Abstract:
Nerve apposition on nicotinic acetylcholine receptor clusters
and invagination of the post-synaptic membrane (i.e. secondary
fold formation) occur by embryonic day 18.5 at the
neuromuscular junctions (NMJs) in mouse skeletal muscles.
Finding the molecules expressed at the NMJ at this stage of
development may help elucidating how the strong linkage
between a nerve terminal and a muscle fiber is established.
Immunohistochemical analyses indicated that the membraneanchored
matrix metalloproteinase regulator RECK was enriched
at the NMJ in adult skeletal muscles. Confocal and
electron microscopy revealed the localization of RECK
immunoreactivity in secondary folds and subsynaptic intracellular
compartments in muscles. Time course studies indicated
that RECK immunoreactivity becomes associated with
the NMJ in the diaphragm at around embryonic day 18.5 and
thereafter. These findings, together with known properties of
RECK, support the hypothesis that RECK participates in NMJ
formation and/or maintenance, possibly by protecting extracellular
components, such as synaptic basal laminae, from
proteolytic degradation.
