Smooth Muscle Action Potentials

[Transformers]

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In skeletal muscle, we have the end plate potential (ach binds, triggers entry of Na+, Apotential, which propagates to trigger opening of Ca2+ channels of SER)...

In smooth muscle (single unit specifically which have gap junctions aka electrical synapses), dont these Na+ ions travel from one cell tot he next, depolarize the next cell, causing entry of Ca2+ ions from the ECF, which then mediates the contraction of smooth muscle?

I ask this, because basically, there was a queston in the TBR bio:

The conduction velocity of APotentials along smooth muscle fiber is low because activation of:
1.) Na2+ channels
2.) Ca2+ channels

I put down Na2+ because AP velocity is dictated by Na2+ ions correct in smooth muscle, while contraction is mediated by Ca2+ ions....but apparently the answer is Ca2+ channels

From my understanding the ONLY cells I am aware of from physiology that can impact AP velocity are the AUTORHYTHMIC cells in your cardiac cells which have that funny current and whose depolarizations and triggering of Action potentials are mediated by the entry of Ca2+ ions...

So where did I go wrong?

 

[Doodl3s]

In skeletal muscle, we have the end plate potential (ach binds, triggers entry of Na+, Apotential, which propagates to trigger opening of Ca2+ channels of SER)...

In smooth muscle (single unit specifically which have gap junctions aka electrical synapses), dont these Na+ ions travel from one cell tot he next, depolarize the next cell, causing entry of Ca2+ ions from the ECF, which then mediates the contraction of smooth muscle?

I ask this, because basically, there was a queston in the TBR bio:

The conduction velocity of APotentials along smooth muscle fiber is low because activation of:
1.) Na2+ channels
2.) Ca2+ channels

I put down Na2+ because AP velocity is dictated by Na2+ ions correct in smooth muscle, while contraction is mediated by Ca2+ ions....but apparently the answer is Ca2+ channels

From my understanding the ONLY cells I am aware of from physiology that can impact AP velocity are the AUTORHYTHMIC cells in your cardiac cells which have that funny current and whose depolarizations and triggering of Action potentials are mediated by the entry of Ca2+ ions...

So where did I go wrong?

No, afaik Na+ will move down the axon inducing the potential, however once the Na+ reaches the end of the axon, it allows in Ca+ which triggers the release of neurotransmitters. These transmitters hit the next dendrite to induce their Apotential. the Na+ cascade happens SUPER fast, while in this case, the limiting step if you will, is getting these neurotransmitters released due to increase in Ca+....
i THINK thats right, but i may be wrong cause your question is specific to certain cell types, so i hope someone can confirm this for me

EDIT: from the two paragraphs you gave anyway, even if i had NO idea about the question, the final step is that release of Ca2+... so...

 

[sagtig]

I'm pretty sure Ca channels make the depolarization remain at plateau thereby keeping i depolarized for a longer time, and preventing it from repolarizing

 

[Transformers]

guys guys, I am not talking about NEURONS HERE...When you electrical synapses in muscle (remember, muscle cells are excitable themselves too), and you have gap junctions to transmit the depolarizing stimulus to trigger the action potential, what is getting transferred between the connexin gap junction channels, is it Na+ or Ca2+?

But lets say we are talking about neurons in the case of the INITIAL neural stimulus to the first unit of single unit smooth muscle tissue; how does norepinephrine trigger action potentials?

 

[sagtig]

Norepinephrine is a neurotransmitter, by binding to the receptors, it opens Ca channels

 

[Transformers]

wait, so is there no end-plate potential in smooth muscle cells? In skeletal muscles, Na+ enters, depoloraizes the cell, that AP gets propagated down into the T-Tubules; in smooth muscles, are there basically no AP propogation and simply the entry of Ca2+ from the ECF which then cause Ca2+ release from the SER and activation of MLCKinase, which phophorylates myosin to initiate contraction...?

thanks.

 

[redlight]

In skeletal muscle, we have the end plate potential (ach binds, triggers entry of Na+, Apotential, which propagates to trigger opening of Ca2+ channels of SER)...

In smooth muscle (single unit specifically which have gap junctions aka electrical synapses), dont these Na+ ions travel from one cell tot he next, depolarize the next cell, causing entry of Ca2+ ions from the ECF, which then mediates the contraction of smooth muscle?

I ask this, because basically, there was a queston in the TBR bio:

The conduction velocity of APotentials along smooth muscle fiber is low because activation of:
1.) Na2+ channels
2.) Ca2+ channels

also, not sure if this is relevant, but check out
http://en.wikipedia.org/wiki/Action_potential#Muscular_action_potentials
scroll down to cardiac action potentials... it seems as though opening of calcium channels slows down the action potential by causing a voltage plateau of sorts