The mechanisms and possible sites of acetylcholine release during chick primary sensory neuron differentiation

Corsetti, Veronica; Mozzetta, Chiara; Biagioni, Stefano; Tocco, Gabriella Augusti; Tata, Ada Maria

doi:10.1016/j.lfs.2012.08.026

Cited by 12 publications

(16 citation statements)

References 39 publications

(51 reference statements)

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“…A role for endogenous ACh in regulating this pathway is supported by our measurement of secreted ACh detected in the culture medium, approximately 16 nmoles/ml (16 μM), which far exceeds estimations of the ACh K D of 0.2-0.4 nM for the M 1 R taken from studies with rat brain neurons (46,47). These data also correspond well with extracellular levels of ACh in the range of 0.1 to 0.6 nM detected using microdialysis in human and rat skin (48,49). Thus, it is feasible that endogenously released ACh could act on M 1 R at nerve endings in the skin.…”

Section: Discussionsupporting

confidence: 82%

“…In vitro work in the current study (Supplemental Figure 3, C-E) and in vivo studies in adult rat utilizing immunohistochemistry for the peripheral form of ChAT reveal that the protein is present in the cell body, axon, and nerve endings in the skin (25,48). Furthermore, compartmented cultures using Campenot chambers of embryonic chick sensory neurons demonstrated secretion of ACh within the cell body compartment and also within the distal axonal compartment (49), emphasizing that ACh could be derived from sites along the whole sensory neuron axis. The best-characterized role of M 1 R in the PNS is in sympathetic neurons, where it mediates the M current (50).…”

Section: Discussionsupporting

confidence: 49%

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Selective antagonism of muscarinic receptors is neuroprotective in peripheral neuropathy

Calcutt¹,

Smith²,

Frizzi³

et al. 2017

Journal of Clinical Investigation

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Section: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 49%

Selective antagonism of muscarinic receptors is neuroprotective in peripheral neuropathy

Calcutt¹,

Smith²,

Frizzi³

et al. 2017

Journal of Clinical Investigation

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“…Together, our data demonstrate that ACh represents an additional molecule active in regulating axon‐SC cross‐talk. As recently demonstrated, ACh can be released along cholinergic axons (Corsetti et al, ) and, therefore, contribute to the modulation of axon‐ensheathing, SC proliferation and differentiation. Lack or low levels of ACh, together with high levels of NRG1, may favor SC proliferation, while high levels of ACh would arrest SC proliferation and direct them to a differentiation program towards a myelinating phenotype.…”

Section: Discussionmentioning

confidence: 90%

M2 muscarinic receptor activation regulates schwann cell differentiation and myelin organization

Uggenti

Stefano

Costantino

et al. 2014

Developmental Neurobiology

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Glial cells express acetylcholine receptors. In particular, rat Schwann cells express different muscarinic receptor subtypes, the most abundant of which is the M2 subtype. M2 receptor activation causes a reversible arrest of the cell cycle. This negative effect on Schwann cell proliferation suggests that these cells may possibly progress into a differentiating program. In this study we analyzed the in vitro modulation, by the M2 agonist arecaidine, of transcription factors and specific signaling pathways involved in Schwann cell differentiation. The arecaidine-induced M2 receptor activation significantly upregulates transcription factors involved in the promyelinating phase (e.g., Sox10 and Krox20) and downregulates proteins involved in the maintenance of the undifferentiated state (e.g., c-jun, Notch-1, and Jagged-1). Furthermore, arecaidine stimulation significantly increases the expression of myelin proteins, which is accompanied by evident changes in cell morphology, as indicated by electron microscopy analysis, and by substantial cellular re-distribution of actin and cell adhesion molecules. Moreover, ultrastructural and morphometric analyses on sciatic nerves of M2/M4 knockout mice show numerous degenerating axons and clear alterations in myelin organization compared with wild-type mice. Therefore, our data demonstrate that acetylcholine mediates axon-glia cross talk, favoring Schwann cell progression into a differentiated myelinating phenotype and contributing to compact myelin organization.

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“…6) makes it plausible that a similar regulation mechanism exists for the cholinergic locus in mammals and birds, which may produce as a result the dual and/or individual expression of both VAChT and ChAT proteins. A specific downregulation of VAChT expression concomitant with an increase in the expression of ChAT has been reported in neurons of the dorsal root ganglia of the chick (Corsetti et al, 2012). Therefore, it is possible that a downregulation of the cholinergic locus may occur in the Ipc cells, which is specifically strong for the VAChT gene, leaving a diminished or "leaky" expression for the ChAT gene.…”

Section: A Possible Downregulation Of the Cholinergic Locus In The Ipmentioning

confidence: 96%

The isthmic nuclei providing parallel feedback connections to the avian tectum have different neurochemical identities: Expression of glutamatergic and cholinergic markers in the chick (Gallus gallus)

González-Cabrera

Garrido-Charad

Roth

et al. 2015

J of Comparative Neurology

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Retinal inputs to the optic tectum (TeO) triggered by moving stimuli elicit synchronized feedback signals from two isthmic nuclei: the isthmi parvocelullaris (Ipc) and isthmi semilunaris (SLu). Both of these nuclei send columnar axon terminals back to the same tectal position receiving the retinal input. The feedback signals from the Ipc seem to act as an attentional spotlight by selectively boosting the propagation of retinal inputs from the tectum to higher visual areas. Although Ipc and SLu nuclei are widely considered cholinergic because of their immunoreactivity for choline acetyltransferase (ChAT), contradictory findings, including the expression of the vesicular glutamate transporter 2 (VGluT2) mRNA in Ipc neurons, have raised doubts about the purely cholinergic nature of this nucleus. In this study, in chicks, we revise the neurochemical identity of the isthmic nuclei by using in situ hybridization assays for VGluT2 along with three cholinergic markers: the vesicular acetylcholine transporter (VAChT), the high-affinity choline transporter (CHT1) and ChAT. We found that neurons in the SLu showed strong mRNA expression of all three cholinergic markers, whereas the expression of VAChT mRNA in the Ipc was undetectable in our essays. Instead, Ipc neurons exhibited a strong expression of VGluT2 mRNA. Immunohistochemistry assays showed VGluT2 immunoreactivity in the TeO codistributing with anterogradely labeled Ipc axon-terminal boutons, further supporting a glutamatergic function for the Ipc nucleus. Therefore, our results strongly suggest that, in the chick, whereas the feedback from the SLu to the TeO is indeed cholinergic, the feedback from the Ipc has a marked glutamatergic component.

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The mechanisms and possible sites of acetylcholine release during chick primary sensory neuron differentiation

Cited by 12 publications

References 39 publications

Selective antagonism of muscarinic receptors is neuroprotective in peripheral neuropathy

Selective antagonism of muscarinic receptors is neuroprotective in peripheral neuropathy

M2 muscarinic receptor activation regulates schwann cell differentiation and myelin organization

The isthmic nuclei providing parallel feedback connections to the avian tectum have different neurochemical identities: Expression of glutamatergic and cholinergic markers in the chick (Gallus gallus)

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