Effects of neurotransmitters on astrocyte glycogen stores in vitro

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. beta-Adrenergic (KD = 88 pM; Bmax = 51 fmol/mg of protein), serotonin (KD = 70 nM; Bmax = 44 pmol/mg of protein), and muscarinic cholinergic receptors (KD = 79 pM; Bmax = 44 fmol/mg of protein) were found to be present on astrocyte membranes using [3H]dihydroalprenolol, [3H]serotonin, and [3H]quinuclidinyl benzilate, respectively, as ligands. Astrocyte cultures exposed to noradrenaline but not specific alpha- and beta-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 alpha- and beta-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.