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Previous studies of the development of cholinergic sympathetic innervation of sweat glands in rat footpads suggested that these terminals initially exhibit noradrenergic properties which are lost as the glands and their innervation mature. We have treated neonatal and adult rats with 6-hydroxydopamine (6-OHDA), a toxic congener of norepinephrine, and compared its effects on the cholinergic sympathetic innervation of sweat glands and the noradrenergic sympathetic innervation of the iris, salivary gland, and blood vessels. As reported by others, 6-OHDA treatment of neonates caused the destruction of noradrenergic fibers in the iris and salivary gland but did not affect other fibers projecting to these targets that stain for acetylcholinesterase (AChE). We found that 6-OHDA treatment of neonatal animals also caused the destruction of the sympathetic axons in immature sweat glands that possess catecholamine histofluorescence and tyrosine-hydroxylase-like immunoreactivity. Furthermore, when such animals were examined as adults, we found no AChE staining, vasoactive intestinal peptide (VIP)-like immunoreactivity, or characteristic sympathetic axonal varicosities. However, the denervated glands were invested by a plexus of sensory axons, some of which exhibited substance P-like immunoreactivity (SP-IR). An increase in the number of SP-IR fibers also occurred in the sympathetically denervated irides of these animals. Chronic treatment of neonates with guanethidine, another adrenergic sympathetic neurotoxin, resulted in similar loss of cholinergic sweat gland innervation. Treatment of adults rats with doses of 6-OHDA identical to those used to treat neonates caused the loss of noradrenergic fibers from the iris, salivary gland, and many blood vessels but did not noticeably affect AChE and VIP staining or axonal ultrastructure in the sweat glands. However, treatment with higher doses of 6-OHDA did cause significant axonal degeneration. The response of the sympathetic innervation of developing but not mature sweat glands to 6-OHDA provides evidence for a transition from noradrenergic to cholinergic phenotype during the development of sympathetic neurons in vivo similar to the transition observed in cell culture. The sprouting of sensory axons may be caused by NGF-like trophic influences present in some sympathetically denervated tissues.

Mature sympathetic neurons contain one or more neuropeptides in addition to a classical neurotransmitter. We compared the development of two peptides, neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP), in rat superior cervical (SCG) and stellate ganglia. NPY immunoreactivity (-IR) was first detected at embryonic day (E) 12.5. It was of similar immunofluorescence intensity in almost all tyrosine hydroxylase (TH)-IR cells. In contrast, VIP-IR, of variable fluorescence intensity, appeared at E14.5 in a subset of TH-IR cells in the stellate ganglion but not in SCG. Both peptides were present in bromodeoxyuridine-labeled neuronal precursors as well as neurons. The intensity of NPY immunofluorescence increased until E16.5. Subsequently, while it continued to increase in some neurons, the intensity decreased in others so that at birth approximately 55% of SCG and stellate neurons were NPY-IR. Developmental changes in NPY concentration, determined by radioimmunoassay, were similar in both ganglia, increasing between E14.5 and E16.5 and then decreasing 60% between E16.5 and birth. VIP expression differed from that of NPY. The proportion of VIP-IR cells began to decrease the day after VIP-IR was first detected. Although VIP-IR was present in one-third of E14.5 TH-IR stellate cells, at birth only 2% were VIP-IR. VIP-IR, measured by radioimmunoassay, was uniformly severalfold more concentrated in the stellate than SCG, and its concentration decreased throughout embryonic development, 40% between E14.5 and E16.5 and 95% by birth. In situ hybridization revealed detectable mRNA for both NPY and VIP at E14.5 in stellate ganglion and mRNA for NPY, but not VIP, in SCG. Initially, ganglionic neuropeptide mRNA appeared uniformly distributed but became heterogeneous. Our data indicate that features of the diverse peptidergic phenotypes expressed by sympathetic neurons are present when peptides are first detected while others arise subsequently. The final acquisition of peptidergic phenotypic diversity is complex, entailing both early induction in many cells and subsequent restriction to specific subpopulations.

Depolarization has been shown to alter the biosynthesis of a number of neurotransmitters and neuromodulators. In the rat superior cervical ganglion (SCG), for example, depolarization has been reported to increase catecholamine biosynthesis and to decrease the level of substance P. We have recently found that, although the level of vasoactive intestinal peptide (VIP)-like immunoreactivity (IR) is normally low in the SCG, it increases significantly 48 hr after adult ganglia are deafferented in situ or placed in organ culture. Both manipulations decrease electrical activity of postganglionic neurons. To determine whether the increases in ganglionic VIP-IR could be a consequence of decreased depolarization of sympathetic neurons, the effect of depolarization on the expression of VIP-IR was examined in organ cultures of neonatal and adult SCG. Depolarization with elevated K+ (30 mM) or veratridine (1.5 microM) amplified, rather than blocked, the increases in VIP-IR content seen after 24 hr. Further, it increased the number of detectable VIP-IR neuronal cell bodies and processes. The stimulatory effects of veratridine were prevented by TTX. Since similar changes in expression of VIP-IR were evident in dissociated cell cultures of the SCG, cell-cell interactions requiring intact ganglionic architecture are not necessary for altered peptide expression. Elevating the concentration of Mg2+ blocked the ability of K+ and veratridine to increase VIP-IR in dissociated cell culture, raising the possibility that the effects of depolarization on VIP-IR are mediated by increased Ca2+ entry. The depolarizing conditions that increased VIP-IR also increased substance P-IR. While higher concentrations of veratridine (50 microM) blocked the elevation of both VIP- and substance P-IR induced by explantation, they produced significant neuronal death. Since depolarization with either 30 mM KCl or 1.5 microM veratridine increases expression of VIP-IR in neonatal and adult ganglia, decreased depolarization is unlikely to cause the increases in VIP- and substance P-IR that occur in culture. Furthermore, our data raise the possibility that sympathetic nerve activity in vivo can increase expression of these peptides.