The third week started with a quiz again. One question of the quiz was about the cause of Alzheimer’s disease which is that the neurons fill up with neurofilaments and eventually die. As this had not been discussed in the lecture and wasn’t mentioned in the course book it was a tough question but also very interesting. In the exercise session, we discussed the different answering possibilities that were offered to the question and to which diseases they belonged, e.g. the degeneration of myelin sheaths in the central nervous system as a cause for multiple sclerosis. I hope that there will be more about diseases caused by defects in the neurons in one of the next lectures.
In the lecture, we first studied the different phases of the action potential and what happens in each of them with the concentration levels of potassium and sodium. This was terminated with a brief introduction to the patch-clamp-method which allows the study of single or multiple ion channels in a membrane. We went on to the different factors for the conduction velocity of the action potentials which are myelination and the thickness of the axon. The purpose of myelin-sheaths around the axons of neurons is mainly electrical insulation but it also decreases the capacitance in the axon so that it is easier for the action potential to travel. If the myelin-sheath isn’t intact anymore, signals that travel along the axon are slowed or stopped completely. Apart from the earlier mentioned multiple sclerosis there are several other diseases affecting the myelin-sheath, e.g. the Guillain-Barre syndrome.
Apart from characterizing neurons through their structure, for example pyramidical cells or stellate cells, which was discussed last week, neurons can also be classified by their behaviour in respect of the frequency of their action potentials. There are for example neurons with consistent action potentials that might have the function to transport a signal continuously over a certain time span while there are other neurons that only transmit a few action potentials at a high frequency which might be to transmit only the strength of a signal.
From there we went on to synapses between neurons. Synapses can exist between an axon and a dendrite, an axon and a soma or between two axons and one axon can also have multiple synapses. For chemical synapses, a neurotransmitter has to be synthesized, converted and stored in transporter proteins in the pre-synaptic neuron and then be released into the synaptic cleft, in response to an influx of calcium ions through voltage-gated calcium channels in the pre-synaptic membrane. I wonder, if this process could be interrupted in any way, for example using drugs and what consequences that would have.