week 2 quiz

it is important for fine tune movement
evaluates success of movement nd how we need to fine tune this movement to be more successful

-70 to -90
inside a muscle fiber it is about 70 mv more negstive compared to outside of the neuron

Na and K
Na wants to move into the cell
K wants to move out fo the cell

chemical driving factors
Na/K pump
Differ in permeability
Cl conductance

leak channels for both Na and K
membrane more permable to K then to Na

helps maintain the negative charge inside the cell

-55 once this is reached once enugh sodium in the cell the AP will happen

Depolarization-increase in charge this si the Na entering the cell
REpolarization- decrease in charge shoving posassium out of the cell
hyperpolartization- when we go beyond the resting (stops from Ap to go backwards)

dont get weaker as the progate down long distances
if it did then it would lead to a decrease/ wouldn't have any unison and it would lead to a weaker contraction and it wouldnt be smooth

action potential arrives at axon terminal of motor neuron

voltage-gated Ca+ channels open, Ca+ enteraxon terminal

Ca+ entry causes Ach vesciales to fuse to axon terminal membrane and release Ach into synaptic cleft

Ach diffuses acorss synaptic cleft and binds to receptor on ion channel embedded into sarcolemma

Ach bind open ion channel that allows simulatneous entry of na into the muscle fiber and K out of the muscle fiber
more Na enters than K exits which leads to the change in membrane potential called the end plate potential

as nore Ach binds, end plate potential triggers action potential which then goes down the cell Bi-directionally

starts at the end of step 6 of NMJ
voltage receptors DHPR along T tubule membrane trigger opening of RYR Ca channel leading to Ca being released inside the cell

Ca binds to troponin (the ball) causing tropomyosin (the rope) to move and expoe binding sites on actin
at this point mysion is preenegerized from the previous contraction
lose Pi here

prengerized myosin with ADP attaches to exposed active sites
bond strength is middle as Pi is lost but we still have the ADP inhibiting full bonding

lose ADP
now have very strong binding
POWER STROKE
mysion is able (due to strong bond) to pull actin
mysion pull asychonously which is what allows us to keep the pull we have on actin and have a full/powerful contraction

ATP binds to mysion causing a conformation change weakening attachement to actin
cleft is now open

Myosin hydrolazes ATP ad gains the engery the comes from ATP turing into ADP and Pi
this is how mysion becomes engerized and storges for the next contraction

voltage sensor embedded along T tubule
tells ryan that there has been a voltage change and it needs to open

Ca+ release channels

pump Ca back into the SR
some enzyme here that breaks down ATP and use it to put Ca back into SR

since death Ca channels opens and that leads to contraction and stayed contraction because there isnt any ATP to bring Ca back
also no ATP means that there isnt any way to relase Mysion from action allowinf relaxion