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Action potential

An action potential is the local membrane potential created as a nerve impulse is transmitted. They set the pace of thought and action, constrain the sizes of evolving anatomies and enable centralized control and coordination of organs and tissues. Table of contents showTocToggle("show","hide") 1 Basic features 2 Underlying mechanism 3 Initiation 4 Wave propagation 5 Saltatory propagation 6 Detection and observation 7 Detailed features Basic features When a biological cell or patch of membrane undergoes an action potential -- or electrical excitation -- the polarity of the transmembrane voltage swings rapidly from negative to positive and back. Within any one excitable cell, consecutive action potentials typically are indistinguishable. Also between different cells the amplitudes of the voltage swings tend to be roughly the same. But the speed and simplicity of action potentials vary significantly between cells, in particular between different cell types. Minimally, an action potential involves a depolarization, a repolarization and finally a hyperpolarization (or "undershoot"). In specialized muscle cells of the heart, such as the pacemaker cells, a plateau phase of intermediate voltage may precede repolarization. Underlying mechanism The transmembrane voltage changes that take place during an action potential result from changes in the permeability of the membrane to specific ions, the internal and external concentrations of which cells maintain in an imbalance. In the axon fibers of nerves, depolarization results from the inward rush of sodium ions, while repolarization and hyperpolarization arise from an outward rush of potassium ions. Calcium ions make up most or all of the depolarizing currents at an axon's presynaptic terminus, in muscle cells (including the heart's) and in some dendrites. The imbalance of ions that makes possible not only action potentials but the resting cell potential arises through the work of pumps, in particular the sodium-potassium exchanger. Changes in membrane permeability and the onset and cessation of ionic currents reflect the opening and closing of voltage-gated ion channels, which provide portals through the membrane for ions. Residing in and spanning the membrane, these enzymes sense and respond to changes in transmembrane potential. Initiation Action potentials are triggered by an initial depolarization to the point of threshold. This threshold potential varies but generally is about 15 millivolts above the resting potential of the cell. Typically action potential initiation occurs at a synapse, but may occur anywhere along the axon. In his discovery of "animal electricity," Luigi Galvani elicited an action potential through contact of his scalpel with the sciatic motor nerve of a frog he was dissecting, causing one of its legs to kick as in life. Wave propagation In the fine fibers of simple (or unmyelinated) axons, action potentials propagate as waves, which travel at speeds up to 120 meters per second. The propagation speed of these impulses is faster in fatter fibers than in thin ones, other things being equal. In their Nobel prize-winning work uncovering the wave nature and ionic mechanism of action potentials, Alan Hodgkin and Andrew Huxley performed experiments on the giant fiber of Atlantic squid. Responsible for initiating flight, this axon is fat enough to be seen without a microscope (100 to 1000 times larger than is typical). This is assumed to reflect an adaptation for speed. Indeed, the velocity of nerve impulses in these fibers is among the fastest in nature. Saltatory propagation Many neurons have insulating sheaths of myelin surrounding their axons, which enable action potentials to travel faster than in unmyelinated axons of the same diameter. The myelin sheathing normally runs along the axon in sections about 1 mm long, punctuated by unsheathed nodes of Ranvier. Because the salty cytoplasm of the axon is electrically conductive, and because the myelin inhibits charge leakage through the membrane, depolarization at one node is sufficient to elevate the voltage at a neighboring node to the threshold for action potential initiation. Thus in myelinated axons, action potentials do not propagate as waves, but recur at successive nodes and in effect hop along the axon. This mode of propagation is known as saltatory conduction. The disease multiple sclerosis (MS) is due to a breakdown of myelin sheathing, and degrades muscle control by destroying axons' ability to conduct action potentials. Detection and observation Action potentials (APs) are measured with the recording techniques of electrophysiology. In the case of an archetypal nerve action potential on an oscilloscope, the relatively large swing to a more positive value, followed by the repolarization recovery and undershoot together trace an arc that could be described as a distorted sine wave -- or like the blips on hospital EKG machines that can be seen on TV (these EKG waves are a smear of all the action potentials in one heartbeat, so they enact more slowly than any individual AP and have a somewhat more complicated shape). In an unmyelinated axon that is firing an action potential, the transmembrane potential at any instant will vary from point to point along the fiber, with its amplitude depending on whether the AP wave has reached that point or passed it, and how long ago. A recording from a single point will show the various stages of the action potential enacted -- depolarization, repolarization, hyperpolarization -- as the wave passes. Detailed features Prototypically, depolarization and repolarization together are complete in about two milliseconds, while undershoots can last hundreds of milliseconds, depending on the cell. In neurons, the exact length of the roughly two-millisecond delay in repolarization can have a strong effect on the amount of neurotransmitter released at a synapse. The duration of the hyperpolarization determines a nerve's refractory period (how long until it may conduct another action potential) and hence the frequency at which it will fire under continuous stimulation. Both of these properties are subject to biological regulation, primarily (among the mechanisms discovered so far) acting on ion channels selective for potassium. In pacemaker and other cardiac muscle cells, inward calcium currents determine shape and duration of the plateau phase, which in turn controls the strength and duration of contraction. See ventricular action potential, atrial action potential, and pacemaker action potential for more details.

The above article is adapted from from Wikipedia All Wikipedia article text is available under the terms of the GNU Free Documentation License



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Recent Action_potential related patents

From USPTO:




from PUBMED
1:  Stucky CL, Medler KA, Molliver DC. 
 The P2Y agonist UTP activates cutaneous afferent fibers.
Pain. 2004 May;109(1-2):36-44. 
PMID: 15082124 

2:  Drew GM, Vaughan CW. 
 Multiple metabotropic glutamate receptor subtypes modulate GABAergic
neurotransmission in rat periaqueductal grey neurons in vitro.
Neuropharmacology. 2004 Jun;46(7):927-34. 
PMID: 15081789 

3:  Han JS, Bird GC, Neugebauer V. 
 Enhanced group III mGluR-mediated inhibition of pain-related synaptic
plasticity in the amygdala.
Neuropharmacology. 2004 Jun;46(7):918-26. 
PMID: 15081788 

4:  Li GR, Sun H, To J, Tse HF, Lau CP. 
 Demonstration of calcium-activated transient outward chloride current and
delayed rectifier potassium currents in Swine atrial myocytes.
J Mol Cell Cardiol. 2004 Apr;36(4):495-504. 
PMID: 15081309 

5:  Axmacher N, Draguhn A. 
 Inhibition of GABA release by presynaptic ionotropic GABA receptors in
hippocampal CA3.
Neuroreport. 2004 Feb 9;15(2):329-34. 
PMID: 15076763 

6:  Martin RL, McDermott JS, Salmen HJ, Palmatier J, Cox BF, Gintant GA. 
 The utility of hERG and repolarization assays in evaluating delayed cardiac
repolarization: influence of multi-channel block.
J Cardiovasc Pharmacol. 2004 Mar;43(3):369-79. 
PMID: 15076220 

7:  Hopfield JJ. 
 Encoding for computation: Recognizing brief dynamical patterns by exploiting
effects of weak rhythms on action-potential timing.
Proc Natl Acad Sci U S A. 2004 Apr 9 [Epub ahead of print] 
PMID: 15075391 

8:  Klop WM, Hartlooper A, Briare JJ, Frijns JH. 
 A new method for dealing with the stimulus artefact in electrically evoked
compound action potential measurements.
Acta Otolaryngol. 2004 Mar;124(2):137-43. 
PMID: 15072415 

9:  Hug U, Burg D, Baldi SV, Meyer VE. 
 Compression neuropathy of the radial palmar thumb nerve.
Chir Main. 2004 Feb;23(1):49-51. 
PMID: 15071968 

10:  Taylor CM, Marta CB, Claycomb RJ, Han DK, Rasband MN, Coetzee T, Pfeiffer
SE. 
 Proteomic mapping provides powerful insights into functional myelin biology.
Proc Natl Acad Sci U S A. 2004 Mar 30;101(13):4643-8. Epub 2004 Mar 19. 
PMID: 15070771 

11:  Liu K, Liao YH, Wang ZH, Li SL, Wang M, Zeng LL, Tang M. 
 Effects of autoantibodies against beta(1)-adrenoceptor in hepatitis virus
myocarditis on action potential and L-type Ca(2+) currents.
World J Gastroenterol. 2004 Apr 15;10(8):1171-5. 
PMID: 15069720 

12:  Liang CL, Nelson O, Yazdani U, Pasbakhsh P, German DC. 
 Inverse relationship between the contents of neuromelanin pigment and the
vesicular monoamine transporter-2: Human midbrain dopamine neurons.
J Comp Neurol. 2004 May 17;473(1):97-106. 
PMID: 15067721 

13:  Chiang CE, Wang TM, Luk HN. 
 Inhibition of L-type ca current in Guinea pig ventricular myocytes by
cisapride.
J Biomed Sci. 2004 May-Jun;11(3):303-14. 
PMID: 15067213 

14:  Brasnjo G, Otis TS. 
 Isolation of glutamate transport-coupled charge flux and estimation of
glutamate uptake at the climbing fiber-Purkinje cell synapse.
Proc Natl Acad Sci U S A. 2004 Apr 5 [Epub ahead of print] 
PMID: 15067125 

15:  Abi-Gerges N, Philp K, Pollard C, Wakefield I, Hammond TG, Valentin JP. 
 Sex differences in ventricular repolarization: from cardiac electrophysiology
to Torsades de Pointes.
Fundam Clin Pharmacol. 2004 Apr;18(2):139-51. 
PMID: 15066127 

16:  Clerc N, Furness JB. 
 Intrinsic primary afferent neurones of the digestive tract.
Neurogastroenterol Motil. 2004 Apr;16 Suppl 1:24-7. 
PMID: 15066000 

17:  Trukhanov KA, Lazareva ES, Maksimov GV, Lebedev VM, Spasskii AV. 
 [Effects of high energy charged particles on conduction of nerve rhythmic
excitation]
Radiats Biol Radioecol. 2004 Jan-Feb;44(1):52-5. Russian. 
PMID: 15060941 

18:  Thaler C, Gray AC, Lipscombe D. 
 Cumulative inactivation of N-type CaV2.2 calcium channels modified by
alternative splicing.
Proc Natl Acad Sci U S A. 2004 Apr 13;101(15):5675-9. Epub 2004 Apr 01. 
PMID: 15060274 

19:  Sirjani DB, Salt AN, Gill RM, Hale SA. 
 The influence of transducer operating point on distortion generation in the
cochlea.
J Acoust Soc Am. 2004 Mar;115(3):1219-29. 
PMID: 15058343 

20:  Suzuki A, Shirakawa I, Noguchi K, Kishi H, Sugi H. 
 Recovery of Action Potentials and Twitches after K-contractures in Frog
Skeletal Muscle.
Zoolog Sci. 2004 Mar;21(3):251-5. 
PMID: 15056919 

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Note again ... some material here is adapted from from Wikipedia All Wikipedia article text is available under the terms of the GNU Free Documentation License

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