scholarly journals SIZES OF END PLATE COMPARTMENTS, DENSITIES OF ACETYLCHOLINE RECEPTOR AND OTHER QUANTITATIVE ASPECTS OF NEUROMUSCULAR TRANSMISSION

1973 ◽  
Vol 21 (9) ◽  
pp. 769-778 ◽  
Author(s):  
MIRIAM M. SALPETER ◽  
MOHYEE E. ELDEFRAWI
Keyword(s):  
Surface Area ◽  
Acetylcholine Receptor ◽  
Neuromuscular Transmission ◽  
Nerve Impulse ◽  
Synaptic Cleft ◽  
Postsynaptic Membrane ◽  
Optimal Response ◽  
End Plate

The area of the postsynaptic membrane and the volume of the synaptic cleft were calculated for the end plates of the diaphragm and sternomastoid of mouse and rat. From these dimensions we were able to extrapolate, from data given by others on acetylcholine (ACh) released during neuromuscular transmission and on ACh receptor per whole end plate, to densities in the postneural compartments. The concentration of ACh in the cleft per nerve impulse was found to be ~ 10–5 M and the density of ACh receptor was between 5 and 10 x l03/µ2 of postsynaptic membrane. (This is approximately a factor of 2 to 3 higher than that for acetylcholinesterase at this site.) From these values we conclude that the concentration of ACh receptor in the plane of the postsynaptic membrane is considerably higher than that of ACh in the cleft during neuromuscular transmission. In addition the ACh itself is present at considerably higher concentrations than necessary to give optimal response. We calculated that the acytelcholinesterase plus ACh receptor together would occupy about 25% of the surface area of the postsynaptic membrane.

scholarly journals Pathological mechanisms in experimental autoimmune myasthenia gravis. II. Passive transfer of experimental autoimmune myasthenia gravis in rats with anti-acetylcholine recepotr antibodies.

1976 ◽  
Vol 144 (3) ◽  
pp. 739-753 ◽  
Author(s):  
J M Lindstrom ◽  
A G Engel ◽  
M E Seybold ◽  
V A Lennon ◽  
E H Lambert
Keyword(s):  
Myasthenia Gravis ◽  
Nerve Stimulation ◽  
Neuromuscular Transmission ◽  
Postsynaptic Membrane ◽  
Passive Transfer ◽  
Autoimmune Response ◽  
End Plate ◽  
Experimental Autoimmune Myasthenia Gravis ◽  
Autoimmune Myasthenia ◽  
Experimental Autoimmune

Passive transfer of experimental autoimmune myasthenia gravis (EAMG) was achieved using the gamma globulin fraction and purified IgG from sera of rats immunized with Electrophus electricus (eel) acetylcholine receptor (AChR). This demonstrates the critical role of anti-AChR antibodies in impairing neuromuscular transmission in EAMG. Passive transfer of anti-AChR antibodies from rats with chronic EAMG induced signs of the acute phase of EAMG in normal recipient rats, including invasion of the motor end-plate region by mononuclear inflammatory cells. Clinical, eletrophysiological, histological, and biochemical signs of acute EAMG were observed by 24 h after antibody transfer. Recipient rats developed profound weakness and fatigability, and the posture characteristic of EAMG. Striking weight loss was attributable to dehydration. Recipient rats showed large decreases in amplitude of muscle responses to motor nerve stimulation, and repetitive nerve stimulation induced characteristic decrementing responses. End-plate potentials were not detectable in many muscle fibers, and the amplitudes of miniature end-plate potentials were reduced in the others. Passively transferred EAMG more severely affected the forearm muscles than diaphragm muscles, though neuromuscular transmission was impaired and curare sensitivity was increased in both muscles. Some AChR extracted from the muscles of rats with passively transferred EAMG was found to be complexed with antibody, and the total yield of AChR per rat was decreased. The quantitative decrease in AChR approximately paralleled in time the course of clinical and electrophysiological signs. The amount of AChR increased to normal levels and beyond at the time neuromuscular transmission was improving. The excess of AChR extractable from muscle as the serum antibody level decreased probably represented extrajunctional receptors formed in response to functional denervation caused by phagocytosis of the postsynaptic membrane by macrophages. The amount of antibody required to passively transfer EAMG was less than required to bind all AChR molecules in a rat's musculature. The effectiveness of samll amounts of antibody was probably amplified by the activation of complement and by the destruction of large areas of postsynaptic membrane by phagocytic cells. A self-sustaining autoimmune response to AChR was not provoked in animals with passively transferred EAMG.

scholarly journals Effect of lanthanum ions on neuromuscular transmission in insects

1983 ◽  
Vol 107 (1) ◽  
pp. 405-414
Author(s):  
H. Washio ◽  
T. Miyamoto
Keyword(s):  
Neuromuscular Transmission ◽  
Nerve Impulse ◽  
Postsynaptic Membrane ◽  
Muscle Fibres ◽  
Excitatory Postsynaptic Potential ◽  
Bathing Medium ◽  
Insect Muscle ◽  
Lanthanum Ions ◽  
Postsynaptic Action ◽  
Ventral Muscle

The effect of extracellular lanthanum on neuromuscular transmission was studied in cockroach leg muscle and larval mealworm ventral muscle by means of microelectrodes. Miniature excitatory postsynaptic potential (MEPSP) frequency was markedly increased after lanthanum was added, in the presence and absence of calcium. The potentiation by La3+ was suppressed in a high Ca2+ saline and enhanced in the absence of Ca2+. Lanthanum ions blocked neuromuscular transmission at a concentration as low as 0.1 mM. The quantal content estimated by the failure method was reduced by 80% in the presence of 0.1 mM-La3+. The reduction in the EPSP amplitude by La3+ may be due to a decrease in the amount of transmitter released by a nerve impulse. The response to L-glutamate applied iontophoretically was also reduced in the presence of La3+. It seems unlikely that La3+ and L-glutamate were competing for a common binding site on the postsynaptic membrane since the apparent maximum of the dose-response curve for glutamate-induced depolarization was reduced in the presence of La3+. External recording of MEPSPs showed that adding lanthanum to the bathing medium increased the time constant of decay of the potential. These results suggest that lanthanum does indeed have a postsynaptic action in addition to its prejunctional action in insect muscle fibres.

scholarly journals Model of Postsynaptic Membrane Deactivation

2018 ◽  
Vol 63 (10) ◽  
pp. 919 ◽  
Author(s):  
A. N. Vasilev ◽  
O. V. Kulish
Keyword(s):  
Time Dependence ◽  
Time Distribution ◽  
Nerve Impulse ◽  
Synaptic Cleft ◽  
Postsynaptic Membrane ◽  
Space Time ◽  
Mediator Release ◽  
Activation Time

A model has been proposed to describe the deactivation of a postsynaptic membrane after its excitation by transmitting a nerve impulse across the synapse. In particular, the process of mediator release in the form of choline from the postsynaptic membrane and its diffusive excretion from the synaptic cleft are considered. The time dependence of the number of activated receptors, the dependence of the maximum number of activated receptors on the activation time, and the space-time distribution of the choline concentration in the synaptic cleft are calculated.

Nicardipine inhibits axon conduction but causes dual changes of acetylcholine release in the mouse motor nerve

1989 ◽  
Vol 67 (12) ◽  
pp. 1493-1498 ◽  
Author(s):  
C. C. Chang ◽  
L. C. Chiou ◽  
L. L. Hwang ◽  
S. J. Hong ◽  
C. Y. Huang
Keyword(s):  
Acetylcholine Receptor ◽  
Neuromuscular Transmission ◽  
Acetylcholine Release ◽  
Motor Nerve ◽  
Neuromuscular Block ◽  
Resting Membrane Potential ◽  
Receptor Desensitization ◽  
End Plate ◽  
Agonist Action ◽  
Release Of Acetylcholine

The effects of nicardipine, a dihydropyridine Ca2+-channel antagonist, on neuromuscular transmission and impulse-evoked release of acetylcholine were compared with those of nifedipine. In the isolated mouse phrenic nerve diaphragm, nicardipine (50 μM), but not nifedipine (100 μM), induced neuromuscular block, fade of tetanic contraction, and dropout or all-or-none block of end-plate potentials. Nicardipine had no significant effect on the resting membrane potential and the amplitude of miniature end-plate potentials but increased the frequency and caused the appearance of large size miniature potentials. The quantal contents of evoked end-plate potentials were increased. In the presence of tubocurarine, however, nicardipine depressed the amplitude of end-plate potentials. The compound nerve action potential was also decreased. It is concluded that nicardipine blocks neuromuscular transmission by acting on Na+ channels and inhibits axonal conduction. Nicardipine appeared to affect the evoked release of acetylcholine by dual mechanisms, i.e., an enhancement presumably by an agonist action on Ca2+ channels, like Bay K 8644 and nifedipine, and inhibition by an effect on Na+ channels, like verapamil and diltiazem. In contrast with its inactivity on the amplitude of miniature end-plate potentials, depolarization of the end plate in response to succinylcholine was greatly depressed. The contractile response of baby chick biventer cervicis muscle to exogenous acetylcholine was noncompetitively antagonized by nicardipine (10 μM), but was unaffected by nifedipine (30 μM). These results may implicate that nicardipine blocks the postsynaptic acetylcholine receptor channel by enhancing receptor desensitization or by a use-dependent effect.Key words: nicardipine, calcium channel antagonists, neuromuscular transmission, acetylcholine release, acetylcholine receptor desensitization.

scholarly journals The versatile synapse

1984 ◽  
Vol 112 (1) ◽  
pp. 199-224
Author(s):  
R. M. Pitman
Keyword(s):  
Ion Channels ◽  
Nerve Impulse ◽  
Synaptic Cleft ◽  
Ionic Species ◽  
Postsynaptic Membrane ◽  
Voltage Dependent ◽  
Biochemical Systems ◽  
Characteristics Analysis ◽  
Neurotransmitter Substances ◽  
Neurotransmitter Substance

‘Typically’ chemical synaptic transmission takes place when an influx of calcium ions during a presynaptic nerve impulse triggers exocytosis of neurotransmitter substance from synaptic vesicles. The neurotransmitter diffuses across the synaptic cleft and occupies receptors embedded in the subsynaptic membrane. This interaction (directly or via a second messenger) operates characteristic ion channels and produces an increase in the postsynaptic membrane permeability to particular ions. Depending on the ionic species to which the postsynaptic membrane becomes more permeable, the physiological response will be an excitatory or an inhibitory postsynaptic potential. The action of neurotransmitters may be terminated either by enzymic inactivation or by cellular uptake mechanisms. Over the last decade it has become clear that a neurotransmitter substance may exert a number of different actions on a single postsynaptic neurone. These may involve opening or closure of either voltage-independent or voltage-dependent ion channels. It is also possible that in some instances transmitters may act on neuronal biochemical systems to modify the physiology of postsynaptic cells without directly altering their electrical characteristics. Analysis of the postsynaptic actions of neurotransmitter substances has become further complicated by the increasing body of evidence which indicates that more than one transmitter substance (one of which may be a peptide) can be released from a single presynaptic neurone. The significance of such dual transmitter systems has yet to be fully elucidated. The efficacy of transmission across many synapses may be modified by either presynaptic or postsynaptic mechanisms; both transmitter release and postsynaptic responsiveness may depend on the recent history of a single synapse, on synaptic inputs from other neurones or on circulating neuroactive substances.

The measurement of synaptic delay, and the time course of acetylcholine release at the neuromuscular junction

1965 ◽  
Vol 161 (985) ◽  
pp. 483-495 ◽  
Keyword(s):  
Neuromuscular Junction ◽  
Time Course ◽  
Nerve Impulse ◽  
Postsynaptic Membrane ◽  
Synaptic Delay ◽  
Time Interval ◽  
Conduction Time ◽  
Inward Current ◽  
End Plate ◽  
Statistical Fluctuations

Focal recording from active spots of a neuromuscular junction was used to measure the ‘synaptic delay’ between terminal axon spike and end-plate current (e.p.c.). Synaptic delay is defined as the time interval between peak of inward current through the presynaptic membrane and commencement of inward current through the postsynaptic membrane. By substituting magnesium for calcium in the medium, and by adjustable electrophoretic application of calcium from the recording electrode, the e.p.c. can be restricted to the small portion of a single junction which is in contact with the microelectrode, and the statistical average amplitude of the e.p.c. can be reduced to less than quantal unit size. Under these conditions, the latency of the unit components of the e.p.c. can be determined and its statistical fluctuations studied. The synaptic delay at a single end-plate spot has a minimum value, at 20 °C, of 0.4 to 0.5 ms and a modal value of about 0.75 ms. There is considerable fluctuation of the measured intervals during a series of nerve impulses; over 50 % occur within a range of 0.5 ms, the rest being spread out in declining fashion over a further 1 to 4 ms. These latency fluctuations are shown to be a statistical consequence of the quantal process of transmitter release. The contribution of various factors to the minimum synaptic delay are discussed. Terminal conduction time has been effectively eliminated by the method of focal recording. Diffusion of acetylcholine towards the receptors, and its reaction with them must cause delays whose exact values are uncertain, but whose extreme upper limits can be shown to make up only a small part of the observed minimum delay. It is concluded that the synaptic interval arises chiefly from a delay in the release of transmitter after the arrival of the nerve impulse.

Na current density at and away from end plates on rat fast- and slow-twitch skeletal muscle fibers

1992 ◽  
Vol 262 (1) ◽  
pp. C229-C234 ◽  
Author(s):  
R. L. Ruff
Keyword(s):  
Skeletal Muscle ◽  
Current Density ◽  
Muscle Fibers ◽  
Postsynaptic Membrane ◽  
Na Current ◽  
End Plate ◽  
Skeletal Muscle Fibers ◽  
Slow Twitch ◽  
Slow Twitch Fibers ◽  
Fast Twitch

Na current density and membrane capacitance were studied with the loose patch voltage clamp technique on rat fast- and slow-twitch skeletal muscle fibers at three different regions on the fibers: 1) the end plate border, 2) greater than 200 microns from the end plate (extrajunctional), and 3) on the end plate postsynaptic membrane. Fibers were treated with collagenase to improve visualization of the end plate and to enzymatically remove the nerve terminal. The capacitance of membrane patches was similar on fast- and slow-twitch fibers and patches of membrane on the end plate had twice the capacitance of patches elsewhere. For fast- and slow-twitch fibers, the sizes of the Na current normalized to the area of the patch were as follows: end plate greater than end plate border greater than extrajunctional. For both types of fibers, the amplitudes of the Na current normalized to the capacitance of the membrane patch were as follows: end plate approximately end plate border greater than extrajunctional. At each of the three regions, the Na current densities were larger on fast-twitch fibers and fast-twitch fibers had a larger increase in Na current density at the end plate border compared with extrajunctional membrane.

Effects of long-term administration of ambenonium chloride on motor end-plate fine structure and acetylcholine receptor in rat

1981 ◽  
Vol 51 (1) ◽  
pp. 69-79 ◽  
Author(s):  
Ryuji Hazama ◽  
Mitsuhiro Tsujihata ◽  
Masataka Mori ◽  
Masaharu Takamori ◽  
Kazutake Mori ◽  
...  
Keyword(s):  
Fine Structure ◽  
Acetylcholine Receptor ◽  
End Plate ◽  
Motor End Plate ◽  
Term Administration

scholarly journals Momentary alteration of the postsynaptic membrane during transmission of a single nerve impulse.

1989 ◽  
Vol 86 (5) ◽  
pp. 1717-1720 ◽  
Author(s):  
Y. Dunant ◽  
L. M. Garcia-Segura ◽  
D. Muller ◽  
A. Parducz
Keyword(s):  
Nerve Impulse ◽  
Postsynaptic Membrane ◽  
Single Nerve

NEUROMUSCULAR TRANSMISSION AND ACETYLCHOLINE RECEPTOR ANTIBODIES IN RHEUMATOID ARTHRITIS PATIENTS ON D-PENICILLAMINE

The Lancet ◽  
1980 ◽  
Vol 315 (8161) ◽  
pp. 203 ◽  
Author(s):  
Z. Argov ◽  
L. Nicholson ◽  
P.R.W. Fawcett ◽  
F.L. Mastaglia ◽  
M. Hall
Keyword(s):  
Rheumatoid Arthritis ◽  
Acetylcholine Receptor ◽  
Neuromuscular Transmission ◽  
Receptor Antibodies
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