This helped me understand CICR and positive feedback. Thank you.
I thought this is a Cardiac muscle. In the skeletal muscle, the Ca++ would not enter where the DHP is; the depolarization of the membrane, would lead to a conformational change and then opens the ryanodine receptor to release the Ca++...
Excellent explanation. Thank you!
Tnx for your complete explained 👌🏻👌🏻
Love you my biggest confusion was the opening of L type calcium channel.
Don't name the video Cardiac Muscle Physiology if you're talking about SKELETAL Muscles
he's not talking about skeletal muscle because there is no CICR in skeletal muscle, only in smooth and cardiac muscle. So his title is correct
@@alexislauga9360 unless I’m mistaken, I think he accidentally says skeletal muscle at 4:25 instead of cardiac muscle, which might be what’s causing the confusion to myself and others
this video saved me THX A LOOOOOOOOT
Not all heroes wear capes
anyone find this guy talking is so pleasant?
Thanks so much idk why other videos kept leaving this out
Excellent Explanation.....Thanks...
What about phospholumbane ??? It inhibits wht and how?
May I know where to find the next video? You really help me a lot. Thank you
+Kevin Tokoph thank you so much! Your videos are awesome! I get it now about the troponin and actin
And what do we mean by calcium sequestration and the calcium transient in cardiac muscle?
Where does the sodium come from? When an AP is propagated, calcium gated channels open, and exocytose across the cleft, so I don't follow the origin of sodium
4:25 here did you mean to say “cardiac muscle” instead of “skeletal muscle”?
what’s the difference between l-type t-type calcium channels
L-type calcium channels are found in the myocardial cells, whereas T-type calcium channels are found in the pacemaker/conduction cells (e.g., SA node).
Why is action potential conducted in sarcolemma
Oh...now I get it.
So does Cardiac and Smooth muscle use the same mechanism to contract?
nope! smooth muscles do not have well defined sarcoplasmic reticulum and instead have caveolae. Smooth muscle contraction is heavily reliant on extracellular calcium.
@@arthur5771 it is but caveolae are more rudimentary unlike the t tubules of the heart and skeletal muscles
😍
where is next video ineed it plzz
Why in the heck did my A&P prof skip this? Seems like a pretty important step in muscle cell contraction
Because it's CARDIAC muscle? You only wrote muscle cell so I assume you did skeletal muscle which does not have calcium-induced calcium release
Does anyone know how "Calcium Induced Calcium Release" works in CARDIAC muscle. In skeletal muscle thats ok, some say DHPR is mechanically linked to Ryanodine and some say Ryanoide is Ca sensitive, doesnt really make a huge difference. But for real what happens in heart, they just say "CICR" and move on. Is it currently unkown to mankind or unsignificant enough to literally not talk about it?
everything explained in this video IS what happens in cardiac muscle, not really skeletal muscle
@@NotKoiy but i thought SR of cardiac muscle does not have a lot of calcium hence the need for CICR?
My understanding is that in SKELETAL muscle the AP goes down the T tubule to the DHP rec which goes thru a conformational change which opens the ryanodine receptors and allows the Ca to leak out into the cytoplasm. So there is only 1 source of calcium used for muscle contraction; also it is more of a mechanical response than an electric one in response to the original stimulus. In CARDIAC muscle you have Ca induced Ca release. Thus extracellular calcium causes the release of more Ca from the SR, and both of these calcium sources go into the cytosol and attach to the troponin C to contract the muscle.
Agree
Well summarized
but i thought SR of cardiac muscle does not have a lot of calcium hence the need for CICR?
@@arthur5771i believe it is the extracellular space during the initial excitation that does not contain a lot of calcium. Once RYR opens and there is efflux of Ca2+ from the SR, it goes into the sarcoplasm to bind to troponin C.