Target-Dependent Development of the Vesicular Acetylcholine Transporter in Rodent Sweat Gland Innervation

Guidry, Guy; Landis, Story C.

doi:10.1006/dbio.1998.8929

Cited by 54 publications

(43 citation statements)

References 46 publications

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“…We first examined whether denervated nerves would regenerate during the 3-mo tracing period, which would confound our conclusions. In normal digit tips (n = 12), the epidermis and hair follicles on the dorsal side contain sensory innervations, whereas sweat glands on the ventral side are innervated by sympathetic nerves, which have been previously shown to be necessary for sweat gland maturation during limb development (28,29). Consistent with these reports, control digits showed robust label of beta III tubulin in epidermal appendages ( Fig.…”

Section: Resultssupporting

confidence: 82%

Clonal analysis reveals nerve-dependent and independent roles on mammalian hind limb tissue maintenance and regeneration

Rinkevich

Montoro²,

Muhonen³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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The requirement and influence of the peripheral nervous system on tissue replacement in mammalian appendages remain largely undefined. To explore this question, we have performed genetic lineage tracing and clonal analysis of individual cells of mouse hind limb tissues devoid of nerve supply during regeneration of the digit tip, normal maintenance, and cutaneous wound healing. We show that cellular turnover, replacement, and cellular differentiation from presumed tissue stem/progenitor cells within hind limb tissues remain largely intact independent of nerve and nerve-derived factors. However, regenerated digit tips in the absence of nerves displayed patterning defects in bone and nail matrix. These nerve-dependent phenotypes mimic clinical observations of patients with nerve damage resulting from spinal cord injury and are of significant interest for translational medicine aimed at understanding the effects of nerves on etiologies of human injury.pattern formation | peripheral nerve | stem cell T he regrowth of vertebrate appendages has been considered a classic model system for interrogating the mechanisms and requirements for tissue/organ generation and regeneration across various phyla (1-5). Urodeles regenerate entire limbs by proliferation of fate-restricted stem and progenitor cells and form a blastema, the collection of cells at the interface of stump and wound epidermis, in a process mediated by nerve-derived factors (6-10). In Urodeles, surgical denervation before amputation results in the inhibition of blastema formation, and ultimately results in regeneration failure. Evidence from fish and amphibians suggests that nerve dependence may be a function of a threshold level of nerve factors with a direct correlation between nerve fibers and degree of regeneration (3,11,12) and supports the idea that nerve dependence may be an evolutionarily conserved requirement for the regeneration of vertebrate limb tissues.Mammalian limbs consist of multiple tissues that are derived from various embryonic origins and germ layers, including embryonic ectoderm, embryonic mesoderm, and embryonic neuralcrest. Recent lineage-tracing studies have demonstrated that tissue-resident stem and progenitor cells that are fate-restricted in their developmental potential are responsible for appendage regeneration of fish, salamanders, and mice (13-16). These cumulative data demonstrate that fate-restricted stem/progenitors as cells of origin, rather than dedifferentiation or transdifferentiation of terminally differentiated cells, represents an evolutionarily conserved cellular mechanism that explains the observed regrowth of the vertebrate appendages.Collectively, the commonalities of nerve dependence and stem/ progenitor fate restriction across vertebrate phyla further highlight the possibility that nerve dependence on appendage regrowth may take place within mammals, and possibly humans. In support of this, human clinical reports indicate that skin complications are manifested in response to spinal cord injury (SCI), suggesting a...

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Section: Resultssupporting

confidence: 82%

Clonal analysis reveals nerve-dependent and independent roles on mammalian hind limb tissue maintenance and regeneration

Rinkevich

Montoro²,

Muhonen³

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…We analyzed Satb2 and Vacht coexpression in sections of rat stellate ganglion at three developmental stages, embryonic day 18 (E18), P1/P2, and P30, that is, before (E18, P1/P2) and after (P30) the innervation of one of the cholinergic target tissues, the forepaw sweat glands (Guidry and Landis, 1998). At E18 and P1/P2, we found a small number of postganglionic sympathetic neurons positive for Vacht immunoreactivity, as previously reported .…”

Section: Satb2 Expression In Vivo Labels a Subpopulation Of Cholinergsupporting

confidence: 66%

The Sympathetic Neurotransmitter Switch Depends on the Nuclear Matrix Protein Satb2

Apostolova

Loy²,

Dorn³

et al. 2010

J. Neurosci.

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Sympathetic neurons can switch their neurotransmitter phenotype from noradrenergic to cholinergic on exposure to neuropoietic cytokines in vitro and in vivo. Here, we provide evidence that this transspecification is regulated by the chromatin architecture protein Satb2. Treatment with the neuropoietic cytokines ciliary neurotrophic factor (CNTF) and leukemia inhibitory factor rapidly and strongly increases Satb2 transcript and protein levels in cultures of rat superior cervical ganglia neurons.

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“…This correlates with the timing of the transmitter phenotype switch during sweat gland innervation. The postnatal increase in the number of VIP-and VAChT-positive cells suggests that the cholinergic sympathetic neurons have not already become committed during embryonic development (Schäfer et al, 1997), and supports the notion that the gp130-dependent population is generated by target-induced differentiation (Guidry and Landis, 1998). Conversely, the gp130-independent population represents cells that acquired cholinergic properties during embryonic stages, most likely independently of target innervation.…”

Section: Quantitative Analysis Of Tuj1-ir Is Shown In (C) (D-f) Sweasupporting

confidence: 58%

Target-dependent specification of the neurotransmitter phenotype:cholinergic differentiation of sympathetic neurons is mediated in vivo by gp130 signaling

et al. 2006

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Sympathetic neurons are generated through a succession of differentiation steps that initially lead to noradrenergic neurons innervating different peripheral target tissues. Specific targets, like sweat glands in rodent footpads, induce a change from noradrenergic to cholinergic transmitter phenotype. Here, we show that cytokines acting through the gp130 receptor are present in sweat glands. Selective elimination of the gp130 receptor in sympathetic neurons prevents the acquisition of cholinergic and peptidergic features (VAChT, ChT1, VIP) without affecting other properties of sweat gland innervation. The vast majority of cholinergic neurons in the stellate ganglion, generated postnatally, are absent in gp130-deficient mice. These results demonstrate an essential role of gp130-signaling in the target-dependent specification of the cholinergic neurotransmitter phenotype.

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Target-Dependent Development of the Vesicular Acetylcholine Transporter in Rodent Sweat Gland Innervation

Cited by 54 publications

References 46 publications

Clonal analysis reveals nerve-dependent and independent roles on mammalian hind limb tissue maintenance and regeneration

Clonal analysis reveals nerve-dependent and independent roles on mammalian hind limb tissue maintenance and regeneration

The Sympathetic Neurotransmitter Switch Depends on the Nuclear Matrix Protein Satb2

Target-dependent specification of the neurotransmitter phenotype:cholinergic differentiation of sympathetic neurons is mediated in vivo by gp130 signaling

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