Tuesday, 27 March 2007

human biology - How do the brain and nerves create electrical pulses?

So, let us introduce some keywords.



The "electrical pulse" that "is sent from between brain and nerves" is called an Action Potential (AP). This is then propagated along a nerve fiber until the target organ.



Basically, a neuronal cell has a body and several long extended structures that "sprout" from the cell body. Dendrites receive signals from other cells and they convey signals towards the cell body by creating small electrical currents. The axon is a single "sprout" that is usually much thinner and longer than the dendrites and it conveys action potentials from the near the cell body to target cells and organs. Some axons can be as long as 80-90 cm (imagine!)! At the place where axon leaves the nerve cell body there is a small protrusion called the axon hillock.



The AP originates at a special part of the axon called the axon initial segment (AIS). The initial segment is the first part of the axon as it leaves the cell body and sits immediately after the axon hillock.



The electrical pulse is the short electrical discharge, that can be seen as a sudden movement of many charged particles from one place to another. In our cells we have ions of Na+ (sodium), K+ (potassium) and Cl- (chloride) (and in some cases also Ca2+) that constitute these charged particles.



There are two types of driving forces for these particles: besides the potential gradient, e.g. the difference in the total charge in two different places there is also another force called concentration gradient, e.g. the difference in concentration at two different places. These force can point into opposite directions, and thus by exploiting one force (let's say concentration gradient) we can influence another one.



What we need here again is a so-called semi-permeable membrane, this is just a barrier for ions, but only for specific ones. We need this because our main ions -- Na+ and K+ -- are both positively charged. Therefore the cell membrane acts as a semi-permeable membrane, letting K+ into the cells and Ca2+ ions outwards but not the opposite. Therefore we have two concentration gradients: Na+ (outside is the peak) and K+ (inside is the peak).



In order to start the pulse we need to initiate a massive ionic drift from one place to another. This is done by the cell, and the first event here is the drastic change (increase) of the permeability for Na+ ions. Na+ ions massively enter the cell and their charges, moved into the cell, form the upstroke of the action potential.



The protective mechanism of the cell immediately start working against the Na+ invasion and open the reserve shunts -- the K+ channels. K+ leaves the cell, taking away some charge and this is revealed as the decay of the action potential. But potassium channels are generally slower, that is why the decay of the pulse is more steady, not as sharp as the upstroke.



You might be wondering now: what triggers the rapid change of membrane permeability then? There are several factors here that may contribute into this process.



  1. Potential change of the membrane. Sodium and potassium channels are voltage-sensitive, meaning if you manage to change the resting potential of the membrane, formed due to concentration gradients and normally being about -90..-80 mV (millivolts) up to about -40 mV it will trigger the sodium channels. This is how the impulse propagates -- having originated at one place it just decreases the resting potential of the adjacent membrane area, sodium enters the cell there and the AP travels along the nerve. The AIS is the site of AP initiation because this part of the cell has a very high density of voltage-gated sodium channels.


  2. Chemical agents, called neurotransmitters, can be detected by receptors on the cell membrane. Some of these receptors are ion channels themselves and open directly when neurotransmitter is bound. Other receptors act through intracellular signals to open ion channels. This is how the signal appears at the sites of nerve cell contacts -- neurotransmitters, like acetylcholine or adrenaline, just act here as triggers for membrane permeability.


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