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process involving progressive loss o f distal ends o f nerve terminals. If adhesion by PSCs
does indeed occur, then these observations suggest that PSCs mediate adhesion by release of
attachment molecules that bind nerve terminals to the extracellular matrix. In the absence of
PSCs, nerve terminals would continue to be maintained by attachment to the reservoir of
such molecules in the matrix. However, once these molecules are depleted by normal
turnover, retraction would set in. Nerve terminal processes under new PSC sprouts would
have fewest o f these attachment molecules to bind to, and would be most vulnerable to
retraction, as is observed. A primary role for PSCs in attachment would also explain the
lack o f acute effects on physiology or ultrastructure after PSC ablation.
Therefore, maybe Virchow was right: glial cells may be “glue” - but “smart glue,”
which detect synaptic activity, which can extend when this activity is disrupted or in
response to regeneration after injury, and which can dictate the pattern o f innervation. Nerve
terminal growth, per se, appears to be intrinsic to nerve terminals and likely regulated by
activity, but guidance and maintenance may involve local adhesion factors from PSCs,
bound to the extracellular matrix, and interacting with anchoring complexes such as
integrins.
New tricks for an old dog: PSCs at the neuromuscular junction
The present studies identify several previously unappreciated functions of
perisynaptic glial cells at the vertebrate NMJ, the synapse that has served for almost a
century as a prototype, yielding the fundamental principles o f synapse structure, synapse
formation and synaptic transmission. However, numerous other questions remain regarding
the roles o f PSCs at the NMJ. Based on current knowledge or speculation, PSCs could be
involved in synapse formation, synaptic growth and stabilization, maturation o f synaptic
111
R e p r o d u c e d with p erm issio n of th e copyright ow n er. F u rth e r rep ro d u ctio n prohibited w ithout p erm issio n .
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| Title | The role of perisynaptic glial cells in synapse formation, maintenance, and regeneration. - Page 121 |
| Repository email | cisadmin@lib.usc.edu |
| Full text | process involving progressive loss o f distal ends o f nerve terminals. If adhesion by PSCs does indeed occur, then these observations suggest that PSCs mediate adhesion by release of attachment molecules that bind nerve terminals to the extracellular matrix. In the absence of PSCs, nerve terminals would continue to be maintained by attachment to the reservoir of such molecules in the matrix. However, once these molecules are depleted by normal turnover, retraction would set in. Nerve terminal processes under new PSC sprouts would have fewest o f these attachment molecules to bind to, and would be most vulnerable to retraction, as is observed. A primary role for PSCs in attachment would also explain the lack o f acute effects on physiology or ultrastructure after PSC ablation. Therefore, maybe Virchow was right: glial cells may be “glue” - but “smart glue,” which detect synaptic activity, which can extend when this activity is disrupted or in response to regeneration after injury, and which can dictate the pattern o f innervation. Nerve terminal growth, per se, appears to be intrinsic to nerve terminals and likely regulated by activity, but guidance and maintenance may involve local adhesion factors from PSCs, bound to the extracellular matrix, and interacting with anchoring complexes such as integrins. New tricks for an old dog: PSCs at the neuromuscular junction The present studies identify several previously unappreciated functions of perisynaptic glial cells at the vertebrate NMJ, the synapse that has served for almost a century as a prototype, yielding the fundamental principles o f synapse structure, synapse formation and synaptic transmission. However, numerous other questions remain regarding the roles o f PSCs at the NMJ. Based on current knowledge or speculation, PSCs could be involved in synapse formation, synaptic growth and stabilization, maturation o f synaptic 111 R e p r o d u c e d with p erm issio n of th e copyright ow n er. F u rth e r rep ro d u ctio n prohibited w ithout p erm issio n . |
