Ion channels are membrane proteins found on cell membrane lipid layer that is composed of several sub-units of proteins forming a pore. Ion channel is a place for the ions transport the body to perform at the cell membrane, small molecules that can not penetrate the double lipid layer can penetrate cell membranes easily through the channel protein. The larger the molecule, its penetration ability declined rapidly. Ion channels can function as ion transport, setting up an electric potential across the cell membrane and cell signals.

Based on how teraktivasinya, the ion channels can be classified into:
1. Voltage activated ion channels (voltage-gated channels)
This channel responds to changes in membrane potential, eg Na and K ion channels in nerve cells, and Ca channels in nerve cells
2. Ligand activated ion channels (ligand-gated channel) responds to ligands located in the extracellular region, eg, nicotinic acetylcholine receptor
3. Intracellular molecules activated ion channels,
Responds to intracellular compounds, eg Ca and cAMP
4. Ion channels activated by mechanical forces (stretch-activated channel)
Responds to mechanical forces arising from the stretching / shrinking local surrounding membrane ion channels.
5. Ion channels connect Protein G
Activated ion channels when activated G protein, eg, acetylcholine receptor muskarinik
There are four kinds of ion channels, namely Channel Sodium, Calcium Channel, Canal Chloride and potassium channel. Sodium Channels are integral membrane proteins that form ion channels that funnel of sodium ions into the cell plasma membrane. There are a lot of sodium channel in nerve cells and muscle cells. The structure consists of sodium channel subunits-α and-β subunits. At the time of subunit-α expressed by the cell, α-subunit can form a sodium ion channels that funnel through the gate voltage. -Α subunit has four repeated domains, named I - IV and each domain consists of six segments or transmembrane helices and named S1 - S6. S4 region acts as a sodium channel voltage sensor.

Sodium channel has a gate for the regulation of channel permeability. opening and closing the gate occurs in the outer channel of the cell membrane. Opening and closing of gates arranged in two ways, namely:
1. Gate voltage.
At the moment there is a strong negative charge on the inside of the cell membrane, sodium at the outer gate will be closed, and vice versa when the inside of the membrane loses the negative charge, this gate will be open all of a sudden, allowing large amounts of sodium ions to flow in through the pore- sodium pore.
2. Chemical gate.
The gates will open as a channel protein binding of other molecules with proteins, this will cause changes in the protein molecule so that the gate will open or closed. For example the effect of acetylcholine channel.

Sodium channel responsible for forwarding the action potential / nerve impulses. Action potential initiated at the time of nerve fibers stimulated, the sodium gates will open. Positively charged sodium ions move into the cell, changing the resting potential (polarization) to action potential (depolarization). Action potential propagates along the nerve fiber with speed and amplitude fixed. Local electrical current spread to adjacent areas of membrane. This causes the number of sodium gates open and cause depolarization wave propagates along the nerve. In this way, signals or nerve impulses are transmitted from one side in the nervous system to the other side. One is a sodium channel abnormalities in Brugada syndrome. Brugada syndrome is a type of congenital heart electrical abnormalities that can tragically claimed the lives of men aged about 30 when falling asleep. Brugada syndrome patients previously in good health and even risk factors for coronary heart disease may not be found and the structure of the heart was also normal.


These disorders can actually be detected by electrocardiography (ECG). Abnomalitas heart rhythm Brugada syndrome is the presence of right heart block file (Right Bunddle Branch Block, RBBB) with ST segment elevation in right heart sandapan that are sometimes not obvious. Previously, this abnormality is less so ignored the doctors because patients healthy and fit until the Brugada brothers from Barcelona, in 1992 detected a linkage such ECG abnormalities. They found the existence of death and arrhythmia attacks (the heart's electrical interference), malignant in eight patients with normal heart structure. Genetic defect responsible for electrical cardiac dysfunction in this syndrome was first identified in 1998. It is still unanswered is why this lethal syndrome are more prevalent in Southeast Asia and more often strike men than women (8:1). What also remains a question is that although Brugada syndrome may be present in various ages, why the attack mostly occurs on top of life, namely in young adulthood? Finally, the mystery of sudden death during sleep that began unfolding when the Brugada brothers reported their observations in the Journal of the American College of Cardiology, 1992. Brugada syndrome occurs when there are defects of genes coding for sodium channel, namely the gene SCN5A on chromosome 3. Inherited mutations in genes that cause the opening of ion channels occurs more rapidly and lasts much longer. This situation can lead to a malignant arrhythmia called ventricular fibrillation. Ventricular fibrillation is a disorder of the electrical activity in the chambers of the heart which is the main blood pump engine. As a result the muscles of the heart beat is not known so that blood can not be pumped throughout the body including the brain. If this situation is not corrected immediately with defibrillator paddles (defibrillator), then the victim will be injured brain due to lack of oxygen and eventually can result in death. Often this syndrome is ventricular fibrillation in the heart of the blaze when the dominance effect of vagal nerve, for example during sleep.