Protein Phosphorylation and Phospholipid Metabolism in the Superior Cervical Ganglion

Abstract

Our laboratory has been interested in the mechanisms by which neuronal activity regulates neuronal metabolism. Specifically, we have been studying the mechanisms by which neuronal activity regulates tyrosine hydroxylase (tyrosine 3-monooxygenase, EC 1.14.16.2) activity and catecholamine synthesis in the superior cervical ganglion (SCG). The SCG is a prototypical sympathetic ganglion. The noradrenergic principal neurons in this ganglion innervate the pineal gland, the salivary glands, the thyroid gland, smooth muscles of the iris, and blood vessels in the head and neck. These neurons are innervated by preganglionic sympathetic nerves whose cell bodies lie in the intermediolateral column of the spinal cord and which release acetylcholine (ACh) as their classical neurotransmitter. The principal ganglionic neurons contain both nicotinic and muscarinic cholinergic receptors. Stimulation of the nicotinic receptors produces a rapid depolarization that is due to a generalized increase in the permeability of the neurons to cations. Nicotinic stimulation typically leads to the generation of action potentials in the neurons. Stimulation of the muscarinic receptors produces a slower depolarization that is due at least in part to the inhibition of K⁺ efflux from the cells. These neurons also contain voltage-sensitive Ca²⁺ channels; depolarization activates these channels and thereby causes an additional influx of Ca^2x into the cells. Finally, the pre-ganglionic neurons contain a variety of peptides in addition to ACh; the physiological effects of these peptides have not yet been determined.