Neuromuscular transmission in the murine mutants “motor end-plate disease” and “jolting”

Mice with the inherited disorder “motor end-plate disease” suffered from a progressive neuromuscular weakness and muscular wasting. The weakness resulted from a failure of evoked transmitter release from the motor nerve terminals. The failure in transmission was all-or-nothing in nature. The numbers...

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Veröffentlicht in:Journal of the neurological sciences 1986-12, Vol.76 (2), p.239-253
Hauptverfasser: Harris, J.B., Pollard, Sandra L.
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description Mice with the inherited disorder “motor end-plate disease” suffered from a progressive neuromuscular weakness and muscular wasting. The weakness resulted from a failure of evoked transmitter release from the motor nerve terminals. The failure in transmission was all-or-nothing in nature. The numbers of muscle fibres in skeletal muscle and myelinated axons in several major nerve trunks were no different from normal. The loss in muscle bulk was caused by the neuromuscular defect and not from a loss of motor units or muscle fibres. The inherited murine disorder “jolting” was allelic with “motor end-plate disease”. Affected “jolting” mice suffered no detectable morphological abnormality in skeletal muscle or peripheral nerve. The physiological properties of skeletal muscle and the characteristics of neuromuscular transmission were indistinguishable from normal.
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The weakness resulted from a failure of evoked transmitter release from the motor nerve terminals. The failure in transmission was all-or-nothing in nature. The numbers of muscle fibres in skeletal muscle and myelinated axons in several major nerve trunks were no different from normal. The loss in muscle bulk was caused by the neuromuscular defect and not from a loss of motor units or muscle fibres. The inherited murine disorder “jolting” was allelic with “motor end-plate disease”. Affected “jolting” mice suffered no detectable morphological abnormality in skeletal muscle or peripheral nerve. The physiological properties of skeletal muscle and the characteristics of neuromuscular transmission were indistinguishable from normal.</description><subject>Action Potentials</subject><subject>Age Factors</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cell Count</subject><subject>Electric Stimulation</subject><subject>Female</subject><subject>Jolting</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Potentials</subject><subject>Mice</subject><subject>Mice, Neurologic Mutants</subject><subject>Motor end-plate disease</subject><subject>Motor Endplate - physiopathology</subject><subject>Mouse</subject><subject>Muscles - pathology</subject><subject>Muscles - physiopathology</subject><subject>mutants</subject><subject>Nerve Fibers, Myelinated - pathology</subject><subject>nerve transmission</subject><subject>Nervous system involvement in other diseases. Miscellaneous</subject><subject>Neurology</subject><subject>Neuromuscular Diseases - pathology</subject><subject>Neuromuscular Diseases - physiopathology</subject><subject>Neuromuscular Junction - pathology</subject><subject>Neuromuscular Junction - physiopathology</subject><subject>neuromuscular junctions</subject><subject>Neuromuscular transmission</subject><subject>Peripheral Nerves - pathology</subject><subject>Synaptic Transmission</subject><issn>0022-510X</issn><issn>1878-5883</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1986</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFu1DAQQC0EKtuWPwApB1SVQ-g4jmPngoSqtiBV5QISN-PYE3CV2IvtVOqtH9L-XL-EpLvaYzmNNPNmNPOGkLcUPlKgzQlAVZWcws9j2XxogYqqZC_IikohSy4le0lWO-Q12U_pGgAaKds9sseg4kyIFfl1hVMM45TMNOhY5Kh9Gl1KLvjC-SL_wWKcovNLyNrnVDze3Y8hh1igt-V60BkL6xLqhI93D4X2diGuw5Cd_z1nDsmrXg8J32zjAflxfvb99Et5-e3i6-nny9LUVOSS9ZSD0MxKIaylBnTfI-8r6AC0rmRb0Za1zAihjeBtB7w20Bjeaeygblt2QI42c9cx_J0wZTWfYXAYtMcwJSVERUHU8F-Q1k3DWC1nsN6AJoaUIvZqHd2o462ioJYPqEWvWvQq2ainDyg2t73bzp-6Ee2uaat8rr_f1nUyeuhn48alHSaBSf50z6cNhrO0G4dRJePQG7QuosnKBvf8Hv8A6bmmmw</recordid><startdate>19861201</startdate><enddate>19861201</enddate><creator>Harris, J.B.</creator><creator>Pollard, Sandra L.</creator><general>Elsevier B.V</general><general>Elsevier Science</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>M7Z</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>19861201</creationdate><title>Neuromuscular transmission in the murine mutants “motor end-plate disease” and “jolting”</title><author>Harris, J.B. ; Pollard, Sandra L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c417t-3f1507a3d877dd1c0affe5f20b00aa289219393c77ac759b054c06c5baeb04993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1986</creationdate><topic>Action Potentials</topic><topic>Age Factors</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cell Count</topic><topic>Electric Stimulation</topic><topic>Female</topic><topic>Jolting</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Potentials</topic><topic>Mice</topic><topic>Mice, Neurologic Mutants</topic><topic>Motor end-plate disease</topic><topic>Motor Endplate - physiopathology</topic><topic>Mouse</topic><topic>Muscles - pathology</topic><topic>Muscles - physiopathology</topic><topic>mutants</topic><topic>Nerve Fibers, Myelinated - pathology</topic><topic>nerve transmission</topic><topic>Nervous system involvement in other diseases. 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The weakness resulted from a failure of evoked transmitter release from the motor nerve terminals. The failure in transmission was all-or-nothing in nature. The numbers of muscle fibres in skeletal muscle and myelinated axons in several major nerve trunks were no different from normal. The loss in muscle bulk was caused by the neuromuscular defect and not from a loss of motor units or muscle fibres. The inherited murine disorder “jolting” was allelic with “motor end-plate disease”. Affected “jolting” mice suffered no detectable morphological abnormality in skeletal muscle or peripheral nerve. The physiological properties of skeletal muscle and the characteristics of neuromuscular transmission were indistinguishable from normal.</abstract><cop>Shannon</cop><pub>Elsevier B.V</pub><pmid>3025377</pmid><doi>10.1016/0022-510X(86)90172-3</doi><tpages>15</tpages></addata></record>
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source MEDLINE; ScienceDirect Journals (5 years ago - present)
subjects Action Potentials
Age Factors
Animals
Biological and medical sciences
Cell Count
Electric Stimulation
Female
Jolting
Male
Medical sciences
Membrane Potentials
Mice
Mice, Neurologic Mutants
Motor end-plate disease
Motor Endplate - physiopathology
Mouse
Muscles - pathology
Muscles - physiopathology
mutants
Nerve Fibers, Myelinated - pathology
nerve transmission
Nervous system involvement in other diseases. Miscellaneous
Neurology
Neuromuscular Diseases - pathology
Neuromuscular Diseases - physiopathology
Neuromuscular Junction - pathology
Neuromuscular Junction - physiopathology
neuromuscular junctions
Neuromuscular transmission
Peripheral Nerves - pathology
Synaptic Transmission
title Neuromuscular transmission in the murine mutants “motor end-plate disease” and “jolting”
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