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@MissShenava -- I'm not aware of any mitochondria in the synaptic cleft, however there are plenty of mitochondria inside of the presynaptic and postsynaptic cells. They are needed in order to have enough ATP to power exocytosis by the presynaptic membrane (exocytosis is a form of active transport). In the postsynaptic cell ATP is required by the sodium/potassium pumps that help set up and maintain resting potential. I'm sure there are more reasons, but those come to mind first.

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Acetylcholine is a neurotransmitter for skeletal muscles (somatic motor pathways) but is also used in both sympathetic and parasympathetic innervation (autonomic motor pathways). Norepinephrine is a neurotransmitter that is used in the last step of a sympathetic autonomic motor pathway. Complicated enough for you :)

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Calcium ions are at higher concentration outside of cells. Cells tend to pump Ca++ outside of their membranes (and into their smooth endoplasmic reticulum). So, the fluid around the axon terminal is where the Ca++ comes from :)

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Yes, the Ca++ entering the axon terminal activates motor proteins involved with exocytosis of the neurotransmitter. If you want the details on how this works take a look at the wikipedia page on exocytosis.

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9:23 for the rundown

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There is not really a relationship between Parkinson's disease and the neuromuscular junction. The tremors are actually initiated up in the brain where the actual problem appears to be. The only relationship to the neuromuscular junction is that motor areas of the brain are sending signals to those junctions leading to the tremors that the person experiences, but those signals appear to be due to an imbalance of neurotransmitters happening in those motor areas rather than at the junctions.

great video. would have liked a more thorough explanation... of course this is only partially complete/true. As this process differs slightly in cardiomyocytes vs skeletal muscle cells.. i was hoping for a description of cardio-selectivity in Calcium channel blockers, versus non-cardioselective dihydropyridines... and specifically how the excitation-coupling process differs in these two places... One is calcium induced calcium release at ryanodine channels (as is shown here) and the other is mechanical induced ryanodine channel calcium release. ...id like to know more about that please.. if you get a chance to expand on this topic. Andrew

Who is watching it in 2018

Dr. Hartung, after watching this video segment i'm guessing that Tetanus would also prohibit the breakdown of AcetylCholine in the Synaptic Cleft i.e. similar to your nerve gas example.

Yes, as I understand noradrenaline is another word for norepinephrine and vise versa :)

There is no direct relationship between ACh and Ca++ that I am aware of. Take a look at my other video on the sliding filament theory to see where Ca++ comes into play in skeletal muscle contraction. You are correct about smooth muscle. For smooth muscle Ca++ comes into the cells from the outside during contraction. There is also other differences between skeletal muscle and smooth muscle contraction.

I thought the right speaker in my headphones was broken. :/ Thanks though it was very helpful!

Nope, actually tetanus has its effects by a different mechanism. It damages motor neurons that send inhibitory signals affecting muscle contraction. Without the inhibitory signals muscles tend to stay contracted. Wikipedia has a good page on tetanus. Take a look if you have time.

nice vid

I like this video, it´s really helpful, but there is one thing I don´t understand and I can´t find how it works. What happend when Ca++ comes into axon, how it is possible that it starts exocytosis ?

Thank you. I was not aware of this. I looked up a few papers on it and it looks like the majority of fibers innervating eccrine sweat glands do use ACh. A good review can be found... Shebasaki, M. et al. Neural control and mechanisms of eccrine sweating during heat stress and exercise. American Physiological Society. 2006. PMID: 16614366

Hello! Is it possible to make a video of the t-tubule system? I heard you mention it in a video, but I can't find it explained.

There are mitochondria present in the synaptic cleft, why are mitochondria essential for for the transmission of impulses across the cleft for muscular contraction? Thanks

Where did the Ca++ in the motor neuron part come from? Thanks

Is norepinephrine the same as noradrenaline?

Awesome thank you! I have one question.. which way does sodium and potassium rushes in and out? And how much of each?

How equilibrium potential of any particular ion achieved? Why the resting membrane potential is much close to Ex to Na ??

is there relationship between the neuromuscular junction with Parkinson's sufferers who experience tremors?

I thought the 90mv is the resting potential for nonexcitable cells..according to guyton's book the resting potential for excitable cells is about 70mv.

I have learned that acetylcholine is a parasympathetic neurotransmitter. then how come in this case, it stimulates contraction, which is sympathetic response? I am assuming that the muscle you drew is not a skeletal muscle. I m probably wrong, so... thanks!