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acetylcholine receptors that are available for binding, symptomatic treatment consists of using an acetylcholinesterase inhibitor to reduce the breakdown of acetylcholine in the neuromuscular junction, so that enough acetylcholine will be present for the small number of unblocked receptors. A congenital abnormality caused by a deficiency in end-plate acetylcholine esterase (AChE) might be a pathophysiologic mechanism for myasthenic gravis. In a study on a patient with AChE deficiency, doctors noted that he had developed severe proximal and truncal muscle weakness with jittering in other muscles. It was found that a combination of the jitter and blocking rate of the acetylcholine receptors caused a reduced end-plate potential similar to what is seen in cases of myasthenia gravis. Research of motor unit potentials (MUPs) has led to possible clinical applications in the evaluation of the progression of pathological diseases to myogenic or neurogenic origins by measuring the irregularity constant related. Motor unit potentials are the electrical signals produced by motor units that can be characterized by amplitude, duration, phase, and peak, and the irregularity coefficient (IR) is calculated based on the peak numbers and amplitudes.
280:
depolarization of the sarcolemma (muscle cell membrane). The small depolarization associated with the release of acetylcholine from an individual synaptic vesicle is called a miniature end-plate potential (MEPP), and has a magnitude of about +0.4mV. MEPPs are additive, eventually increasing the end-plate potential (EPPs) from about -100mV up to the threshold potential of -60mV, at which level the voltage-gated ion channels in the postsynaptic membrane open, allowing a sudden flow of sodium ions from the synapse and a sharp spike in depolarization. This depolarization voltage spike triggers an action potential which propagates down the postsynaptic membrane leading to muscle contraction. It is important to note that EPPs are not action potentials, but that they trigger action potentials. In a normal muscular contraction, approximately 100-200 acetylcholine vesicles are released causing a depolarization that is 100 times greater in magnitude than a MEPP. This causes the membrane potential to depolarize +40mV (100 x 0.4mV = 40mV) from -100mV to -60mV where it reaches threshold.
199:. During fetal development acetylcholine receptors are concentrated on the postsynaptic membrane and the entire surface of the nerve terminal in the growing embryo is covered even before a signal is fired. Five subunits consisting of four different proteins from four different genes comprise the nicotinic acetylcholine receptors therefore their packaging and assembly is a very complicated process with many different factors. The enzyme muscle-specific kinase (MuSK) initiates signaling processes in the developing postsynaptic muscle cell. It stabilizes the postsynaptic acetylcholine receptor clusters, facilitates the transcription of synaptic genes by muscle fiber nuclei, and triggers differentiation of the axon growth cone to form a differentiated nerve terminal. Substrate laminin induces advanced maturation of the acetylcholine receptor clusters on the surfaces of myotubes.
224:. Large dense core vesicles contain neuropeptides and large neurotransmitters that are created in the cell body of the neuron and then transported via fast axonal transport down to the axon terminal. Small clear core vesicles transport small molecule neurotransmitters that are synthesized locally in the presynaptic terminals. Finalized neurotransmitter vesicles are bound to the presynaptic membrane. When an action potential propagates down the motor neuron axon and arrives at the axon terminal, it causes a depolarization of the axon terminal and opens calcium channels. This causes the release of the neurotransmitters via vesicle exocytosis.
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neuromuscular junction even without a signal from the axon. These small depolarizations are not enough to reach threshold and so an action potential in the postsynaptic membrane does not occur. During experimentation with MEPPs, it was noticed that often spontaneous action potentials would occur, called end plate spikes in normal striated muscle without any stimulus. It was believed that these end plate spikes occurred as a result of injury or irritation of the muscles fibers due to the
20:
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88:(α-MN) and the skeletal muscle fiber. In order for a muscle to contract, an action potential is first propagated down a nerve until it reaches the axon terminal of the motor neuron. The motor neuron then innervates the muscle fibers to contraction by causing an action potential on the postsynaptic membrane of the neuromuscular junction.
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During the action potential before the hyperpolarization phase, the membrane is unresponsive to any stimulation. This inability to induce another action potential is known as the absolute refractory period. During the hyperpolarization period, the membrane is again responsive to stimulations but it
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and have two distinct patterns: small and large. Small end plate spikes have a negative onset without signal propagation and large end plate spikes resemble motor unit potentials (MUPs). Muscle spindles are sensory receptors that measure muscle elongation or stretch and relay the information to the
67:
and the contents are released into the neuromuscular junction. These neurotransmitters bind to receptors on the postsynaptic membrane and lead to its depolarization. In the absence of an action potential, acetylcholine vesicles spontaneously leak into the neuromuscular junction and cause very small
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During repolarization, the sodium channels begin to become inactivated, causing a net efflux of potassium ions. This causes the membrane potential to drop down to its resting membrane potential of -100mV. Hyperpolarization occurs because the slow-acting potassium channels take longer to deactivate,
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Threshold is when the summation of MEPPs reaches a certain potential and induces the opening of the voltage-gated ion channels. The rapid influx of sodium ions causes the membrane potential to reach a positive charge. The potassium ion channels are slower-acting than the sodium ion channels and so
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When an action potential causes the release of many acetylcholine vesicles, acetylcholine diffuses across the neuromuscular junction and binds to ligand-gated nicotinic receptors (non-selective cation channels) on the muscle fiber. This allows for increased flow of sodium and potassium ions, causing
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is an autoimmune disease, where the body produces antibodies targeted against the acetylcholine receptor on the postsynaptic membrane in the neuromuscular junction. Muscle fatigue and weakness, worsened with use and improved by rest, is the hallmark of the disease. Because of the limited amount of
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The synaptic vesicles of acetylcholine are clear core synaptic vesicles with a diameter of 30 nm. Each acetylcholine vesicle contains approximately 5000 acetylcholine molecules. The vesicles release their entire quantity of acetylcholine and this causes miniature end plate potentials (MEPPs)
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After exocytosis, vesicles are recycled during a process known as the synaptic vesicle cycle. The retrieved vesicular membranes are passed through several intracellular compartments where they are modified to make new synaptic vesicles. They are then stored in a reserve pool until they are needed
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Normally the resting membrane potential of a motor neuron is kept at -70mV to -50 with a higher concentration of sodium outside and a higher concentration of potassium inside. When an action potential propagates down a nerve and reaches the axon terminal of the motor neuron, the change in membrane
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Miniature end plate potentials are the small (~0.4mV) depolarizations of the postsynaptic terminal caused by the release of a single vesicle into the synaptic cleft. Neurotransmitter vesicles containing acetylcholine collide spontaneously with the nerve terminal and release acetylcholine into the
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is a disorder where presynaptic calcium channels are subjected to autoimmune destruction which causes fewer neurotransmitter vesicles to be exocytosed. This causes smaller EPPs due to less vesicles being released. Often the smaller EPPs do not reach threshold which causes muscle weakness and
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Unlike the reserve pool, the readily releasable pool of synaptic vesicles is ready to be activated. Vesicle depletion from the readily releasable pool occurs during high frequency stimulation of long duration and the size of the evoked EPP reduces. This neuromuscular depression is due to less
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attaches to the acetylcholine receptors and inhibits acetylcholine binding. This causes less signal propagation and small EPPs that do not reach threshold. By analyzing brain processes with acetylcholine, doctors can measure how much beta amyloid is around and use it to judge its effects on
154:. Voltage gated ion channels are responsive to changes in membrane voltage which cause the voltage gated ion channel to open and allows certain ions to pass through. Ligand gated ion channels are responsive to certain molecules such as neurotransmitters. The binding of a
23:
A sample endplate potential (EPP; an average of 10 single EPPs) is shown at the top, and sample miniature endplate potentials (mEPPs) are shown at the bottom. Note the differences in the scales on the X- and Y-axes. Both are taken from recordings at the mouse neuromuscular
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for
Physiology or Medicine for statistically determining the quantal size of acetylcholine vesicles based on noise analysis in the neuromuscular junction. Using a book on mechanical statistics, he was able to infer the size of individual events going on at the same time.
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depolarizations in the postsynaptic membrane. This small response (~0.4mV) is called a miniature end plate potential (MEPP) and is generated by one acetylcholine-containing vesicle. It represents the smallest possible depolarization which can be induced in a muscle.
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is the enzyme that synthesizes acetylcholine and is often used as a marker in research relating to acetylcholine production. Neurons that utilize acetylcholine are called cholinergic neurons and they are very important in muscle contraction, memory, and learning.
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When a vesicle releases its neurotransmitters via exocytosis, it empties its entire contents into the synaptic cleft. Neurotransmitter release from vesicles is therefore stated to be quantal because only whole numbers of vesicles can be released. In 1970,
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as the membrane potential starts to peak, the potassium ion channels open and causes an outflux of potassium to counteract the influx of sodium. At the peak, the outflux of potassium equals the influx of sodium, and the membrane does not change polarity.
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Once the membrane potential reaches threshold, an action potential occurs and causes a sharp spike in membrane polarity. There are five phases of an action potential: threshold, depolarization, peak, repolarization, and hyperpolarization.
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voltage causes the calcium voltage gated ion channels to open allowing for an influx of calcium ions. These calcium ions cause the acetylcholine vesicles attached to the presynaptic membrane to release acetylcholine via
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neurotransmitter release during stimulation. In order for depletion not to occur, there must be a balance between repletion and depletion which can happen at low stimulation frequencies of less than 30 Hz.
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Current research is attempting to learn more about end plate potentials and their effect on muscle activity. Many current diseases involve disrupted end plate potential activity. In
Alzheimer patients,
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End plate potentials are produced almost entirely by the neurotransmitter acetylcholine in skeletal muscle. Acetylcholine is the second most important excitatory neurotransmitter in the body following
312:. Several diseases and problems can be caused by the inability of enzymes to clear away the neurotransmitters from the synaptic cleft leading to continued action potential propagation.
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EPP are caused mostly by the binding of acetylcholine to receptors in the postsynaptic membrane. There are two different kinds of acetylcholine receptors: nicotinic and muscarinic.
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Kohara N, Lin TS, Fukudome T, Kimura J, Sakamoto T, et al. (2002). "Pathophysiology of weakness in a patient with congenital end-plate acetylcholinesterase deficiency".
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is the most powerful toxic protein. It prevents release of acetylcholine at the neuromuscular junction by inhibiting docking of the neurotransmitter vesicles.
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that use a second messenger. These receptors are slow and therefore are unable to measure a miniature end plate potential (MEPP). They are located in the
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found in insects blocks potassium channels. Alpha neurotoxin found in snakes binds to acetylcholine receptors and prevents acetylcholine from binding.
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Takeda T, Sakata A, Matsuoka T (1999). "Fractal dimensions in the occurrence of miniature end-plate potential in a vertebrate neuromuscular junction".
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Once the action potential has finished in the neuromuscular junction, the used acetylcholine is cleared out of the synaptic cleft by the enzyme
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506:"Enhanced acetylcholine secretion in neuroblastoma X glioma hybrid NG108-15 cells transfected with rat choline-acetyltransferase CDNA"
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47:. They are called "end plates" because the postsynaptic terminals of muscle fibers have a large, saucer-like appearance. When an
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are ligand gated ion channels for fast transmission. All acetylcholine receptors in the neuromuscular junction are nicotinic.
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Cole RN, Reddel SW, Gervasio OL, Phillips WD (2008). "Anti-MuSK patient antibodies disrupt the mouse neuromuscular junction".
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Prives J, Professor of
Pharmacology, State University of New York at Stony Brook. Interviewed by Pierre Watson. 2008-11-18.
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which includes the senses of touch, vision, and hearing. It was the first neurotransmitter to be identified in 1914 by
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requires a much higher input to induce an action potential. This phase is known as the relative refractory period.
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to the receptor on the ion channel protein causes a conformational change which allows the passing of certain ions.
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ion channels. There are two types of ion channels involved in the neuromuscular junction and end plate potentials:
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Van
Lunteren E, Moyer M (2005). "Modulation of biphasic reate of end-plate potential recovery in rat diaphragm".
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causes a massive influx of calcium at the axon terminal and leads to an overflow of neurotransmitter release.
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Partanen J (1999). "End plate spikes in the human electromyogram. Revision of the fusimotor theory".
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which blocks the sodium ion channels and prevents an action potential on the postsynaptic membrane.
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Sellin LC, Molgo J, Thornquist K, Hansson B, Thesleff S (1996). "On the possible origin of
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to occur which are less than 1mV in amplitude and not enough to reach threshold.
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All neurotransmitters are released into the synaptic cleft via exocytosis from
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947:, Stahlberg E (2004). "Modeling studies on irregular motor unit potentials".
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Patient with myasthenia gravis showing typical symptom of eyelid droop
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Purves D, Augustine G, et al. "Electrical
Signals of Nerve Cells."
109:. Acetylcholine is synthesized in the cytoplasm of the neuron from
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The neuromuscular junction is the synapse that is formed between an
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881:. Sinauer Associates, Inc: Sunderland, Massachusetts, 2008. 25-39.
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Progress in Neuro-Psychopharmacology & Biological
Psychiatry
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Signal transmission from nerve to muscle at the motor end plate.
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miniature end plate potentials at the neuromuscular junction".
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is a poison found in the certain poisonous fishes such as
483:. Philadelphia, PA: Saunders, Elsevier inc. p. 224.
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again for transport and release of neurotransmitters.
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271:spinal cord or brain for the appropriate response.
216:. Two kinds of neurotransmitter vesicles exist:
35:) are the voltages which cause depolarization of
553:Lin S, Landmann L, Ruegg MA, Brenner HR (2008).
504:Kimura Y; Oda Y; Deguchi T; Higashida H (1992).
802:Pflügers Archiv: European Journal of Physiology
130:The polarization of membranes is controlled by
59:, vesicles carrying neurotransmitters (mostly
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344:fatigue in patients. Many animals use
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257:Miniature end plate potentials (MEPPs)
348:to defend themselves and kill prey.
16:Voltages associated with muscle fibre
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275:Threshold potential ("All or None")
195:such as in the vagus nerve and the
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341:Lambert–Eaton myasthenic syndrome
1067:Lateralization of brain function
479:Boron, W.; Boulpaep, E. (2012).
1138:Somatosensory evoked potentials
297:so the membrane overshoots the
575:10.1523/JNEUROSCI.5590-07.2008
193:parasympathetic nervous system
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857:10.1016/S0928-4257(99)80146-6
767:10.1016/S0278-5846(99)00050-0
999:Muscle and the neuromuscular
961:10.1016/j.clinph.2003.10.031
664:Biological Procedures Online
658:Teressa G, Prives J (2008).
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845:Journal of Physiology-Paris
189:G protein-coupled receptors
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376:produced by the bacteria
222:small clear core vesicles
218:large dense core vesicles
171:into the synaptic cleft.
148:voltage-gated ion channel
119:Choline acetyltransferase
949:Clinical Neurophysiology
945:Hausmanowa-Petrusewicz I
152:ligand-gated ion channel
1143:Visual evoked potential
562:Journal of Neuroscience
284:Action potential phases
1227:Long-term potentiation
1179:Postsynaptic potential
1123:Bereitschaftspotential
430:Neuromuscular junction
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197:gastrointestinal tract
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72:Neuromuscular junction
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1062:Intracranial pressure
378:Clostridium botulinum
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316:Clinical applications
175:Postsynaptic membrane
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1232:Long-term depression
1207:Axoplasmic transport
798:giant or slow-rising
420:Muscarinic receptors
310:acetylcholinesterase
242:University of London
185:Muscarinic receptors
162:Presynaptic membrane
103:somatosensory system
29:End plate potentials
1403:End-plate potential
1388:Uterine contraction
1222:Synaptic plasticity
1214:/Nerve regeneration
617:Annals of Neurology
440:Nicotinic receptors
405:Alzheimer's disease
370:black widow spiders
181:Nicotinic receptors
101:. It controls the
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1169:Membrane potential
1034:Physiology of the
902:Muscle & Nerve
814:10.1007/BF02207269
709:Muscle & Nerve
481:Medical Physiology
455:Tetraethylammonium
362:Tetraethylammonium
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568:(13): 3333–3340.
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425:Myasthenia gravis
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41:neurotransmitters
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61:acetylcholine
58:
54:
53:axon terminal
50:
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1323:Eye movement
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943:Zalewska E,
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670:(1): 58–65.
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510:FEBS Letters
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460:Tetrodotoxin
415:Motor neuron
350:Tetrodotoxin
331:beta amyloid
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238:Bernard Katz
234:
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126:Ion channels
95:
83:
57:motor neuron
51:reaches the
32:
28:
27:
1360:Muscle tone
1055:Wakefulness
358:triggerfish
346:neurotoxins
246:Nobel Prize
1435:Categories
1416:Myogenesis
1333:Locomotion
1189:Inhibitory
1184:Excitatory
466:References
354:pufferfish
264:electrodes
203:Initiation
169:exocytosis
115:acetyl-CoA
107:Henry Dale
65:exocytosed
1378:Isometric
1200:Long term
1164:Chronaxie
1098:Sensation
645:205340971
368:found in
240:from the
136:potassium
99:glutamate
24:junction.
1383:Isotonic
1318:Movement
1313:Exercise
1305:Exertion
977:43828995
969:15036049
930:45891411
922:11932977
783:30988488
775:10621955
737:31071429
729:15654692
694:19461953
637:18384168
602:18659773
594:18367600
384:See also
244:won the
144:chloride
1297:muscles
1050:Arousal
994:Muscles
865:4961877
830:8748384
822:8584425
685:2683546
585:6670584
540:4956377
532:1468577
140:calcium
111:choline
1093:Reflex
1077:Memory
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156:ligand
142:, and
132:sodium
63:) are
1344:Other
1243:Other
1072:Sleep
973:S2CID
926:S2CID
861:S2CID
826:S2CID
779:S2CID
733:S2CID
641:S2CID
598:S2CID
558:(PDF)
536:S2CID
55:of a
1328:Gait
1128:P300
1107:Both
965:PMID
918:PMID
818:PMID
771:PMID
725:PMID
690:PMID
633:PMID
590:PMID
528:PMID
485:ISBN
356:and
220:and
187:are
150:and
113:and
33:EPPs
957:doi
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910:doi
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680:PMC
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31:(
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