ArticleThe Journal of physiology2003
Functional analysis of neurotransmission at beta2-laminin deficient terminals.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 67 citations in OpenAlex.
- Review of the Pathology of Muscle in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026Review
- Ageing-induced weakness of mouse NMJs is associated with reduced active zone density, synaptic event kinetics and presynaptic calcium entry.The Journal of physiology · 2025Article
- Extracellular matrix and synapse formation.Bioscience reports · 2023Article
- Brain derived neurotrophic factor/tropomyosin related kinase B signaling impacts diaphragm neuromuscular transmission in a novel rat chemogenetic model.Frontiers in cellular neuroscience · 2022Article
- A Role of Lamin A/C in Preventing Neuromuscular Junction Decline in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- An improved method for culturing myotubes on laminins for the robust clustering of postsynaptic machinery.Scientific reports · 2020Article
- The Synaptic Vesicle Glycoprotein 2: Structure, Function, and Disease Relevance.ACS chemical neuroscience · 2019Review
- Conditional Inactivation ofG3 (Bethesda, Md.) · 2019Article
- Muscle-restricted nuclear receptor interaction protein knockout causes motor neuron degeneration through down-regulation of myogenin at the neuromuscular junction.Journal of cachexia, sarcopenia and muscle · 2018Article
- Presynaptic active zones of mammalian neuromuscular junctions: Nanoarchitecture and selective impairments in aging.Neuroscience research · 2018Review
- Shaping Synapses by the Neural Extracellular Matrix.Frontiers in neuroanatomy · 2018Review
- The Structure of Human Neuromuscular Junctions: Some Unanswered Molecular Questions.International journal of molecular sciences · 2017Review
- Functional decline at the aging neuromuscular junction is associated with altered laminin-α4 expression.Aging · 2017Article
- The role of laminins in the organization and function of neuromuscular junctions.Matrix biology : journal of the International Society for Matrix Biology · 2017Review
- Focal segmental glomerulosclerosis: molecular genetics and targeted therapies.BMC nephrology · 2015Review
- Loss of β2-laminin alters calcium sensitivity and voltage-gated calcium channel maturation of neurotransmission at the neuromuscular junction.The Journal of physiology · 2015Article
- Perlecan antagonizes collagen IV and ADAMTS9/GON-1 in restricting the growth of presynaptic boutons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Role of exercise in maintaining the integrity of the neuromuscular junction.Muscle & nerve · 2014Review
- Laminin β2 gene missense mutation produces endoplasmic reticulum stress in podocytes.Journal of the American Society of Nephrology : JASN · 2013Article
- Disruption of basal lamina components in neuromotor synapses of children with spastic quadriplegic cerebral palsy.PloS one · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
beta2-Laminin is important for the formation of neuromuscular junctions in vertebrates. Previously, we have inactivated the gene that encodes for beta2-laminin in mice and observed predominantly prejunctional structural defects. In this study, we have used both intra- and extracellular recording methods to investigate evoked neurotransmission in beta2-laminin-deficient mice, from postnatal day 8 (P8) through to day 18 (P18). Our results confirmed that there was a decrease in the frequency of spontaneous release, but no change in the postjunctional response to such release. Analysis of evoked neurotransmission showed an increase in the frequency of stimuli that failed to elicit an evoked postjunctional response in the mutants compared to litter mate controls, resulting in a 50 % reduction in mean quantal content at mutant terminals. Compared to littermate controls, beta2-laminin-deficient terminals showed greater synaptic depression when subjected to high frequency stimulation. Furthermore, the paired pulse ratio of the first two stimuli was significantly lower in beta2-laminin mutant terminals. Statistical analysis of the binomial parameters of release showed that the decrease in quantal content was due to a decrease in the number of release sites without any significant change in the average probability of release. This suggestion was supported by the observation of fewer synaptic vesicle protein 2 (SV2)-positive varicosities in beta2-laminin-deficient terminals and by ultrastructural observations showing smaller terminal profiles and increased Schwann cell invasion in beta2-laminin mutants; the differences between beta2-laminin mutants and wild-type mice were the same at both P8 and P18. From these results we conclude that beta2-laminin plays a role in the early structural development of the neuromuscular junction. We also suggest that transmitter release activity may act as a deterrent to Schwann cell invasion in the absence of beta2-laminin.
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