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- AHP
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出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2016/04/13 00:05:00」(JST)
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Schematic of an electrophysiological recording of an action potential, showing the various phases that occur as the voltage wave passes a point on a cell membrane. The afterhyperpolarisation is one of the processes that contribute to the refactory period.
Afterhyperpolarization, or AHP, describes the hyperpolarizing phase of a neuron's action potential where the cell's membrane potential falls below the normal resting potential. This is also commonly referred to as an action potential's undershoot phase. AHPs have been segregated into "fast", "medium", and "slow" components that appear to have distinct ionic mechanisms and durations. While fast and medium AHPs can be generated by single action potentials, slow AHPs generally develop only during trains of multiple action potentials.
During single action potentials, transient depolarization of the membrane opens more voltage-gated K+ channels than are open in the resting state, many of which do not close immediately when the membrane returns to its normal resting voltage. This can lead to an "undershoot" of the membrane potential to values that are more polarized ("hyperpolarized") than was the original resting membrane potential. Ca2+-activated K+ channels that open in response to the influx of Ca2+ during the action potential carry much of the K+ current as the membrane potential becomes more negative. The K+ permeability of the membrane is transiently unusually high, driving the membrane voltage VM even closer to the K+ equilibrium voltage EK. Hence, hyperpolarization persists until the membrane K+ permeability returns to its usual value.[1]
Medium and slow AHP currents also occur in neurons.[2] The ionic mechanisms underlying medium and slow AHPs are not yet well understood, but may also involve M current and HCN channels for medium AHPs,[3] and ion-dependent currents[4] and/or ionic pumps for slow AHPs.[5][6]
References
- ^ Purves et al., p. 37; Bullock, Orkand, and Grinnell, p. 152.
- ^ M. Shah, and D. G. Haylett. Ca2+ Channels Involved in the Generation of the Slow Afterhyperpolarization in Cultured Rat Hippocampal Pyramidal Neurons. J Neurophysiol 83: 2554-2561, 2000.
- ^ N. Gu, K. Vervaeke, H. Hu, and J.F. Storm, Kv7/KCNQ/M and HCN/h, but not KCa2/SK channels, contribute to the somatic medium afterhyperpolarization and excitability control in CA1 hippocampal pyramidal cells, Journal of Physiology 566:689-715 (2005).
- ^ R. Andrade, R.C. Foehring, and A.V. Tzingounis, Essential role for phosphatidylinositol 4,5-bisphosphate in the expression, regulation, and gating of the slow afterhyperpolarization current in the cerebral cortex, Frontiers in Cellular Neuroscience 6:47 (2012).
- ^ J.H. Kim, I. Sizov, M. Dobretsov, and H. Von Gersdorff, Presynaptic Ca2+ buffers control the strength of a fast post-tetanic hyperpolarization mediated by the a3 Na+/K+-ATPase, Nature Neuroscience 10:196-205 (2007).
- ^ A.T. Gulledge, S. Dasari, K. Onoue, E.K. Stephens, J.M. Hasse, and D. Avesar, A sodium-pump-mediated afterhyperpolarization in pyramidal neurons., Journal of Neuroscience 33:13025-13041 (2013).
English Journal
- Redistribution of Kv2.1 ion channels on spinal motoneurons following peripheral nerve injury.
- Romer SH1, Dominguez KM2, Gelpi MW3, Deardorff AS4, Tracy RC5, Fyffe RE6.Author information 1Department of Neuroscience, Cell Biology and Physiology, 202 University Hall, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: Shannon.romer@wright.edu.2Department of Surgery Boonshoft School of Medicine, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: Kmdominguez@juno.com.3Department of Neuroscience, Cell Biology and Physiology, 202 University Hall, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: gelpi.2@wright.edu.4Department of Neuroscience, Cell Biology and Physiology, 202 University Hall, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: deardorff.2@wright.edu.5Department of Neuroscience, Cell Biology and Physiology, 202 University Hall, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: robert.tracy@osumc.edu.6Department of Neuroscience, Cell Biology and Physiology, 202 University Hall, Wright State University, 3640 Colonel Glenn Hwy, Dayton, OH 45435, USA. Electronic address: robert.fyffe@wright.edu.AbstractPathophysiological responses to peripheral nerve injury include alterations in the activity, intrinsic membrane properties and excitability of spinal neurons. The intrinsic excitability of α-motoneurons is controlled in part by the expression, regulation, and distribution of membrane-bound ion channels. Ion channels, such as Kv2.1 and SK, which underlie delayed rectifier potassium currents and afterhyperpolarization respectively, are localized in high-density clusters at specific postsynaptic sites (Deardorff et al., 2013; Muennich and Fyffe, 2004). Previous work has indicated that Kv2.1 channel clustering and kinetics are regulated by a variety of stimuli including ischemia, hypoxia, neuromodulator action and increased activity. Regulation occurs via channel dephosphorylation leading to both declustering and alterations in channel kinetics, thus normalizing activity (Misonou et al., 2004; Misonou et al., 2005; Misonou et al., 2008; Mohapatra et al., 2009; Park et al., 2006). Here we demonstrate using immunohistochemistry that peripheral nerve injury is also sufficient to alter the surface distribution of Kv2.1 channels on motoneurons. The dynamic changes in channel localization include a rapid progressive decline in cluster size, beginning immediately after axotomy, and reaching maximum within one week. With reinnervation, the organization and size of Kv2.1 clusters do not fully recover. However, in the absence of reinnervation Kv2.1 cluster sizes fully recover. Moreover, unilateral peripheral nerve injury evokes parallel, but smaller effects bilaterally. These results suggest that homeostatic regulation of motoneuron Kv2.1 membrane distribution after axon injury is largely independent of axon reinnervation.
- Brain research.Brain Res.2014 Feb 14;1547:1-15. doi: 10.1016/j.brainres.2013.12.012. Epub 2013 Dec 16.
- Pathophysiological responses to peripheral nerve injury include alterations in the activity, intrinsic membrane properties and excitability of spinal neurons. The intrinsic excitability of α-motoneurons is controlled in part by the expression, regulation, and distribution of membrane-bound ion chan
- PMID 24355600
- Electrophysiological and Morphological Properties of Rat Supratrigeminal Premotor Neurons Targeting the Trigeminal Motor Nucleus.
- Nakamura S, Nakayama K, Mochizuki A, Sato F, Haque T, Yoshida A, Inoue T.Author information Showa University School of Dentistry.AbstractThe electrophysiological and morphological characteristics of premotor neurons in the supratrigeminal region (SupV) targeting the trigeminal motor nucleus (MoV) were examined in neonatal rat brainstem slice preparations using Ca2+ imaging, whole-cell recordings and intracellular biocytin labeling. First, we screened SupV neurons that showed a rapid rise in [Ca2+]i after single-pulse electrical stimulation of the ipsilateral MoV. Subsequent whole-cell recordings were generated from the screened SupV neurons, and their antidromic responses to MoV stimulation were confirmed. We divided the antidromically activated premotor neurons into 2 groups according to their discharge patterns during the steady-state in response to 1-s depolarizing current pulses: those firing at a frequency higher (HF neurons, n = 19) or lower (LF neurons, n = 17) than 33 Hz. In addition, HF neurons had a narrower action potential and a larger afterhyperpolarization than LF neurons. Intracellular labeling revealed that the axons of all HF neurons (6/6) and half of the LF neurons (4/9) entered the MoV from its dorsomedial aspect, whereas the axons of the remaining LF neurons (5/9) entered the MoV from its dorsolateral aspect. Furthermore, the dendrites of 3 HF neurons penetrated into the principal sensory trigeminal nucleus (Vp), whereas the dendrites of all LF neurons were confined within the SupV. These results suggest that the types of SupV premotor neurons targeting the MoV with different firing properties have different dendritic and axonal morphologies, and these SupV neuron classes may play unique roles in diverse oral motor behaviors, such as suckling and mastication.
- Journal of neurophysiology.J Neurophysiol.2014 Feb 5. [Epub ahead of print]
- The electrophysiological and morphological characteristics of premotor neurons in the supratrigeminal region (SupV) targeting the trigeminal motor nucleus (MoV) were examined in neonatal rat brainstem slice preparations using Ca2+ imaging, whole-cell recordings and intracellular biocytin labeling. F
- PMID 24501266
- Concomitant changes in afterhyperpolarization and twitch following repetitive stimulation of fast motoneurones and motor units.
- Krutki P, Mrówczyński W, Raikova R, Celichowski J.Author information Department of Neurobiology, University School of Physical Education, 27/39 Królowej Jadwigi St., 61-871, Poznan, Poland.AbstractThe study aimed at determining changes in a course of motoneuronal afterhyperpolarization (AHP) and in contractile twitches of motor units (MUs) during activity evoked by increasing number of stimuli (from 1 to 5), at short interspike intervals (5 ms). The stimulation was applied antidromically to spinal motoneurones or to isolated axons of MUs of the medial gastrocnemius muscle within two separate series of experiments on anesthetized rats. Alterations in the amplitude and time parameters of the AHP of successive spikes were compared to changes in force and time course of successive twitches obtained by mathematical subtraction of tetanic contractions evoked by one to five stimuli. The extent of changes of the studied parameters depended on a number of applied stimuli. The maximal modulation of the AHP and twitch parameters (a prolongation and an increase in the AHP and twitch amplitudes) was typically observed after the second pulse, while higher number of pulses at the same frequency did not induce so prominent changes. One may conclude that changes observed in parameters of action potentials of motoneurons are concomitant to changes in contractile properties of MU twitches. This suggests that both modulations of the AHP and twitch parameters reflect mechanisms leading to force development at the beginning of MU activity.
- Experimental brain research.Exp Brain Res.2014 Feb;232(2):443-52. doi: 10.1007/s00221-013-3752-5. Epub 2013 Nov 8.
- The study aimed at determining changes in a course of motoneuronal afterhyperpolarization (AHP) and in contractile twitches of motor units (MUs) during activity evoked by increasing number of stimuli (from 1 to 5), at short interspike intervals (5 ms). The stimulation was applied antidromically to
- PMID 24202237
Japanese Journal
- Electrophysiological characteristics of IB4-negative TRPV1-expressing muscle afferent DRG neurons
- Rat GnRH Neurons Exhibit Large Conductance Voltage- and Ca2+-Activated K+ (BK) Currents and Express BK Channel mRNAs
- Membrane properties of rat medial vestibular nucleus neurons in vivo
- Neuroscience research : the official journal of the Japan Neuroscience Society 59(2), 215-223, 2007-10-01
- NAID 10024417564
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- Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Afterhyperpolarization describes the part of an inactivation phase of an action potential where the membrane falls below the normal resting potential. Both medium and slow ...
- Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual... ... File:Action potential.svg Afterhyperpolarization, or AHP, describes the hyperpolarizing phase of a neuron's action potential where the ...
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- afterhyperpolarization、oxaceprol