Neuromuscular transmission in the murine mutants “motor end-plate disease” and “jolting”☆
References (27)
- et al.
A comparative study of “denervation” in muscles from mice with inherited progressive neuromuscular disorders
Exp. Neurol.
(1974) - et al.
A modular system of instruments for simple experiments on skeletal muscle using intracellular microelectrode techniques
Brit. J. Pharmacol.
(1977) - et al.
Electrophysiological studies of a motor nerve in “motor end-plate disease” of the mouse
- et al.
Abnormal electrophysiological and anatomical characteristics of cerebellar Purkinje cells in the mutant mouse jolting
J. Physiol. (Lond.)
(1985) - et al.
Abnormal nerve function in hereditary motor end-plate disease (med) of the mouse
- et al.
A cerebellar abnormality in the mouse with motor end-plate disease
Neuropath. Appl. Neurobiol.
(1985) - et al.
Hereditary motor end-plate disease in the mouse: light and electron microscopic studies
J. Neurol. Neurosurg. Psychiat.
(1970) - et al.
Electrophysiological studies of neuromuscular transmission in hereditary “motor end-plate disease” of the mouse
J. Physiol. (Lond.)
(1971) An Introduction to Recombinant DNA
(1985)- et al.
“Motor end-plate disease” and the mutant “jolting” (medjo) mouse
J. Physiol. (Lond.)
(1982)
Reversal of paralysis in nerve-muscle preparations isolated from animals with hereditary motor end-plate disease
Brit. J. Pharmacol.
The relationship between endplate size and transmitter release in normal and dystrophic muscles of the mouse
J. Physiol. (Lond.)
Pharmacological aspects of neuromuscular transmission in the isolated diaphragm of the dystrophic (Rej 129) mouse
Brit. J. Pharmacol.
Cited by (27)
Mouse Models of Dystonia
2015, Movement Disorders: Genetics and Models: Second EditionChapter 2 Reliability of neuromuscular transmission and how it is maintained
2008, Handbook of Clinical NeurologyCitation Excerpt :For example, failure of the nerve impulse to depolarize the nerve terminal leads to greatly reduced release. An example of this is seen in the naturally occurring mouse mutant motor endplate disease (med) (Harris and Pollard, 1986). In this mouse, a profound impairment of quantal ACh release results from a mutation in the gene encoding the voltage‐gated sodium channel in the nerve (SCN8a) (Burgess et al., 1995; Kohrman et al., 1996).
Mouse models of dystonia
2005, Movement DisordersMouse Models of Dystonia
2004, Movement Disorders: Genetics and Models: Second EditionThe absence of resurgent sodium current in mouse spinal neurons
1999, Brain Research
- ☆
This work was supported by grants from the Muscular Dystrophy Group of Great Britain and the National Fund for Research into Crippling Diseases.
Part of this work was incorporated into a Ph.D. thesis submitted to the University of Newcastle upon Tyne by Sandra Pollard.
- ∗
Present address: ICI Plc., Central Toxicology Laboratory, Alderley Park, Macclesfield, Cheshire, U.K.