Action potential
An action potential is a message in the form of an electrical impulse caused by a rapid change in a cell's membrane potential.
When a stimulus reaches the threshold at the axon hillock, an action potential is generated.
An action potential relies on many protein channels. In a neurone, the Potassium leak channel and Sodium-Potassium pump maintain the resting potential. The voltage gated sodium channels and the voltage gated potassium channels are involved in the progression of an action potential along the membrane.
The action potential progression can be separated into several steps;
- Voltage channels are closed and the Potassium (K+) leak channel and the sodium (Na+) pump maintain the resting membrane potential of -70 mV. The Sodium/Potassium Pump (ATPase) is responsible for maintaining the membrane potential at -70mv, the protein actively pumps three sodium ions out of the cell and pumps two potassium ions into the cell.
- The neurone becomes stimulated. The voltage gated sodium channels begin to open and the membrane potential begins to slowly depolarises and sodium enters the cell down its concentration gradient. All the voltage-gated Sodium channels open when the membrane potential reaches around -55 mV and there's a large influx of Sodium, causing a sharp rise in voltage. As the potential nears +30mV, the rate of depolarisation slows down as the voltage-gated Sodium channels become saturated and inactivate, preventing further sodium ions from entering the cell.
- Voltage gated potassium channels open, and potassium leaves the cell down its concentration gradient. The depolarization of the cell stops and repolarisation can occur through these voltage-gated Potassium channels.
- Voltage gated sodium channels are completely deactivated and potassium floods out through the voltage gated potassium channels,
- Voltage gated potassium channels are slow to close, and therefore hyperpolarisation occurs. This is where the membrane potential drops below the resting potential of -70 mV as potassium continues to leave.
- Once the voltage gated potassium channels close, the resting state can be re-established through the Potassium leak channel and Sodium pump.
The action potential travels along the neurone's axon via current loops in order to reach the axon terminal.
An action potential is a transient, electrical signal, which is caused by a rapid change in resting membrane potential (-70 mV). This occurs when the threshold potential (-55 mV) is reached, this causes a rapid opening in the voltage-gated sodium channels leading to an influx of sodium ions into the cell. The threshold potential also causes a slow opening of voltage-gated potassium channels leading to the efflux of potassium ions out of the cell. This causes the cell to depolarise, meaning the inside of the cell is now more positive compared to the outside.
The action potential starts in the axon hillock as there is a high density of voltage-gated sodium channels here, it is also where graded potentials need to reach the threshold potential to cause an action potential. If the graded potential do not reach the supratheshold level, then an action potential is not triggered and the graded potential is known as subthreshold[1]. Above the threshold, increase in the strength of a stimulus will not increase the size or the amplitude of the corresponding action potential. The strength of a stimulus, or the size of a graded potential, is indicated by the frequency of action potentials travelling along a neurone.
The action potential travels via current loops. In myelinated axons its jumps from node of ranvier to Node of Ranvier, this is a process known as saltatory conduction.
There are two main factors which affect the conduction velocity: the myelination of the axon and the axon diameter. As myelin sheath acts as an electrical insulator, the current cannot pass through the myelinated areas and will have to jump from node to node (saltatory conduction). When the diameter of the axon is increased, there is more room for local current flow, therefore, the internal membrane resistance decreases, and in turn, increases the conduction velocity.
An example of myelination-related disease is Multiple Sclerosis, which causes the immune system to attack the myelin sheath, resulting in demyelination of the axon. When the axon is demyelinated, the conduction velocity will drastically decrease, therefore, the action potential travels slower to the effector (e.g. muscle), leading to the loss of movement.
The point at which the membrane of an axon is depolarised causes a local circuit to be set up between the depolarized region and the region either side of it. This also causes the resting at regions either side to become depolarized. In this way, the action potential sweeps along the axon.
The refractory period prevents the action potential from travelling backwards. There are two types of refractory periods, the absolute refractory period and the relative refractory period. The absolute refractory period is when the membrane cannot generate another action potential, no matter how large the stimulus is. This is because the voltage-gated sodium ion channels are inactivated. The relative refractory period is when the membrane can produce another action potential, if the stimulus is larger than normal. This is because some of the voltage-gated sodium ion channels have recovered and the voltage-gated potassium ion channels are still open. The relative refractory period is the period of hyperpolarization after an action potential[2].
Action potentials in neurons are also known as "nerve impulses" or "spikes"[3][4].
- Problems to action potential can lead to some abnormalities to the ECG curve especially to cardiac muscle. This may happened due to the abnormality of the gene that encode for the Sodium or Potassium ion channels which then cause some changes happen in the action potential curve subsequently lead to abnormal ECG curve. When there is a problem to Potassium K+ channel happened, it will lead to Early After Depolarisation (EAD) symptom to happen that is mechanism on how a long QT syndrome happened. LONG QT syndrome have a prolonged QT interval because depolarisation phase has been prolonged too.
- Secondly, Brugada syndrome mainly happened because some abnormality happened to the Sodium Na+ channel in right ventricle epicardium. This will lead to an abnormal ST elevation or cove shaped of T wave in V1-V3 chest lead. It is causes by mutation to SCN5A (sodium channel gene) which provide instruction for making Na channels.
References
- ↑ http://www.ncbi.nlm.nih.gov/books/NBK11104/
- ↑ The McGill Physiology Virtual Lab, Refractory Period. Available at: http://www.medicine.mcgill.ca/physio/vlab/cap/refract.htm (Last accessed 9.11.13)
- ↑ Silverthorn, D. (2012). Human physiology. 5th ed. San Francisco California: Pearson Education, p.261.
- ↑ http://www.ncbi.nlm.nih.gov/books/NBK11104/
