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The Journal of Neuroscience, September 1, 2000, 20(17):6529-6539
Structural and Functional Alterations of Neuromuscular Junctions
in NCAM-Deficient Mice
Victor F.
Rafuse,
Luis
Polo-Parada, and
Lynn T.
Landmesser
Department of Neurosciences, Case Western Reserve University,
School of Medicine, Cleveland, Ohio 44106-4975
The role of neural cell adhesion molecule (NCAM) in the
development and maturation of the neuromuscular junction (NMJ) was explored by characterizing structurally and functionally NMJs from
postnatal day 11 (P11) to P30 +/+, +/ , and / NCAM null mutant mice. Differences in NCAM levels resulted in alterations in the
size and shape of NMJs, with / NMJs being smaller. Additionally both the withdrawal of polyneuronal innervation and the selective accumulation of synaptic vesicle protein in the presynaptic terminal were delayed. These observations suggest that the bidirectional signaling responsible for these events is impaired at / NMJs. Functionally, miniature end plate potential size, end
plate potential size, and quantal content did not differ from that of
wild type under either normal or low release conditions. However at
normal release conditions, / NMJs, unlike +/+ NMJs, lacked
paired-pulse facilitation. The most striking abnormality was the
inability of NCAM null junctions to maintain transmitter output with
repetitive stimuli. Combined electrophysiological and
FM1-43-labeling studies suggest that NCAM null junctions are
unable either to dock or to mobilize a sufficient number of vesicles at
high but physiological rates of transmitter release. Taken together our
observations show that many aspects of transmission are normal and,
thus, that many presynaptic and postsynaptic molecules have assembled
properly in the absence of NCAM. However, the fact that NCAM was
required for specific aspects of transmission, including paired-pulse
facilitation and reliable transmission with repetitive stimuli,
suggests that NCAM either is directly involved in these processes or is
required for the proper organization and/or function of other molecules underlying these processes.
Key words:
NCAM; synaptic depression; FM1-43; synapse elimination; neuromuscular transmission; synapse maturation
Copyright © 2000 Society for Neuroscience 0270-6474/00/20176529-11$05.00/0
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