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Endocrinology, Vol 134, 91-96, Copyright © 1994 by Endocrine Society

ARTICLES

Protein kinase A regulates nicotinic cholinergic receptors and subunit messenger ribonucleic acids in PC 12 cells

TC Madhok, HS Beyer and BM Sharp
Department of Medicine, Hennepin County Medical Center, Minneapolis, Minnesota.

To delineate mechanisms regulating the expression of neuronal nicotinic cholinergic receptors (nAcChRs), we studied the cAMP-dependent second messenger system. PC 12 cells were grown in (Bu)2cAMP (0.001-1.0 mM) or vehicle for 7 days, and specific [3H] nicotine binding was measured. (Bu)2cAMP (0.1 mM) increased specific binding 2- and 4-fold at 3 and 7 days, respectively, whereas 1.0 mM enhanced binding 4-fold at both time intervals. Cells grown in 8-bromo-cAMP (1.0 mM) showed a 2-fold increase in [3H]nicotine binding at 3 days. Forskolin (10-100 microM), in combination with isobutyl-methylxanthine (1.0 mM), enhanced [3H]nicotine binding 2- to 3-fold at 7 days; forskolin or isobutyl- methylxanthine alone had no effect. Specific [3H] nicotine binding to PC 12 cell mutants (A126.1B2 and A123.7), deficient in cAMP-responsive protein kinase A types I and II, were unaffected by (Bu)2cAMP. Northern gel analysis of nAcChR subunit messenger RNAs showed that the alpha-3, alpha-5, and beta-4 subunits were significantly decreased by (Bu)2cAMP at 4 h. However, (Bu)2cAMP caused an increase in the beta-2 messenger RNA transcript at 4 h, which returned to baseline by 24 h. These studies indicate that the cAMP-protein kinase A system regulates expression of nAcChR by PC 12 cells. These studies also suggest that enhancement of [3H]nicotine binding by activated protein kinase A may not involve synthesis of new receptor subunit proteins.


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