excitation contraction coupling.wmv
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- Опубліковано 23 сер 2024
- Description of excitation contraction coupling... how a neuronal signal causes a muscle fiber to contract. Recorded at Glen Oaks Community College, Centreville, Michigan by Dr Ren Allen Hartung.
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I have been studying and trying to understand excitation contraction coupling for the past 2 weeks..I had ALL the correct pieces to this puzzle, but I just couln't see the whole the picture. It was driving me crazy..especially since I knew this is going to be on the final...I watched your video the first time and BAM!!!...it just clicked...sometimes it just takes another perspective..You truely have a gift..Thank you so much!
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Exam tomorrow. You've explained everything I needed to know in a concise way. I get it now... can't thank you enough!!!
Thank you very much, incredibly helpful in explaining in better detail than a 50 min class lecture!
Thank you so much for this video. I was getting scared I wasn't going to understand this lol, You broke it down and made it easy to understand and see what is going on. Thanks so much!
I'm writing a short essay on excitation-contraction coupling and unfortunately was extremely confused & had no idea where to start -- there's a lot going on! Your explanation made it a lot clearer! Thank you!
Amazingly explained. This helped for my final for tomorrow. Thanks
I am currently taking A & P at a very respected college but if you were to offer online classes I would opt for your classes in a minute. I really appreciate the understandable way you present. Thank you for all your work. I think Glen Oaks would do well to offer an online program with you teaching. Sincerely, Steve
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Superb elusive limited words spoken by u sir. Thanks
Oh goodness!!! Much better explanation than my physiology professors´ in medical school. Thanks a million!
Thank you so much! I could hug you! You made this so clear and understandable! Please don't stop what you are doing, it has helped me tremendously!
Great videos! I especially appreciated that you pointed out that the next video, sliding filament theory, picks up where this one left off. I am enrolled in a hybrid course on A&P and your videos have helped me where the course lacks in lecture material! Thank you for taking the time to make these.
@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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This was so awesome and helped me understand it much better than how my teacher taught it… thank you
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thanks again..
Elad gross and Lorraine fransis
You taught me more than my professor and my TA combined
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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 :)
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 :)
Just awesome i am struggling with this topic and i pretty much confident about it for my final exam tommorrow..
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This was incredibly helpful. Thank you so much.
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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.
Thank you so much! You cleared it up for me. It's so easy now. (I been reading my textbook and I would get confused but now that I now how it works it's quite simple!)
Thank you Sir... wish you were my professor!!!
Thankyou so much! This has helped me enormously. Wish you were my teacher :)
9:23 for the rundown
Thank you for helping me understand this.
Thank you professor!
Thank you!
Absolutely amazing👍I understood everything now😊
My right ear loved this
very well explained. thank you!
This was so helpful!
Thank you!!
Thank you so much! This helps a lot.
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I'm heading over to Wikipedia now. Thank you sir !
Thanks!
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awesome!
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.
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
tHANK YOU SO MUCH...
thank you this really helps alot !!!!
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Who is watching it in 2018
ThanQ Sir!!!!!
Thank you , that was really helpful.
nice explanation. Thank you
Thx doctor!
Thank you so much
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.
Thank you . im understand by this
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.
Thank you so so so much!!!
This was so helpful!! Thank you!!!
wow! a very nice video
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Yes, as I understand noradrenaline is another word for norepinephrine and vise versa :)
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one word: amazing
I'm taking A & P in my third year in high school, and I gotta say this stuff is confusing! But thanks for explaining!
amazing very helpful thank you!
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 ?
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.
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!
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
Love this video!than you so much!!!!:)
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.
is there relationship between the neuromuscular junction with Parkinson's sufferers who experience tremors?
How equilibrium potential of any particular ion achieved? Why the resting membrane potential is much close to Ex to Na ??
Awesome thank you! I have one question.. which way does sodium and potassium rushes in and out? And how much of each?
Sodium rushes into the cell and potassium rushes out, there is no specific amount though. It's more about the charge changes that their movement creates. Take a look at videos that cover membrane potentials (resting potential and action potentials) to get a better idea of the importance of these ions.
Thank you so much! Yes I was getting the resting and action potentials mixed up!
Is norepinephrine the same as noradrenaline?
Thanks dr . but I would like ask you why you explained Ach? because as I knew that Ach has adifferent effect and oppist to catecholamine , this make me confuseed a little bit>
Sometimes ACh and catecholamines do have opposite effects (that is an accurate simplification for flight or flight responses for example), but not always. It's more complicated than that. Both ACh and epiniphrine can lead to depolarization of the target cell, to hyperpolarization of the target cell, or to other effects. It depends on the particular type of receptor the target cell has.
I thought the right speaker in my headphones was broken. :/
Thanks though it was very helpful!
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
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.
Where did the Ca++ in the motor neuron part come from?
Thanks
Thank you :) It was very helpful :D