what is the role of Cl- channels in membrane and action potentials?
153770
There are potassium ion channel pumps on the cell membrane. This pump pumps out CL ions and bring in K+ ions. It  goes against the flow of diffusion, so energy is needed. When an action potential is created, it oppens Cl- gated channels which, due to the differnt concentrations (more on the outside) the CL rushes back in, creating a change in cell voltage.
752479
an electrical wave that travels down the membrane of a cell
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Strychnine acts as a blocker or antagonist at the inhibitory or strychnine-sensitive Glycine receptor (GlyR), a ligand-gated chloride channel in the spinal cord and the brain.
573250
Certain neurotransmitters contain potassium, and the outward rectifier potassium channel genome component acts as a controller or gate for potassium. The fluctuation in potassium-based neurotransmitters can affect excitability in the neurons.
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A neuromuscular junction is the synapse or junction of the axon terminal of a motoneuron with the motor end plate, the highly-excitable region of muscle fiber plasma membrane responsible for initiation of action potentials across the muscle's surface, ultimately causing the muscle to contract. The signal passes through the neuromusclar junction via the neurotransmitter acetylcholine.
1047759
Cells have openings on their outer membrane - ion pumps. The pumps regulate the concentration of sodium and potassium ions in the cell. The difference in ions in and out of the cell creates an electric potential across the membrane allowing a nerve impulse to propagate along its length. Jens C. Skou won the 1997 Nobel Prize for work in this area. Several ion pumps have now ben described.
837454
Cholesterol is an important component of cell membranes embedded in the hydrophobic areas of the inner region. It is required to control the fluidity of cell membranes. On the one hand, cholesterol breaks up close packing of the phospholipid tails and makes the membrane more fluid. On the other hand, the effect of cholesterol is to reduce leakage of water and ions through the lipid bilayer, probably by reducing the sideways motion of the lipid molecules. Thus, cholesterol regulates the fluidity of the plasma membrane, preventing it from becoming either too rigid or too fluid.
1150529
The Q wave is the start of depolarization of the ventricles, and the T wave is repolarization.  When the interval between the two takes too long, it is long QT syndrome.  This is due to L type calcium channels staying open too long, due to either a genetic defect or certain medications.  Obviously in an infant this would be due to genetics.  The ventricles are signaled to contract electrically.  The signal first causes sodium to rush into the cells, the influx of sodium causes calcium and potassium channels to open, with potassium flowing out and calcium flowing in (helping in muscle contraction).  The L type calcium channels are closed by a timer mechanism that does not work as quickly in people with long QT syndrome, so the calcium channels stay open longer, prolonging the QT interval and delaying repolarization of the ventricle.  And that is what determines a long QT in an infant.
732842
Membrane proteins.\n\nSome membrane proteins act as channel proteins that allow for passive diffusion of solutes across the membrane.\n\nOthers are transport proteins that take part actively (require energy) in transport across the membrane. Some transport proteins may be gated.
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permeability of the cell membrane
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Water is actually the main component of the cytoplasm of a cel, as well as being used in energy production cycles.  As a small, non-polar molecule, water enters the cell by way of passive diffusion called osmosis.  The semi-permeable membrane means that not just anything can cross it.  The only things that can passively cross the membrane are molecules that are, like water, small and non-polar.  Anything else must be actively transported in, or have a channel protein.
796389
chloride shift:\nn.\nThe movement of chloride ions from the plasma into red blood cells as a result of the transfer of carbon dioxide from tissues to the plasma, a process that serves to maintain blood pH.\n\nBicarbonate and chloride ions are transported across the red blood cell membrane in opposite directions by the bicarbonate-chloride carrier protein. \nThe chloride shift is extremely rapid, occurring within 1 second. \nThe chloride shift results in the chloride content of venous blood being greater than that of arterial blood. \n\n(The effect of carbon dioxide in the blood:\nHaemoglobin can also bind carbon dioxide, but to a lesser extent. Carbaminohaemoglobin forms. Some carbon dioxide is carried in this form to the lungs from respiring tissues.\n\nThe presence of carbon dioxide helps the release of oxygen from haemoglobin, this is known as the Bohr effect. This can be seen by comparing the oxygen dissociation curves when there is less carbon dioxide present and when there is more carbon dioxide in the blood.\n\n \n\nWhen carbon dioxide diffuses into the blood plasma and then into the red blood cells (erythrocytes) in the presence of the catalyst carbonic anhydrase most CO2 reacts with water in the erythrocytes and the following dynamic equilibrium is established\n\nH2O + CO2    H2CO3\n\nCarbonic acid, H2CO3, dissociates to form hydrogen ions and hydrogencarbonate ions. This is also a reversible reaction and undissociated carbonic acid, hydrogen ions and hydrogencarbonate ions exist in dynamic equilibrium with one another\n\nH2CO3    H+ + HCO3-\n\nInside the erythrocytes negatively charged HCO3- ions diffuse from the cytoplasm to the plasma. This is balanced by diffusion of chloride ions, Cl-, in the opposite direction, maintaining the balance of negative and positive ions either side. This is called the 'chloride shift'.\n\nThe dissociation of carbonic acid increases the acidity of the blood (decreases its pH). Hydrogen ions, H+, then react with oxyhaemoglobin to release bound oxygen and reduce the acidity of the blood. This buffering action allows large quantities of carbonic acid to be carried in the blood without major changes in blood pH.\n\nHb.4O2 + H+    HHb+ + 4O2\n\n(Hb.4O2 is sometimes written HbO8.)\n\nIt is this reversible reaction that accounts for the Bohr effect. Carbon dioxide is a waste product of respiration and its concentration is high in the respiring cell and so it is here that haemoglobin releases oxygen.\n\n \nNow the haemoglobin is strongly attracted to carbon dioxide molecules. Carbon dioxide is removed to reduce its concentration in the cell and is transported to the lungs were its concentration is lower. This process is continuous since the oxygen concentration is always higher than the carbon dioxide concentration in the lungs. The opposite is true in respiring cells. )
105755
I suspect it is a biochemical process. I skimmed the attached reference, and here is what I was able to pull out: \n\nThere is a complicated process that takes place in the neurons. Chemical action separates positive sodium and potassium ions from anions across a membrane, creating an electric field. Neurotransmitters open ion gateways in the membrane when the field is built up to a certain level. This allows an electromagnetic wave to travel down the nerve. \n\nIt is MUCH more complicated than that, but that is a simplified cartoon version of the events I think.
113785
1. At the neuromuscular juncture, ACh released by the synaptic terminal binds to receptors on the sarcolemma.\n\n2. The resulting change in the transmembrane potential of the muscle fiber leads to the production of action petential that spreads across the entire surface of the muscle fiber and along the T tubules.\n\n3.The sarcoplasmic reticulum releases stored calcium ions, increasing the calcium concentration of the sarcoplasm in and around the sarcomeres.\n\n4. Calcium ions bind to triponin, producing a change in the orientation of the troponin-tropomyosin complex that exposes active sites on the thin filaments (actin). Cross-bridges form when myosin heads bind to the active sites on F actin.\n\n5. The contraction begins as repeated cycles of cross-bridge binding, pivoting, and detatchment occur, powered by the hydrolysis of ATP. These events produce filament sliding, and the muscle fiber shortens.
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Cl is an halogene, like F or Br.  They all have the properties to kill germs (Cl in pool water, F in toothpaste, Br in surgical antiseptics).
276026
"As the action potential envelops the bouton (the terminal bouton at the end of the axon), the synaptic vesicles attach to the bouton membrane at the active zone.  Once attached they release their chemical messenger into the synaptic cleft where it diffuses to the post synaptic membrane.  There the chemical messenger combines with a receptor protein, a process that alters the ionic conductance and consequently the membrane potential of the post synaptic cell.  This may initiate an action potential in the post synaptic neuron."\n\nTo summarize:\nThe action potential arrives at the synaptic junction.  There it stimulates the release of the chemical messenger, known as a neurotransmitter, into the synaptic cleft.  If enough neurotransmitter chemicals cross the synaptic cleft and attach to receptors on the 2nd neuron, a new action potential is initiated in the 2nd neuron.
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ions are polar, so they don't mix with the non-polar lipid bilayer. there are protein channels for their transportation, and pumps and all that..