Glucocorticosteroids modulate transmitter choice in developing superior cervical ganglion

Abstract

In vivo the superior cervical ganglion (SCG) is adrenergic with less than 5% of neurones expressing cholinergic properties¹. In vitro these neurones can develop either an adrenergic or cholinergic phenotype, depending on the nature of the culture conditions²: when immature SCG neurones are cultured in the virtual absence of non-neuronal cells they develop adrenergic properties, synthesising noradrenaline (NA) and a negligible amount of acetylcholine (ACh)^3,4; when ganglionic non-neuronal cells are present the neurones develop a cholinergic phenotype, characterised by increased ACh synthesis and a corresponding decrease in NA synthesis⁵. If ganglionic non-neuronal cells release a factor which induces cholinergic properties in vitro, why is the SCG not cholinergic in vivo? In vitro there are none of the presynaptic, postsynaptic, or circulatory hormonal influences normally present in neuronal development. Depolarisation of SCG neurones in vitro prevents the development of cholinergic properties, suggesting that the preganglionic input in vivo may maintain the adrenergic nature of the SCG⁶. However, as prevention of depolarisation of neurones in vivo by preganglionic nerve section does not alter the adrenergic character of the SCG, influences other than the preganglionic input must be involved in preventing the development of cholinergic properties in vivo⁷. Circulatory glucocorticosteroids modulate the induction of neurotransmitter synthetic enzymes in the SCG^8,9 and have been reported to change the expression of adrenergic and cholinergic properties in a pheochromocytoma cell line¹⁰. We present here results suggesting that glucocorticosteroids are involved in specifying the transmitter type used in the SCG.