Stimulation by acetylcholine and inhibition by norepinephrine of transglutaminase activity in superior cervical ganglia excised from adult rats.
Very rapid changes in activity of transglutaminase (TG), a calcium-dependent enzyme contributing to cross-linkage formation of intracellular polypeptide chains, were observed in vitro in rat superior cervical ganglion (SCG) and nodose ganglion (NG) following application of cholinergic or adrenergic agonists and antagonists. In SCG, a tissue rich in synapses, the depolarizing agent acetylcholine (ACh, 0.1 mM) produced an 8.7-fold increase in TG activity within 5 min that lasted for 30 min and returned to control levels by 2 h. In contrast, the ACh-induced increase in TG activity in NG, a tissue containing neuronal cell bodies with few synapses, was more gradual and of smaller magnitude, reaching a peak of approximately 2.4 times control by 30 min that was maintained for at least 2 h. In both tissues the ACh-stimulation was effectively blocked by the nicotinic antagonist, hexamethonium (0.1 mM), whereas the muscarinic antagonist, atropine (0.1 mM), partially blocked the ACh effect in SCG and was without effect in NG. Addition of the hyperpolarizing adrenergic agonists norepinephrine (NE, 50 microM), isoproterenol (0.2 mM) or dopamine (0.1 mM) produced an inhibition of TG activity in SCG but had no effect in NG. The inhibitory effects of the adrenergic agonists in SCG were blocked by the beta-adrenergic antagonist, propranolol (10 microM) and alpha 2-adrenergic antagonist, yohimbine (10 microM). A kinetic study revealed that the ACh-induced stimulation of TG activity in SCG and NG was a result of decrease in apparent Km and an increase in Vmax value, whereas the NE-induced inhibition of SCG enzyme activity was a result of an increased Km and decreased Vmax. 45Ca2+ influx into excised SCG or NG was significantly reduced by the application of either ACh or NE. The ACh inhibition was effectively blocked by either hexamethonium or atropine. The NE inhibition was more effectively blocked by yohimbine than by propranolol. These results suggest that the rapid alterations of TG activity in SCG produced by cholinergic and adrenergic neurotransmitters are attributable to the processes of receptor-mediated depolarization and hyperpolarization, respectively, via modulation of nerve-impulse-induced Ca2+ fluxes during synaptic activity.
Department of Physiology, School of Medicine, Fujita Health University, Aichi, Japan.
M
M
Ando
Y
Y
Nakashima
Y
Y
Nagata
D000109:Acetylcholine / Q000494:pharmacology*; D000332:Aerobiosis; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D005260:Female; D005728:Ganglia, Sympathetic / Q000201:enzymology*; D018738:Hexamethonium; D006584:Hexamethonium Compounds / Q000494:pharmacology; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D009620:Nodose Ganglion / Q000201:enzymology*; D009638:Norepinephrine / Q000494:pharmacology*; D011224:Prazosin / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011503:Transglutaminases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015016:Yohimbine / Q000494:pharmacology
D006584:Hexamethonium Compounds; D015016:Yohimbine; D018738:Hexamethonium; D001285:Atropine; D011433:Propranolol; D011503:Transglutaminases; D007545:Isoproterenol; D000109:Acetylcholine; D002118:Calcium; D009638:Norepinephrine; D011224:Prazosin