Neural accommodation
Neural accommodation or neuronal accommodation occurs when a neuron or muscle cell is depolarised by slowly rising current (ramp depolarisation) in vitro.[1][2] The Hodgkin–Huxley model also shows accommodation.[3] Sudden depolarisation of a nerve evokes propagated action potential by activating voltage-gated fast sodium channels incorporated in the cell membrane if the depolarisation is strong enough to reach threshold. The open sodium channels allow more sodium ions to flow into the cell and resulting in further depolarisation, which will subsequently open even more sodium channels. At a certain moment this process becomes regenerative (vicious cycle) and results in the rapid ascending phase of action potential. In parallel with the depolarisation and sodium channel activation, the inactivation process of the sodium channels is also driven by depolarisation. Since the inactivation is much slower than the activation process, during the regenerative phase of action potential, inactivation is unable to prevent the "chain reaction"-like rapid increase in the membrane voltage.
During neuronal accommodation, the slowly rising depolarisation drives the activation and inactivation, as well as the potassium gates simultaneously and never evokes action potential. Failure to evoke action potential by ramp depolarisation of any strength had been a great puzzle until Hodgkin and Huxley created their physical model of action potential. Later in their life they received a Nobel Prize for their influential discoveries. Neuronal accommodation can be explained in two ways. "First, during the passage of a constant cathodal current through the membrane, the potassium conductance and the degree of inactivation will rise, both factors raising the threshold. Secondly, the steady state ionic current at all strengths of depolarization is outward, so that an applied cathodal current which rises sufficiently slowly will never evoke a regenerative response from the membrane, and excitation will not occur."[3] (quote from Hodgkin and Huxley)
In vivo physiologic condition accommodation breaks down, that is long-duration slowly rising current excites nerve fibers at a nearly constant intensity no matter how slowly this intensity is approached.[4][5]
See also
[edit]References
[edit]- ^ Lucas, K. (1907). "On the rate of variation of the exciting current as a factor in electric excitation". The Journal of Physiology. 36 (4–5): 253–274. doi:10.1113/jphysiol.1907.sp001231. PMC 1533589. PMID 16992906.
- ^ Vallbo, A. B. (1964). "Accommodation Related to Inactivation of the Sodium Permeability in Single Myelinated Nerve Fibres from Xenopus Laevis". Acta Physiologica Scandinavica. 61: 429–444. PMID 14209259.
- ^ a b Hodgkin, A. L.; Huxley, A. F. (1952). "A quantitative description of membrane current and its application to conduction and excitation in nerve". The Journal of Physiology. 117 (4): 500–544. doi:10.1113/jphysiol.1952.sp004764. PMC 1392413. PMID 12991237.
- ^ Hennings, K.; Arendt-Nielsen, L.; Andersen, O. K. (2005). "Breakdown of accommodation in nerve: A possible role for persistent sodium current". Theoretical Biology and Medical Modelling. 2: 16. doi:10.1186/1742-4682-2-16. PMC 1090618. PMID 15826303.
- ^ Baker, M.; Bostock, H. (1989). "Depolarization changes the mechanism of accommodation in rat and human motor axons". The Journal of Physiology. 411: 545–561. doi:10.1113/jphysiol.1989.sp017589. PMC 1190540. PMID 2614732.
External links
[edit]- Interactive Java applet of the HH model Parameters of the model can be changed as well as excitation parameters and phase space plottings of all the variables is possible.
- Direct link to Hodgkin-Huxley model and a Description in BioModels Database
- Hodgkin, A. L.; Huxley, A. F.; Katz, B. (April 1952). "Measurement of current-voltage relations in the membrane of the giant axon of Loligo". The Journal of Physiology. 116 (4): 424–48. doi:10.1113/jphysiol.1952.sp004716. PMC 1392219. PMID 14946712. Direct link to Hodgkin-Huxley paper #1 via PubMedCentral
- Hodgkin, A. L.; Huxley, A. F. (April 1952). "Currents carried by sodium and potassium ions through the membrane of the giant axon of Loligo". The Journal of Physiology. 116 (4): 449–72. doi:10.1113/jphysiol.1952.sp004717. PMC 1392213. PMID 14946713. Direct link to Hodgkin-Huxley paper #2 via PubMedCentral
- Hodgkin, A. L.; Huxley, A. F. (April 1952). "The components of membrane conductance in the giant axon of Loligo". The Journal of Physiology. 116 (4): 473–96. doi:10.1113/jphysiol.1952.sp004718. PMC 1392209. PMID 14946714. Direct link to Hodgkin-Huxley paper #3 via PubMedCentral
- Hodgkin, A. L.; Huxley, A. F. (April 1952). "The dual effect of membrane potential on sodium conductance in the giant axon of Loligo". The Journal of Physiology. 116 (4): 497–506. doi:10.1113/jphysiol.1952.sp004719. PMC 1392212. PMID 14946715. Direct link to Hodgkin-Huxley paper #4 via PubMedCentral
- Hodgkin, A. L.; Huxley, A. F. (August 1952). "A quantitative description of membrane current and its application to conduction and excitation in nerve". The Journal of Physiology. 117 (4): 500–44. doi:10.1113/jphysiol.1952.sp004764. PMC 1392413. PMID 12991237. Direct link to Hodgkin-Huxley paper #5 via PubMedCentral
- Neural Impulses: The Action Potential In Action by Garrett Neske, The Wolfram Demonstrations Project
- Interactive Hodgkin-Huxley model by Shimon Marom, The Wolfram Demonstrations Project
- ModelDB A computational neuroscience source code database containing 4 versions (in different simulators) of the original Hodgkin–Huxley model and hundreds of models that apply the Hodgkin–Huxley model to other channels in many electrically excitable cell types.