Gene dosage-dependent transmitter release changes at neuromuscular synapses of Cacna1a R192Q knockin mice are non-progressive and do not lead to morphological changes or muscle weakness
- 1 January 2005
- journal article
- Published by Elsevier in Neuroscience
- Vol. 135 (1) , 81-95
- https://doi.org/10.1016/j.neuroscience.2005.04.069
Abstract
No abstract availableKeywords
This publication has 48 references indexed in Scilit:
- Presynaptic Ca2+ Channels Compete for Channel Type-Preferring Slots in Altered Neurotransmission Arising from Ca2+ ChannelopathyNeuron, 2004
- Maintenance of transmitter release from neuromuscular junctions with different patterns of usage ‘in vivo’Journal of Neurocytology, 2003
- Acetazolamide Acts on Neuromuscular Transmission Abnormalities Found in Some MigraineursCephalalgia, 2003
- Migraine — Current Understanding and TreatmentNew England Journal of Medicine, 2002
- Insights from mouse models of absence epilepsy into Ca2+ channel physiology and disease etiology.Cellular and Molecular Neurobiology, 2002
- Neuromuscular transmission in migraineNeurology, 2001
- Splicing of α1A subunit gene generates phenotypic variants of P- and Q-type calcium channelsNature Neuroscience, 1999
- Functional Consequences of Mutations in the Human α1ACalcium Channel Subunit Linked to Familial Hemiplegic MigraineJournal of Neuroscience, 1999
- The probability of transmitter release at a mammalian central synapseNature, 1993
- The relationship between end‐plate size and transmitter release in normal and dystrophic muscles of the mouse.The Journal of Physiology, 1979