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Miniature endplate potentials induced by ammonium chloride, hypertonic shock, and botulinum toxin
Author(s) -
Vautrin J.
Publication year - 1992
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490310213
Subject(s) - tonicity , toxin , ammonium chloride , shock (circulatory) , chemistry , pharmacology , chloride channel , biophysics , medicine , biochemistry , biology , organic chemistry
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 4 Cl) (replacing NaCl, a treatment which is known to raise intracellular p H) MEPP frequencies increased and the amplitudes of. MEPP s decreased. These treatments as well as type A botulinum toxin (BoTx) gradually prolonged the rising phase of some MEPP s , which increased their time‐to‐peak (slow‐MEPP s ; Vautrin and Kriebel: Neuroscience 41:71–88, 1991) and increased eventually their amplitude. Fasciculation after hyperosmotic shock or during NH 4 C1 challenge was blocked by D‐tubocurarine and was due to large slow‐MEPP s that reached threshold for the muscle fiber action potential. The development of fasciculation provided the time course for the development of giant‐MEPP s . 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 NH 4 C1 or hyperosmotic shock. NH 4 C1 delayed BoT x blockage of bell‐MEPP s . Data suggest that BoT x alters the formation of transmitter packets gradually but similarly to other treatments which increase incidence of skew‐MEPP s .