scholarly journals The structure and organization of lanceolate mechanosensory complexes at mouse hair follicles

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Lishi Li ◽  
David D Ginty

In mouse hairy skin, lanceolate complexes associated with three types of hair follicles, guard, awl/auchene and zigzag, serve as mechanosensory end organs. These structures are formed by unique combinations of low-threshold mechanoreceptors (LTMRs), Aβ RA-LTMRs, Aδ-LTMRs, and C-LTMRs, and their associated terminal Schwann cells (TSCs). In this study, we investigated the organization, ultrastructure, and maintenance of longitudinal lanceolate complexes at each hair follicle subtype. We found that TSC processes at hair follicles are tiled and that individual TSCs host axonal endings of more than one LTMR subtype. Electron microscopic analyses revealed unique ultrastructural features of lanceolate complexes that are proposed to underlie mechanotransduction. Moreover, Schwann cell ablation leads to loss of LTMR terminals at hair follicles while, in contrast, TSCs remain associated with hair follicles following skin denervation in adult mice and, remarkably, become re-associated with newly formed axons, indicating a TSC-dependence of lanceolate complex maintenance and regeneration in adults.

2020 ◽  
Vol 29 (4) ◽  
pp. 400-403
Author(s):  
Jiang‐Ping Wei ◽  
Yao Gong ◽  
Hong‐Bing Zhong ◽  
Tim Hua Wang ◽  
Xin‐Hua Liao

2019 ◽  
Vol 116 (19) ◽  
pp. 9168-9177 ◽  
Author(s):  
Emily D. Kuehn ◽  
Shan Meltzer ◽  
Victoria E. Abraira ◽  
Cheng-Ying Ho ◽  
David D. Ginty

Innocuous mechanical stimuli acting on the skin are detected by sensory neurons, known as low-threshold mechanoreceptors (LTMRs). LTMRs are classified based on their response properties, action potential conduction velocity, rate of adaptation to static indentation of the skin, and terminal anatomy. Here, we report organizational properties of the cutaneous and central axonal projections of the five principal hairy skin LTMR subtypes. We find that axons of neurons within a particular LTMR class are largely nonoverlapping with respect to their cutaneous end organs (e.g., hair follicles), with Aβ rapidly adapting-LTMRs being the sole exception. Individual neurons of each LTMR class are mostly nonoverlapping with respect to their associated hair follicles, with the notable exception of C-LTMRs, which exhibit multiple branches that redundantly innervate individual hair follicles. In the spinal cord, LTMR central projections exhibit rostrocaudal elongation and mediolateral compression, compared with their cutaneous innervation patterns, and these central projections also exhibit a fine degree of homotypic topographic adjacency. These findings thus reveal homotypic tiling of LTMR subtype axonal projections in hairy skin and a remarkable degree of spatial precision of spinal cord axonal termination patterns, suggesting a somatotopically precise tactile encoding capability of the mechanosensory dorsal horn.


2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Kazunori Sango ◽  
Hiroko Yanagisawa ◽  
Shizuka Takaku ◽  
Emiko Kawakami ◽  
Kazuhiko Watabe

We have established spontaneously immortalized Schwann cell lines from normal adult mice and rats and murine disease models. One of the normal mouse cell lines, IMS32, possesses some biological properties of mature Schwann cells and high proliferative activities. The IMS32 cells under hyperglycemic and/or hyperlipidemic conditions have been utilized to investigate the pathogenesis of diabetic neuropathy, especially the polyol pathway hyperactivity, glycation, increased oxidative stress, and reduced synthesis of neurotrophic factors. In addition to the mouse cell lines, our current study focuses on the characterization of a normal rat cell line, IFRS1, under normal and high glucose conditions. These Schwann cell lines can be valuable tools for exploring the detailed mechanisms leading to diabetic neuropathy and novel therapeutic approaches against that condition.


2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Robert Louis Hastings ◽  
Michelle Mikesh ◽  
Young il Lee ◽  
Wesley J. Thompson

1982 ◽  
Vol 30 (9) ◽  
pp. 912-918 ◽  
Author(s):  
D Dahl ◽  
N H Chi ◽  
L E Miles ◽  
B T Nguyen ◽  
A Bignami

Antisera to the glial fibrillary acidic (GFA) protein stained a subpopulation of Schwann cells in cryostat sections of rat sciatic nerve by indirect immunofluorescence and by the peroxidase-antiperoxidase (PAP) procedure. The staining pattern was entirely different from that obtained with vimentin antisera, which uniformly decorated endoneurial tubes. Electron microscopic examination of sciatic nerve provided a possible explanation for the relatively small number of Schwann cells decorated by GFA antisera: 10 nm filaments were mainly confined to Schwann cell processes surrounding nonmyelinated axons. A marked increase in GFA-positive Schwann cells and in Schwann cells containing filaments by electron microscopy was observed in sciatic nerves undergoing Wallerian degeneration. Conversely, immunochemical procedures failed to demonstrate the presence of antigen reacting with GFA antisera in extracts of sciatic nerve, both normal and degenerated. These include absorption experiments, double immunodiffusion, immunoaffinity chromatography, and immunoradiometric assay. Two explanations may be considered for these findings: i) Schwann cell intermediate filaments and GFA protein share common antigenic determinants, the immunohistological methods being more sensitive to detect cross-reactivity as compared to immunochemical procedures on tissue extracts; and ii) the binding of anti-GFA to Schwann cell 10 nm filaments is not due to immunological cross-reactivity.


1984 ◽  
Vol 51 (4) ◽  
pp. 777-792 ◽  
Author(s):  
H. J. Ralston ◽  
A. R. Light ◽  
D. D. Ralston ◽  
E. R. Perl

The arborizations and synaptic relationships of intra-axonally stained horseradish peroxidase- (HRP) labeled primary afferent fibers to the dorsal horn of the cat and monkey spinal cord have been studied by light and electron microscopic methods. The light microscopic arborizations of the afferent fiber types (hair follicle afferents, pacinian corpuscle afferents, type I and type II slowly adapting afferents) are similar to those described by Brown and his colleagues (1) in the cat. The synaptic profiles formed by labeled afferents contain rounded synaptic vesicles. In serial thin sections, it was found that single dorsal root axons may make hundreds or thousands of synapses with neuronal structures of the dorsal horn. The vast majority of synaptic contacts are on the dendritic trees of dorsal horn neurons. The synapses made by these low-threshold afferent axons are almost all in the deeper laminae (III-VI) of the dorsal horn. The hair follicle afferent axons and the pacinian corpuscle afferents have numerous vesicle-containing structures that synapse on them to form either axoaxonal synapses or dendroaxonal synapses. The slowly adapting afferent axons are less often found to be postsynaptic to axons or dendrites. It is concluded that different physiological classes of primary afferent axons have different morphological characteristics, both at the light and electron microscopic level.


2000 ◽  
Vol 148 (5) ◽  
pp. 1009-1020 ◽  
Author(s):  
X. Yin ◽  
G.J. Kidd ◽  
L. Wrabetz ◽  
M.L. Feltri ◽  
A. Messing ◽  
...  

This report investigated mechanisms responsible for failed Schwann cell myelination in mice that overexpress P0 (P0tg), the major structural protein of PNS myelin. Quantitative ultrastructural immunocytochemistry established that P0 protein was mistargeted to abaxonal, periaxonal, and mesaxon membranes in P0tg Schwann cells with arrested myelination. The extracellular leaflets of P0-containing mesaxon membranes were closely apposed with periodicities of compact myelin. The myelin-associated glycoprotein was appropriately sorted in the Golgi apparatus and targeted to periaxonal membranes. In adult mice, occasional Schwann cells myelinated axons possibly with the aid of endocytic removal of mistargeted P0. These results indicate that P0 gene multiplication causes P0 mistargeting to mesaxon membranes, and through obligate P0 homophilic adhesion, renders these dynamic membranes inert and halts myelination.


2019 ◽  
Author(s):  
Matthew Grove ◽  
Hyunkyoung Lee ◽  
Huaqing Zhao ◽  
Young-Jin Son

ABSTRACTPreviously we showed that YAP/TAZ promote not only proliferation but also differentiation of immature Schwann cells (SCs), thereby forming and maintaining the myelin sheath around peripheral axons (Grove et al., 2017). Here we show that YAP/TAZ are required for mature SCs to restore peripheral myelination, but not to proliferate, after nerve injury. We find that YAP/TAZ dramatically disappear from SCs of adult mice concurrent with axon degeneration after nerve injury. They reappear in SCs only if axons regenerate. YAP/TAZ ablation does not impair SC proliferation or transdifferentiation into growth promoting repair SCs. SCs lacking YAP/TAZ, however, fail to upregulate myelin-associated genes and completely fail to remyelinate regenerated axons. We also show that both YAP and TAZ are redundantly required for optimal remyelination. These findings suggest that axons regulate transcriptional activity of YAP/TAZ in adult SCs and that YAP/TAZ are essential for functional regeneration of peripheral nerve.


2021 ◽  
Author(s):  
Benayahu Elbaz ◽  
Lite Yang ◽  
Braesen Lee Rader ◽  
Riki Kawaguchi ◽  
Maria Traka ◽  
...  

Schwann cells, the main glial cell in the peripheral nervous system (PNS), ensheath bundles of small unmyelinated axons or form myelin on larger axons. PNS injuries initiate transcriptional reprograming in both Schwann cells and sensory neurons that promotes regeneration. While the factors that initiate the transcriptional reprograming in Schwann cells are well characterized, the full range of stimuli that initiate this reprograming in sensory neurons remain elusive. Here, using a genetic model of Schwann cell ablation, we find that Schwann cell loss results in transient PNS demyelination without overt axonal loss. By profiling sensory ganglia at single-cell resolution we show that this demyelination induces transcriptional reprogramming preferably in proprioceptive and Aβ RA-LTMR neurons. Transcriptional reprogramming is assumed to be a cell-autonomous response of sensory neurons to mechanical axonal injury. By identifying similar reprogramming in non-injured, demyelinated neurons, our study suggests that this reprogramming represents a non-cell-autonomous transcriptional response of sensory neurons to the loss of axon-Schwann cell interactions.


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