bioelectric potentials-3 action...
TRANSCRIPT
BIOELECTRIC POTENTIALS-3Action Piteontal
Yalçın İŞLER, PhDIzmir Katip Celebi University
Department of Biomedical [email protected]
Restong Piteontal• All cells (not just excitable cells) have a restng potental
• The size of the restng potental varies – in excitable cells runs about -65/-80/-100 mV
Excitable Cells
• Neuron • Muscle Cells• Endocrine Cells
Could be stmulated by appropriate chemical and physical stmuli
Action Piteontal
• In response to the appropriate stmulus, the cell membrane of an excitable cell goes through a sequence of depolarizaton from its rest state followed by repolarizaton to that rest state.
Action Piteontal
• The main electrical actvity of excitable cells.• In neurons, they play a central role in cell-to-cell communicaton
• Their main functon is to actvate intracellular processes– In muscle cells;an acton potental is the rst step in the chain of events leading to contracton.
– In beta cells of the pancreas, they provoke release of insulin.
• At restng potental the membrane is more permeable to K+ ions than Na+ ions.
o
oo
Cl)K/pCl(piNa)K/pNa(piKiCl)K/pCl(pNa)K/pNa(pK
log58mV
Axion if Squid (-70 mV)Iion Extracellular Cionceontration Iontracellular Cionceontration
Na+ 460 50K+ 10 400Cl- 540 40
Concentratons are in mM/l
pK: 1.0, pNa: 0.03, pCl: 0.1
mV
o
oo
70545.1400
48.1310log58
540)1.0(50)03.0(400
40)1.0(460)03.0(10log58
Cl)K/pCl(piNa)K/pNa(piKiCl)K/pCl(pNa)K/pNa(pK
log58mV
Equlibrium Potental of K+
EK=(RT/zF) 2,303 log(Ko/Ki) Nernst Equaton
EK=((8,31x293)/(1x96500))x 2,303x log(10/400) =58,1 x log (0.025) =-93 mV
• When the cell is stmulated the sodium permeability of the membrane increases suddenly and allows tremendous numbers of positvely charged sodium ions to difuse to the interior of the cell.
• The normal "polarized" state of -80 millivolts is immediately neutralized by the infowing positvely charged sodium ions, with the potental rising rapidly in the positve directon.
• This is called depolarizaton.
Axion if SquidIion Extracellular Cionceontration Iontracellular Cionceontration
Na+ 460 50K+ 10 400Cl- 540 40
Concentratons are in mM/l
During restng state pK: 1.0, pNa: 0.03, pCl: 0.1 During acton potental pK: 1.0, pNa: 15, pCl: 0.1
mV
o
oo
44540)1.0(50)15(400
40)1.0(460)15(10log58
Cl)K/pCl(piNa)K/pNa(piKiCl)K/pCl(pNa)K/pNa(pK
log58mV
Equlibrium Potental of Na+
ENa=(RT/zF) 2,303 log(Nao/Nai) Nernst Equaton
ENa=((8,31x293)/(1x96500))x 2,303x log(460/50) =58,1 x log (9.2) =56 mV
• Within a few 10,000ths of a second afer the membrane becomes highly permeable to sodium ions, the sodium channels begin to close and the potassium channels open more than normal.
• Then, rapid difusion of potassium ions to the exterior re-establishes the normal negatve restng membrane potental.
• This is called repolarizaton of the membrane.
Two other types of transport channels through the nerve membrane: the viltage-gated sidium aond pitassium chaononels
• The necessary actor in causing both depolarizaton and repolarizaton of the nerve membrane during the acton potental is the voltage-gated sodium channel.
• A voltage-gated potassium channel also plays an important role in increasing the rapidity of repolarizaton of the membrane.
Voltage –gated Na+ Channels• In restng state, actvaton gates
closed, inactvaton gates are open.• As a result of the stmulus (which
exceeds the threshold value) both gates are actvated– Actvaton gate opens -rapid process– Inactvaton gate starts closing -slow
process
• Till the inactvaton gate is closed Na+ ions that enter the cell are depolarized the cell.
• Another important characteristc of the sodium channel inactvaton process is that the inactvaton gate will not reopen untl the membrane potental returns to or near the original restng membrane potental level.
• Therefore, it is usually not possible for the sodium channels to open again without rst repolarizing the nerve ber.
Voltage –gated Na+ Channels
Voltage –gated K+ Channels• When the cell is at rest
– Gate closed
• At threshold voltage – Gate starts opening -slow process
• At peak positvity level – Gate opens– Remains open tll restng membrane potental is restored
• During repolarizaton – Gate starts to close -slow process
• if any event causes enough inital rise in the membrane potental from -90 millivolts toward the zero level, the rising voltage itself causes many voltage-gated sodium channels to begin opening.
• This allows rapid infow of sodium ions, which causes a further rise in the membrane potental, thus opening stll more voltage-gated sodium channels and allowing more streaming of sodium ions to the interior of the ber.
• This process is a positve-feedback cycle that, once the feedback is strong enough, contnues untl all the voltage-gated sodium channels have become actvated (opened).
A Pisitve-Feedback Cycle Opeons the Sidium Chaononels
All ir onione prionciple
• Acton potental will either be generated or not…no gradatons or intensites possible
• Suprathreshild stmulus will elicit same acton potental as elicited by threshold stmulus
• Subthreshild stmulus will not elicit acton potental
Refractiry periid• A new acton potental cannot occur as long as the
membrane is stll depolarized from the preceding acton potental
• shortly afer the acton potental is initated, the sodium channels become inactvated and no amount of excitatory signal applied to these channels at this point will open the inactvaton gates.
• The only conditon that will allow them to reopen is for the membrane potental to return to or near the original restng membrane potental level.
• Then, within another small fracton of a second, the inactvaton gates of the channels open and a new acton potental can be initated.
Refractiry periid1. Absilutely refractiry periidPeriod during which a 2nd acton potental can not be generated. • Afer closure, the inactvaton gates do not reopen untl RMP is restored
2. Relatve refractiry periidPeriod during which 2nd acton potental can be generated but with stronger than normally required stmulus. • Some voltage gated Na+channels
regain their restng con guraton• During this period K+efux
contnues.