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Effects of Neurotransmitters on Astrocyte Glycogen Stores In Vitro
Author(s) -
CambrayDeakin Martin,
Pearce Brian,
Morrow Christine,
Murphy Sean
Publication year - 1988
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.1471-4159.1988.tb01168.x
Subject(s) - astrocyte , endocrinology , medicine , serotonin , glycogen , reserpine , neurotransmitter , receptor , biology , chemistry , central nervous system
We have used receptor binding assays to determine the presence of three neurotransmitter receptors in a crude membrane fraction derived from neonatal rat cortical astrocyte cultures and subsequently determined the effects of transmitter receptor activation on astrocyte glycogen content in vitro. β‐Adrenergic ( K D = 88 p M; B max = 51 fmol/mg of protein), serotonin ( K D = 70 n M; B max = 44 pmol/mg of protein), and muscarinic cholinergic receptors ( K D = 79 p M; B max = 44 fmol/mg of protein) were found to be present on astrocyte membranes using [ 3 H]dihydroalprenolol, [ 3 H]serotonin, and [ 3 H]quinuclidinyl benzilate, respectively, as ligands. Astrocyte cultures exposed to noradrenaline but not specific α‐ and β‐receptor agonists contained 33% less glycogen than controls. Neither serotonin nor carbachol caused alterations in astrocyte glycogen content under normal conditions. Reserpine‐treated cultures, however, responded to serotonin with a 28% decrease in glycogen content and contained higher levels of glycogen than non‐reserpine‐treated controls (a 55% increase). These results show that both noradrenaline and serotonin can evoke astrocyte glycogenolysis and that noradrenergic control of glycogen metabolism is probably exerted through both α‐ and /S ‐receptors. Neurotransmitter control of astrocyte glycogen turnover may represent a form of neuron‐astrocyte signalling in addition to that provided by changes in external potassium concentration.