Nicotinic α7 receptor‐induced adenosine release from perisynaptic Schwann cells controls acetylcholine spillover from motor endplates

2020 ◽  
Vol 154 (3) ◽  
pp. 263-283 ◽  
Author(s):  
José B. Noronha‐Matos ◽  
Laura Oliveira ◽  
Ana R. Peixoto ◽  
Liliana Almeida ◽  
Lilian Martins Castellão‐Santana ◽  
...  
Keyword(s):  
Schwann Cells ◽  
Motor Endplates ◽  
Adenosine Release ◽  
Perisynaptic Schwann Cells

scholarly journals Activity-induced Ca2+ signaling in perisynaptic Schwann cells of the early postnatal mouse is mediated by P2Y1 receptors and regulates muscle fatigue

eLife ◽  
2018 ◽  
Vol 7 ◽  
Author(s):  
Dante J Heredia ◽  
Cheng-Yuan Feng ◽  
Grant W Hennig ◽  
Robert B Renden ◽  
Thomas W Gould
Keyword(s):  
Muscle Fatigue ◽  
Schwann Cells ◽  
Glial Cells ◽  
Nerve Stimulation ◽  
Neural Activity ◽  
Purinergic Receptor ◽  
Cytosolic Calcium ◽  
High Potassium ◽  
Presynaptic Function ◽  
Perisynaptic Schwann Cells

Perisynaptic glial cells respond to neural activity by increasing cytosolic calcium, but the significance of this pathway is unclear. Terminal/perisynaptic Schwann cells (TPSCs) are a perisynaptic glial cell at the neuromuscular junction that respond to nerve-derived substances such as acetylcholine and purines. Here, we provide genetic evidence that activity-induced calcium accumulation in neonatal TPSCs is mediated exclusively by one subtype of metabotropic purinergic receptor. In P2ry1 mutant mice lacking these responses, postsynaptic, rather than presynaptic, function was altered in response to nerve stimulation. This impairment was correlated with a greater susceptibility to activity-induced muscle fatigue. Interestingly, fatigue in P2ry1 mutants was more greatly exacerbated by exposure to high potassium than in control mice. High potassium itself increased cytosolic levels of calcium in TPSCs, a response which was also reduced P2ry1 mutants. These results suggest that activity-induced calcium responses in TPSCs regulate postsynaptic function and muscle fatigue by regulating perisynaptic potassium.

scholarly journals CXCL 12α/ SDF ‐1 from perisynaptic Schwann cells promotes regeneration of injured motor axon terminals

2017 ◽  
Vol 9 (8) ◽  
pp. 1000-1010 ◽  
Author(s):  
Samuele Negro ◽  
Francesca Lessi ◽  
Elisa Duregotti ◽  
Paolo Aretini ◽  
Marco La Ferla ◽  
...  
Keyword(s):  
Schwann Cells ◽  
Motor Axon ◽  
Axon Terminals ◽  
Perisynaptic Schwann Cells

scholarly journals Schwann Cells Overexpressing FGF-2 Alone or Combined with Manual Stimulation Do Not Promote Functional Recovery after Facial Nerve Injury

2009 ◽  
Vol 2009 ◽  
pp. 1-11 ◽  
Author(s):  
Kirsten Haastert ◽  
Maria Grosheva ◽  
Srebrina K. Angelova ◽  
Orlando Guntinas-Lichius ◽  
Emmanouil Skouras ◽  
...  
Keyword(s):  
Facial Nerve ◽  
Schwann Cells ◽  
Function Analysis ◽  
Fibroblast Growth Factor 2 ◽  
Fibroblast Growth ◽  
Nerve Transection ◽  
Motor Endplates ◽  
Adult Rat ◽  
Manual Stimulation ◽  
Facial Nerves

Purpose. To determine whether transplantation of Schwann cells (SCs) overexpressing different isoforms of fibroblast growth factor 2 (FGF-2) combined with manual stimulation (MS) of vibrissal muscles improves recovery after facial nerve transection in adult rat.Procedures. Transected facial nerves were entubulated with collagen alone or collagen plus naïve SCs or transfected SCs. Half of the rats received daily MS. Collateral branching was quantified from motoneuron counts after retrograde labeling from 3 facial nerve branches. Quality assessment of endplate reinnervation was combined with video-based vibrissal function analysis.Results. There was no difference in the extent of collateral axonal branching. The proportion of polyinnervated motor endplates for either naïve SCs or FGF-2 over-expressing SCs was identical. Postoperative MS also failed to improve recovery.Conclusions. Neither FGF-2 isoform changed the extent of collateral branching or polyinnervation of motor endplates; furthermore, this motoneuron response could not be overridden by MS.

scholarly journals THE FINE STRUCTURE OF MOTOR ENDPLATE MORPHOGENESIS

1969 ◽  
Vol 42 (1) ◽  
pp. 154-169 ◽  
Author(s):  
A. M. Kelly ◽  
S. I. Zacks
Keyword(s):  
Fine Structure ◽  
Schwann Cells ◽  
Basal Lamina ◽  
Plasma Membranes ◽  
Muscle Cells ◽  
Motor Endplate ◽  
Intercostal Muscle ◽  
Motor Endplates ◽  
Terminal Axon ◽  
Small Muscle

The fine structure of the developing neuromuscular junction of rat intercostal muscle has been studied from 16 days in utero to 10 days postpartum. At 16 days, neuromuscular relations consist of close membrane apposition between clusters of axons and groups of myotubes. Focal electron-opaque membrane specializations more intimately connect axon and myotube membranes to each other. What relation these focal contacts bear to future motor endplates is undetermined. The presence of a group of axons lying within a depression in a myotube wall and local thickening of myotube membranes with some overlying basal lamina indicates primitive motor endplate differentiation. At 18 days, large myotubes surrounded by new generations of small muscle cells occur in groups. Clusters of terminal axon sprouts mutually innervate large myotubes and adjacent small muscle cells within the groups. Nerve is separated from muscle plasma membranes by synaptic gaps partially filled by basal lamina. The plasma membranes of large myotubes, where innervated, simulate postsynaptic membranes. At birth, intercostal muscle is composed of separate myofibers. Soleplate nuclei arise coincident with the peripheral migration of myofiber nuclei. A possible source of soleplate nuclei from lateral fusion of small cells' neighboring areas of innervation is suspected but not proven. Adjacent large and small myofibers are mutually innervated by terminal axon networks contained within single Schwann cells. Primary and secondary synaptic clefts are rudimentary. By 10 days, some differentiating motor endplates simulate endplates of mature muscle. Processes of Schwann cells cover primary synaptic clefts. Axon sprouts lie within the primary clefts and are separated from each other. Specific neural control over individual myofibers may occur after neural processes are segregated in this manner.

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