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Glial Regulation of α7‐Type Nicotinic Acetylcholine Receptor Expression in Cultured Rat Cortical Neurons
Author(s) -
Jensen Janice J.,
WinzerSerhan Ursula H.,
Leslie Frances M.
Publication year - 1997
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 - 10.1046/j.1471-4159.1997.68010112.x
Subject(s) - nicotinic agonist , astrocyte , receptor , neuroglia , biology , glutamate receptor , acetylcholine receptor , muscarinic acetylcholine receptor , bungarotoxin , alpha 4 beta 2 nicotinic receptor , microbiology and biotechnology , endocrinology , medicine , nicotinic acetylcholine receptor , biochemistry , central nervous system
Primary embryonic cortical cultures were used as an in vitro model to evaluate the influence of glia on developmental expression of α7‐type nicotinic acetylcholine receptors in rat brain. In cells cultured in serum‐containing medium without mitotic inhibitors, specific 125 I‐α‐bungarotoxin binding to α7‐type nicotinic receptors was maximal 4–8 days after plating. Treatment with 5′‐fluorodeoxyuridine (80 µ M ) from 1 to 3 days in vitro significantly reduced glial proliferation and concomitantly increased 125 I‐α‐bungarotoxin binding, whereas plating onto a glial bed layer decreased binding. There was no significant binding to pure glial cultures. Treatment‐induced changes in neuronal binding resulted from alterations in receptor density, with no change in affinity. 5′‐Fluorodeoxyuridine treatment also increased cellular expression of α7 receptor mRNA but had no effect on N ‐[ 3 H]methylscopolamine binding to muscarinic receptors. Glial conditioned medium decreased 125 I‐α‐bungarotoxin binding in both control and 5′‐fluorodeoxyuridine‐treated cultures, suggesting the release of a soluble factor that inhibits α7‐type nicotinic receptor expression. An additional mechanism of glial regulation may involve removal of glutamate from the surrounding medium, as added glutamate (200 µ M ) increased 125 I‐α‐bungarotoxin binding in astrocyte‐poor cultures but not in those that were astrocyte enriched. These results suggest that glia may serve a physiological role in regulating α7‐type nicotinic receptors in developing brain.