Changes in frequency of motor end-plate miniature potentials after transient tetanic stimulation of the motor nerve

1968 ◽  
Vol 66 (5) ◽  
pp. 1179-1181
Author(s):  
M. A. Kamenskaya ◽  
N. P. Loss

At the nerve-muscle junction, a specific process occurs which is not found during the propagation of impulses along nerve or muscle fibres; the nerve impulse causes acetylcholine (Ach) to be released from the motor nerve endings, and this substance depolarizes the end-plate surface of the muscle fibre by a specific chemical reaction. The transient local depolarization of the muscle fibre which is so produced has been called the end-plate potential (e.p.p.). The e.p.p., then, unlike the nerve or muscle impulse, is not itself produced by electric stimulation (direct spread of electric current from nerve to muscle has, in fact, never been demonstrated and appears to be indetectably small). On the other hand, the e.p.p. electrically stimulates the surrounding region of the muscle fibre, and so gives rise to the propagation of a new impulse.


1977 ◽  
Vol 40 (1) ◽  
pp. 95-105 ◽  
Author(s):  
R. Capek ◽  
B. Esplin

1. The transmission in the spinal monosynaptic pathway was studied during repetitive stimulation of a motor nerve by 10 stimuli at 2, 5, or 10 Hz in spinal cats. Initially, the amplitudes of the monosynaptic responses rapidly declined, reaching a plateau after a few stimuli. The level of the plateau was inversely related to the frequency of stimulation. 2. This depression of monosynaptic response was seen only when the same pathway was stimulated; the response elicited from the lateral gastrocnemius was not depressed when preceded by stimulation of the medial gastrocnemius nerve and vice versa. Pretreatment with semicarbazide left the homosynaptic depression unchanged while suppressing the dorsal root reflex. The participation of a depolarization of primary afferents in the described depression is, therefore, unlikely. 3. The decrease of transmitter release by successive volleys, which is the cause of the observed depression, could conceivably be related to the depletion of transmitter stores. 4. A procedure is described, based on this assumption, which allows the calculation of transmitter turnover. The input-output relation in the spinal monosynaptic pathway is used to convert the amplitudes of monosynaptic responses to the amounts of transmitter, both relative to the maximum response. The changes of transmitter release are analyzed under the assumption that each volley releases instantaneously a constant fraction of the transmitter store available for release and that this store is replenished at a constant fraction of the depleted part per second. 5. The values of fractional release per volley were about 0.4, irrespective of frequency of stimulation. 6. The values of fractional replenishment per second ranged from about 1 to 5 on the average, depending directly on the frequency of stimulation. 7. It is suggested that the described procedure might be useful in analyzing drug effects on synaptic transmission.


1982 ◽  
Vol 242 (5) ◽  
pp. C366-C372 ◽  
Author(s):  
D. F. Wilson

The presence and physiological significance of acetylcholine (ACh) receptors on motor nerve terminals was examined at the rat diaphragm neuromuscular junction. Intracellular recording techniques were used to monitor end-plate potentials (EPP), miniature end-plate potentials (MEPP), and resting potentials of the muscle fibers. Muscle action potentials were blocked by the cut-muscle technique. Quantal release was determined by the ratio EPP/MEPP, after correcting for nonlinear summation. Blockade of acetylcholinesterase with eserine and neostigmine was tested to determine the influence of residual ACh on transmitter release. Partial blockade of ACh receptors with curare was examined to further clarify the role of these presynaptic receptors. The experiments demonstrate that residual ACh inhibits transmitter release and that blockade of ACh receptors enhances transmitter release. It is concluded that presynaptic ACh receptors exist and that they serve an important physiological function. It is suggested that the presynaptic ACh receptors normally serve to limit transmitter release in a negative feedback pathway.


1995 ◽  
Vol 132 (2) ◽  
pp. 97-104
Author(s):  
Naoko Tetsuo ◽  
Mitsuhiro Tsujihata ◽  
Akira Satoh ◽  
Toshiro Yoshimura ◽  
Tatsufumi Nakamura ◽  
...  

2003 ◽  
Vol 95 (2) ◽  
pp. 577-583 ◽  
Author(s):  
Jianhua Li ◽  
Nicholas C. King ◽  
Lawrence I. Sinoway

Previous studies have suggested that activation of ATP-sensitive P2X receptors in skeletal muscle play a role in mediating the exercise pressor reflex (Li J and Sinoway LI. Am J Physiol Heart Circ Physiol 283: H2636–H2643, 2002). To determine the role ATP plays in this reflex, it is necessary to examine whether muscle interstitial ATP (ATPi) concentrations rise with muscle contraction. Accordingly, in this study, muscle contraction was evoked by electrical stimulation of the L7 and S1 ventral roots of the spinal cord in 12 decerebrate cats. Muscle ATPi was collected from microdialysis probes inserted in the muscle. ATP concentrations were determined by the HPLC method. Electrical stimulation of the ventral roots at 3 and 5 Hz increased mean arterial pressure by 13 ± 2 and 16 ± 3 mmHg ( P < 0.05), respectively, and it increased ATP concentration in contracting muscle by 150% ( P < 0.05) and 200% ( P < 0.05), respectively. ATP measured in the opposite control limb did not rise with ventral root stimulation. Section of the L7 and S1 dorsal roots did not affect the ATPi seen with 5-Hz ventral root stimulation. Finally, ventral roots stimulation sufficient to drive motor nerve fibers did not increase ATP in previously paralyzed cats. Thus ATPi is not largely released from sympathetic or motor nerves and does not require an intact afferent reflex pathway. We conclude that ATPi is due to the release of ATP from contracting skeletal muscle cells.


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