrinology , chemistry , stimulation , cholinergic , serotonin , cerebral cortex , histamine , neurotransmitter , atropine , biology , receptor , central nervous system , biochemistry
A variety of neurotransmitters elicit a phos‐phoinositide response in the CNS; however, their effects on prostaglandin (PG) formation in the brain are not well characterized. In the present study, we investigated the effect of acetylcholine (ACh) on the synthesis of PCs E and F in slices from various regions of guinea pig brain incubated in glucose‐fortified Krebs‐Henseleit bicarbonate saline. Slices were prewashed in the presence of 1% albumin to reduce basal PG levels followed by incubation for 30 min at 37°C in the presence or absence of ACh. Under these conditions, 5 m M ACh significantly increased the efflux of PGE and PGF from brain regions enriched in muscarinic cholinergic receptors, i.e., cerebral cortex, temporal cortex, corpus striatum, and hippocampus. Depolarization by 45 m M KCl also significantly enhanced PG synthesis, and the relative magnitude of the effect was similar to that of ACh. The stimulation of PG synthesis by ACh was inhibited by 20 μ M atropine, whereas the K + ‐induced stimulation was not. The effects of potassium and ACh were additive at maximally effective ACh concentrations, an observation that suggests that ACh and K + increase PG efflux through independent mechanisms. Norepinephrine, histamine, and serotonin, three other neurotransmitters that evoke a phos‐phoinositide response in the brain, were ineffective in stimulating PG release from brain cortex slices.