Nicotinic receptor binding sites in rat primary neuronal cells in culture: characterization and their regulation by chronic nicotine.

Autor: Dávila-García MI; Department of Pharmacology, Georgetown University School of Medicine, 3900 Reservoir Road, Washington, DC 20007, USA., Houghtling RA, Qasba SS, Kellar KJ
Jazyk: angličtina
Zdroj: Brain research. Molecular brain research [Brain Res Mol Brain Res] 1999 Mar 20; Vol. 66 (1-2), pp. 14-23.
DOI: 10.1016/s0169-328x(98)00344-1
Abstrakt: We have characterized high affinity neuronal nicotinic acetylcholine receptors labeled by [3H]cytisine in primary neuronal cell cultures from fetal rat brains. After 15 days in culture, the highest density of [3H]cytisine binding sites (Bmax approximately 57 fmol/mg protein) was found in cells from the brainstem, which includes the following subcortical brain areas: the septum, thalamus, hypothalamus, midbrain, pons and medulla. A lower density of sites was found in cells from the cerebral cortex, hippocampus, and caudate nucleus. [3H]Cytisine binds to receptors in primary cells from the brainstem and cerebral cortex with a Kd of approximately 0. 5 nM, and the binding is inhibited by the agonists nicotine, acetylcholine, and epibatidine with IC50 values of 1 to 20 nM, and by carbachol and the antagonist dihydro-beta-erythroidine with IC50 values of 0.5 to 1.5 microM. Chronic treatment of neuronal cultures with nicotine for 7 days differentially affected the number of nicotinic receptors in cells from different brain areas; it significantly increased the number of nicotinic binding sites in cells from the cerebral cortex, hippocampus, and caudate, but not in cells from the brainstem. The nicotine-induced increase of receptors in cerebral cortical cultures was not blocked by either mecamylamine or dihydro-beta-erythroidine. These results indicate that primary cultures of rat neuronal cells provide a good model system in which to study and compare the properties and regulation of native neuronal nicotinic acetylcholine receptors.
(Copyright 1999 Elsevier Science B.V.)
Databáze: MEDLINE
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