NEUROMUSCULAR JUNCTION

[pizza1994]

is a neuromuscular junction between a neuron and heart muscle or a neuron and skelton muscle or both? confused about what this junction joins

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[Cawolf]

Skeletal muscle. It is where the motor neuron releases it's neurotransmitter to the motor end plate of a motor unit.

Cardiac muscle has autonomic innervation and does not have a well defined NMJ as seen in skeletal muscle.

 

[pizza1994]

Skeletal muscle. It is where the motor neuron releases it's neurotransmitter to the motor end plate of a motor unit.

Cardiac muscle has autonomic innervation and does not have a well defined NMJ as seen in skeletal muscle.

so then when texts refer to "NMJ" then its a reference to both types of muscle and not a specfic one right?

 

[yanks26dmb]

Am I understanding this correctly...

Motor neuron releases Ach, which in turn causes nor/epinepherine release down the line?

 

[Cawolf]

so then when texts refer to "NMJ" then its a reference to both types of muscle and not a specfic one right?

Unless I am mistaken, I have only heard this term used to describe the specific innervation of skeletal muscle by a motor neuron.

 

[ChEMD]

Am I understanding this correctly...

Motor neuron releases Ach, which in turn causes nor/epinepherine release down the line?

Nope. The motor neuron releases Ach -> binds nicotinic (Ach) receptor and causes it to open (non-specific cation channel) -> depolarization of the end plate -> opening of fast Na channels on the sarcolemma (action potential spreading within the muscle cell) -> opening of dihydropyridine receptors (voltage-gated) on the plasma membrane within T-tubules -> opening of ryanodine receptors on the sacroplasmic reticulum (just Ca channels which are tethered to the dihydropyridine receptor) -> calcium influx into the cell from the SR -> muscle contraction.

 

[Cawolf]

Am I understanding this correctly...

Motor neuron releases Ach, which in turn causes nor/epinepherine release down the line?

No - if you are talking about cardiac muscle - norepi or ach is released by the postganglionic neuron to the target cells.

 

[pizza1994]

Nope. The motor neuron releases Ach -> binds nicotinic (Ach) receptor and causes it to open (non-specific cation channel) -> depolarization of the end plate -> opening of fast Na channels on the sarcolemma (action potential spreading within the muscle cell) -> opening of dihydropyridine receptors (voltage-gated) on the plasma membrane within T-tubules -> opening of ryanodine receptors on the sacroplasmic reticulum (just Ca channels which are tethered to the dihydropyridine receptor) -> calcium influx into the cell from the SR -> muscle contraction.

so is the calcium influx from voltage-gated calcium channels?

 

[ChEMD]

so is the calcium influx from voltage-gated calcium channels?

The primary calcium influx in skeletal muscle cells comes from the opening of the ryanodine receptors on the sarcoplasmic reticulum. These receptors are tethered to the voltage-gated receptors (called dihydropyridine receptors) on the plasma membrane invaginations, called t-tubules. So when the action potential depolarizers the membrane within the t-tubules, the dihydropyridine receptors open, which causes the ryanodine receptors to open, which let Ca out of the SR.

 

[pizza1994]

The primary calcium influx in skeletal muscle cells comes from the opening of the ryanodine receptors on the sarcoplasmic reticulum. These receptors are tethered to the voltage-gated receptors (called dihydropyridine receptors) on the plasma membrane invaginations, called t-tubules. So when the action potential depolarizers the membrane within the t-tubules, the dihydropyridine receptors open, which causes the ryanodine receptors to open, which let Ca out of the SR.

sorry so in human terms basically....an action potential depolarizes t-tubules, and then the voltage-gated calcium channels are all excited and they open and then calcium releasing channels open and then calcium exits the SR and goes to muscle fiber to cause it to contract? is that right?

 

[ChEMD]

sorry so in human terms basically....an action potential depolarizes t-tubules, and then the voltage-gated calcium channels are all excited and they open and then calcium releasing channels open and then calcium exits the SR and goes to muscle fiber to cause it to contract? is that right?

Yes, that's correct. Just realize that the amount of Ca that the voltage-gated Ca channels let in is insignificant and is not required for muscle contraction.

 

[pizza1994]

The primary calcium influx in skeletal muscle cells comes from the opening of the ryanodine receptors on the sarcoplasmic reticulum. These receptors are tethered to the voltage-gated receptors (called dihydropyridine receptors) on the plasma membrane invaginations, called t-tubules. So when the action potential depolarizers the membrane within the t-tubules, the dihydropyridine receptors open, which causes the ryanodine receptors to open, which let Ca out of the SR.

also sorry but Im confused about skeletal muscle and the role of calcium. So why is it that in skeltal muscle the voltage-gated calcium channels dont open? cause right now you are talking about heart muscle, but in skeltal muscle that doesnt happen

 

[ChEMD]

also sorry but Im confused about skeletal muscle and the role of calcium. So why is it that in skeltal muscle the voltage-gated calcium channels dont open? cause right now you are talking about heart muscle, but in skeltal muscle that doesnt happen

I'm not talking about heart muscle. Please read through my posts carefully.

 

[pizza1994]

Yes, that's correct. Just realize that the amount of Ca that the voltage-gated Ca channels let in is insignificant and is not required for muscle contraction.

yeah i donnoe but I would think the amount of Ca you let in is important....because the heart has an SR that isnt as developed as the SR in skeltal muscle and so the heart SR doesnt store enough calcium to allow the muscle to contract.....so thats why voltage-gated Ca channels are crucial for muscle contraction in the heart because they provide the "threshold" for contraction to occur....am I incorrect when I say this? at least this is what i thought

 

[pizza1994]

I'm not talking about heart muscle. Please read through my posts carefully.

right right okay sorry!!!!!! I thought you were talking about heart muscle. ignore my other post!

 

[ChEMD]

yeah i donnoe but I would think the amount of Ca you let in is important....because the heart has an SR that isnt as developed as the SR in skeltal muscle and so the heart SR doesnt store enough calcium to allow the muscle to contract.....so thats why voltage-gated Ca channels are crucial for muscle contraction in the heart because they provide the "threshold" for contraction to occur....am I incorrect when I say this? at least this is what i thought

Well I'm telling you it's not important in skeletal muscle. The primary purpose of the dihydropyridine receptor is to open the ryanodine receptor (although it does, itself, let some Ca in).

You're right-ish about cardiac muscle. Voltage-gated Ca channels do let Ca in during the plateau phase of the action potential, which leads to Ca-induced Ca release from the SR (as in the Ca channel on the SR opens when the Ca concentrations within the cell reach a certain level).

 

[pizza1994]

Yes, that's correct. Just realize that the amount of Ca that the voltage-gated Ca channels let in is insignificant and is not required for muscle contraction.

k im confused too much now. So in skeletal muscle cells the "voltage-gated" calcium channels still open? I thought they do not open and I am saying this because for skeltal muscle in its action potential graph you dont get a "plateau phase."

 

[ChEMD]

http://en.wikipedia.org/wiki/Dihydropyridine_receptor

http://en.wikipedia.org/wiki/Ryanodine_receptor

 

[pizza1994]

http://en.wikipedia.org/wiki/Dihydropyridine_receptor

http://en.wikipedia.org/wiki/Ryanodine_receptor

right so how the action potential occurs is independent from how the muscle contracts right? so the "slow" voltage-gated calcium channels involved in the heart cell action potential are different from the votage-gated calcium channels in T-tubules right? I think there is where my confusion lies.

 

[Cawolf]

As knowledgeable as @ChEMD is in physiology, I think that unless you already have a strong background, trying to understand or memorize to the level of detail he describes would be a mistake if your primary purpose is to score well on the MCAT.

 

[pizza1994]

As knowledgeable as @ChEMD is in physiology, I think that unless you already have a strong background, trying to understand or memorize to the level of detail he describes would be a mistake if your primary purpose is to score well on the MCAT.

yeah but Im just a bit curious now as to how this works...

 

[Cawolf]

Then ignore my last post!

 

[ChEMD]

As knowledgeable as @ChEMD is in physiology, I think that unless you already have a strong background, trying to understand or memorize to the level of detail he describes would be a mistake if your primary purpose is to score well on the MCAT.

I definitely agree with this, I had no clue what any of this stuff was back when I took my MCAT and I did well.

 

[ChEMD]

right so how the action potential occurs is independent from how the muscle contracts right? so the "slow" voltage-gated calcium channels involved in the heart cell action potential are different from the votage-gated calcium channels in T-tubules right? I think there is where my confusion lies.

I think you need to treat the two cells as completely different and stop trying to compare the two until you understand how each works individually.

For a skeletal muscle cell, the action potential starts because the end plate gets depolarized due to the action of the acetylcholine on the Ach receptors. The action potential propagates through the plasma membrane due to fast voltage-gated Na channels. This action potential propagates down into the T-tubules, which causes the dihydropyridine receptors to open (which are technically voltage-gated Ca channels, but the amount of Ca that they let in is insignificant and not necessary to cause skeletal muscle contraction). The dihydropyridine receptors are physically tethered to the ryanodine receptors (which are Ca channels on the sarcoplasmic reticulum (SR) that let Ca flow out into the cytoplasm of the cell). So when the action potential gets down into the T-tubules and opens the dihydropyridine receptor, the ryanodine receptor also opens, which allows a massive amount of Ca out of the SR into the cytoplasm, which leads to muscle contraction through the troponin-tropomyosin mechanism.

In cardiac myocytes, the mechanism is very different. The action potential still propagates through fast voltage-gated Na channels, but now once the cell depolarizes, slow voltage-gated Ca channels open and cause an influx of Ca from the surrounding extracellular fluid, and this happens throughout the action potential plateau as Ca influx and K efflux balance each other out electrically. The Ca that enters during this plateau (through the voltage-gated Ca channels) causes the ryanodine receptor on the SR to open (this version of the ryanodine receptor opens based on Ca concentration within the cell). Once the ryanodine receptors open, calcium flows from the SR into the cytoplasm, leading to contraction, once again through the troponin-tropomyosin mechanism.

This has to be my last post on this subject, sorry haha. I'd suggest trying to find some pictures if you really want to get it, but like I said before, this level of detail is probably way beyond what you need to know for the MCAT. Best of luck!

 

[pizza1994]

I think you need to treat the two cells as completely different and stop trying to compare the two until you understand how each works individually.

For a skeletal muscle cell, the action potential starts because the end plate gets depolarized due to the action of the acetylcholine on the Ach receptors. The action potential propagates through the plasma membrane due to fast voltage-gated Na channels. This action potential propagates down into the T-tubules, which causes the dihydropyridine receptors to open (which are technically voltage-gated Ca channels, but the amount of Ca that they let in is insignificant and not necessary to cause skeletal muscle contraction). The dihydropyridine receptors are physically tethered to the ryanodine receptors (which are Ca channels on the sarcoplasmic reticulum (SR) that let Ca flow out into the cytoplasm of the cell). So when the action potential gets down into the T-tubules and opens the dihydropyridine receptor, the ryanodine receptor also opens, which allows a massive amount of Ca out of the SR into the cytoplasm, which leads to muscle contraction through the troponin-tropomyosin mechanism.

In cardiac myocytes, the mechanism is very different. The action potential still propagates through fast voltage-gated Na channels, but now once the cell depolarizes, slow voltage-gated Ca channels open and cause an influx of Ca from the surrounding extracellular fluid, and this happens throughout the action potential plateau as Ca influx and K efflux balance each other out electrically. The Ca that enters during this plateau (through the voltage-gated Ca channels) causes the ryanodine receptor on the SR to open (this version of the ryanodine receptor opens based on Ca concentration within the cell). Once the ryanodine receptors open, calcium flows from the SR into the cytoplasm, leading to contraction, once again through the troponin-tropomyosin mechanism.

This has to be my last post on this subject, sorry haha. I'd suggest trying to find some pictures if you really want to get it, but like I said before, this level of detail is probably way beyond what you need to know for the MCAT. Best of luck!

omg ya yoo!!!! this makes sense!!! thanks so much! a super-duper internet high-five for you! who knew this was so complex! wow this is epic! btw thanks for taking the time to explain and type all that

 

[ChEMD]

No problem!