Loss of β2-laminin alters calcium sensitivity and voltage-gated calcium channel maturation of neurotransmission at the neuromuscular junction.

@article{Chand2015LossO,
  title={Loss of β2-laminin alters calcium sensitivity and voltage-gated calcium channel maturation of neurotransmission at the neuromuscular junction.},
  author={Kirat K Chand and Kah Meng Lee and Mitja P Schenning and Nickolas A. Lavidis and Peter G. Noakes},
  journal={The Journal of physiology},
  year={2015},
  volume={593 1},
  pages={245-65}
}
KEY POINTS Neuromuscular junctions from β2-laminin-deficient mice exhibit lower levels of calcium sensitivity. Loss of β2-laminin leads to a failure in switching from N- to P/Q-type voltage-gated calcium channel (VGCC)-mediated transmitter release that normally occurs with neuromuscular junction maturation. The motor nerve terminals from β2-laminin-deficient mice fail to up-regulate the expression of P/Q-type VGCCs clusters and down-regulate N-type VGCCs clusters, as they mature. There is… CONTINUE READING

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