Miniature endplate potentials induced by ammonium chloride, hypertonic shock, and botulinum toxin
✍ Scribed by J. Vautrin
- Publisher
- John Wiley and Sons
- Year
- 1992
- Tongue
- English
- Weight
- 798 KB
- Volume
- 31
- Category
- Article
- ISSN
- 0360-4012
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✦ Synopsis
Intracellular recordings were made at the neuromuscular junction (NMJ) of the mouse diaphragm to study alteration of miniature endplate potential (MEPP) amplitude and rise time after different treatments. Following either hyperosmotic shock or 3 to 5 min of incubation in 10 to 50 mM ammonium chloride (NH,CI) (replacing NaCI, a treatment which is known to raise intracellular pH) MEPP frequencies increased and the amplitudes of MEPPs decreased. These treatments as well as type A botulinum toxin (BoTx) gradually prolonged the rising phase of some MEPPs, which increased their time-to-peak (slow-MEPPs; Vautrin and Kriebel: Neuroscience 41:71- 88, 1991) and increased eventually their amplitude. Fasciculation after hyperosmotic shock or during NH,CI challenge was blocked by D-tubocurarine and was due to large slow-MEPPs that reached threshold for the muscle fiber action potential. The development of fasciculation provided the time course for the development of giant-MEPPs. Increased frequency of giant MEPP is accompanied by a block of the nerveevoked muscle contraction. Effects of BoTx on spontaneous release were functionally antagonized either by NH4CI or hyperosmotic shock. NH,CI delayed BoTx blockage of bell-MEPPs. Data suggest that BoTx alters the formation of transmitter packets gradually but similarly to other treatments which increase incidence of skew-MEPPs.