M. Stanke et al., The early expression of VAChT and VIP in mouse sympathetic ganglia is not induced by cytokines acting through LIFR beta or CNTFR alpha, MECH DEVEL, 91(1-2), 2000, pp. 91-96
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
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