Linked Life Data

2388082

Source:http://linkedlifedata.com/resource/pubmed/id/2388082

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1990-9-21
pubmed:abstractText
Neuromuscular synapses in an androgen-sensitive muscle of sexually mature male mice were repeatedly observed over several-month intervals in normal animals and in animals in which testosterone levels were manipulated. In normal bulbocavernosus muscles, pre- and postsynaptic regions of neuromuscular junctions enlarge as muscle fibers grow. After castration, junctional area decreased in parallel with muscle fiber atrophy. When testosterone was resupplied to castrated animals, junctions that previously decreased in size then enlarged in parallel with muscle fiber hypertrophy. Surprisingly, these size changes occurred without loss or addition of motor nerve terminal branches or acetylcholine (ACh) receptor regions. Rather, each nerve terminal branch and underlying receptor region became smaller following castration and reenlarged following testosterone treatment. Several lines of evidence argued that the size changes observed after castration and testosterone treatment were secondary to shrinkage and stretching of the postsynaptic muscle fiber membrane. Following castration, the spaces between synaptic regions decreased in size at the same time and to a similar extent as the regions themselves. Following testosterone replacement, the spaces between synaptic regions expanded and each existing ACh receptor region enlarged. Ultrastructural analysis showed that there was no loss or addition of postsynaptic secondary junctional folds in the muscle fiber membrane (where ACh receptors are located) as junctions shrank and expanded. Rather, folds became more densely packed as muscle fibers atrophied following castration and less densely packed as muscle fibers hypertrophied following testosterone replacement. From these studies of the bulbocavernosus muscle, as from our previous studies of the sternomastoid muscle, we conclude that neuromuscular junction size is directly coupled to muscle fiber size. Androgens modulate muscle fiber volume directly, leading to a change in the surface area of the muscle fiber membrane, which in turn causes the postsynaptic specializations to shrink or expand. The concomitant shrinkage and stretching of motor nerve terminals that we observed can only be accounted for by their adhesion to postsynaptic specializations that are also changing size. Thus adhesion, rather than an interchange of diffusible factors, trophic or otherwise, is likely to be the primary determinant of coordinated pre- and postsynaptic enlargement in growing mammalian skeletal muscles.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0270-6474
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2660-71
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Neuromuscular junctions shrink and expand as muscle fiber size is manipulated: in vivo observations in the androgen-sensitive bulbocavernosus muscle of mice.
pubmed:affiliation
Department of Anatomy and Neurobiology, Washington University School of Medicine, St. Louis, Missouri 63110.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't