Functional analysis of neurotransmission at β2-laminin deficient terminals

Knight, D., Tolley, L. K., Kim, D. K., Lavidis, N. A. and Noakes, P. G. (2003) Functional analysis of neurotransmission at β2-laminin deficient terminals. The journal of physiology, 546 3: 789-800. doi:10.1113/jphysiol.2002.030924

Author Knight, D.
Tolley, L. K.
Kim, D. K.
Lavidis, N. A.
Noakes, P. G.
Title Functional analysis of neurotransmission at β2-laminin deficient terminals
Journal name The journal of physiology   Check publisher's open access policy
ISSN 0022-3751
Publication date 2003-01-01
Sub-type Article (original research)
DOI 10.1113/jphysiol.2002.030924
Open Access Status DOI
Volume 546
Issue 3
Start page 789
End page 800
Total pages 12
Place of publication Oxford
Publisher Blackwell for the Physiological Society
Language eng
Subject C1
320703 Peripheral Nervous System
730104 Nervous system and disorders
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 Schwarm cell invasion in the absence of beta2-laminin.
Keyword Physiology
Frog Neuromuscular-junction
Protein S-laminin
Transmitter Release
Synaptic Cleft
Axon Withdrawal
Probabilistic Secretion
Q-Index Code C1

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Created: Wed, 15 Aug 2007, 12:31:33 EST