The early expression of VAChT and VIP in mouse sympathetic ganglia is not induced by cytokines acting through LIFR beta or CNTFR alpha

Sympathetic ganglia consist of noradrenergic and cholinergic neurons. The c holinergic marker protein vesicular acetylcholine transporter (VAChT) and t he neuropeptide vasoactive intestinal peptide (VIP), co-expressed in mature cholinergic sympathetic neurons, are first detectable during embryonic dev elopment of rat sympathetic ganglia. However, the subpopulation of choliner gic sympathetic neurons which innervates sweat glands in mammalian footpads starts to express VAChT and VIP during the first postnatal weeks, under th e influence of sweat gland-derived signals. In vitro evidence suggests that the sweat gland-derived cholinergic differentiation factor belongs to a gr oup of neuropoietic cytokines, including LIF, CNTF and CT-1, that act throu gh a LIFR beta-containing cytokine receptor. To investigate whether the emb ryonic expression of cholinergic properties is elicited by a related cytoki ne, the expression of VAChT and VIP was analyzed in stellate ganglia of mic e deficient for the cytokine receptor subunits LIFR beta or CNTFR alpha. Th e density of VAChT- and VIP immunoreactive cells in stellate ganglia of new -born animals was not different in LIFR beta(-/-) and CNTFR alpha(-/-) gang lia as compared to ganglia from wild-type mice. These results demonstrate t hat the early, embryonic expression of VAChT and VIP is not induced by cyto kines acting through LIFR beta- or CNTFR alpha-containing receptors. (C) 20 00 Elsevier Science Ireland Ltd. All rights reserved.