Alright, this is an extremely lengthy post which I took care to craft in hope to bring a more wholesome view to this amazing topic yet trying not to put down information in overly-saturated form.
TOFS - totally out of syllabus.
The rest I think are cool information that will bring a better appreication of information in notes =) cheers!
Drop a note if you need to.
1. Why is a myelinated neuron faster in the transmission of signals? Myelin sheath provides an insulating layer which impedes the loss of ions across the membrane thus as an action potential travels down the axon, there is little loss of current/energy and thus improves speed of conduction. (awati for diagram)
2. Since Na+ ion is larger than K+ ion (in the hydrated form), can the K+ ions enter the Na+ channel? (TOFS)No. The conductance of a channel for an ion is not soiely based on size but also the R-groups that line the walls of the channel. Interaction of the ions with the R-groups also contributes to the ion selectivity nature of the channel (in energy terms – we’ll stop here).
3.How is it possible for a given neurotransmitter to produce opposite effects in different tissues? (in notes - For T Flea – if I have not mistaken the question)The post-synaptic potential (excitatory or inhibitory) really depends on the nature of post-synaptic receptor and the ion channels associated with it.
For example, acetylcholine (ACh) released at the neuromuscular junction (NMJ) btw motor neuron and skeletal muscles will bind to its receptor on the Na+ channels at the post-synaptic membrane, opening the Na+ channels* to depolarize the cell (excitatory)
On the other hand, ACh can also be released at the neuromuscular junction between vagus nerve and cardiac muscles will eventually lead to the opening of Cl- channel which will hyperpolarise the cells (efflux of Cl- - inhibitory)
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*
NOTE:
when the ACh-gated ion channel is opened at the neuromuscular junction, the channel is big enough to allow the passing of both Na+ and K+ .
Nonetheless, there is a NET influx of Na+ due to the greater electrochemical gradient thus depolarization (EPSP) is observed, thus it is also correct to make the following reference:
- ACh binds to its receptor on the Na+ channel at its post-synaptic membrane.
4.Since the amplitude of the action potential that arrives at the synaptic terminal is always the same, does that mean that the resulting potential change at the post-synaptic membrane is always the same? Nope.
While the amplitude of an action potential that arrives at the synaptic bulb is always the same, the frequency of the action potentials arriving at the region might be different.
During summation, there are two issues to be noted:
Is the resulting voltage above threshold? If so, what is the strength of the stimulus?
If the resulting voltage/stimulus is above threshold, all the Na+ channels will be opened* for the depolarization phase.
Then comparing a strong and a weak stimulus, the former will generate action potentials at a higher frequency.
Taking the lead from there, having a series of action potential at higher frequency will also mean that synaptic terminal will be depolarized more often and thus increase the rate of neurotransmitter released for a greater response at the post-synaptic membrane.
5. If the synaptic vesicles keep fusing with the pre-synaptic membrane for neurotransmitter release, won’t the synaptic knob just become bigger and bigger?Sounds reasonable but it does not happen because there is constant recycling of synaptic vesicles from the pre-synaptic membrane via endocytosis =)
6.Why is a sensory neuron bipolar/ cell body in the middle somewhere? (TOFS)A bipolar sensory neuron allows the formation of an extensive network of dentrites to receive information from the external environment.
(Oops! After thinking about the question after class, the facilitation of nutrient transport hypothesis does not stand up very well based on what we understand about the distribution of various types of neurons.)
7.Inactivation gate of Na+ channel? (TOFS)The Na+ channel involved in action potential operates on a two-gate system: activation gate and inactivation gate.
At resting membrane potential, the activation gate is closed while inactivation gate is opened.
When threshold potential is reached, the activation gate will open to allow influx of Na+
After some time, a delayed response in inactivation gate will have it closes its gate. Thus forbidding the continual influx of Na+
During hyperpolarization, the activation gate is once again closed while the inactivation gate will open back to norm.
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Some additional notes for you:
- signal transmitted at the NMJ btw motor neuron and skeletal muscles is always excitatory but the EPSP generated has to overcome the threshold potential so that action potential will be initiated by neighbouring voltage-gated Na+ channels for transmission along the muscle fiber.
For neuron-neuron transmission, however, there can be both IPSP and EPSP on the post-synaptic membrane
- action potential – do they all look the same?
This question is posted by me because I don’t know how many of you are going to become doctors so you should be aware that the shape of the action potential we are examining now is for a typical nerve cell but action potential found in the nerves of the hearts is of a different distinct form/shape which is also very interesting. =)
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