*Thick filaments are bipolar, meaning there are heads at either end.
Thin filaments (striated vs. smooth muscle)
Striated: Made up of f-actin, tropomyosin, and troponin.
Smooth: Made up of f-actin and tropomyosin.
Tropomyosin (striated vs. smooth)
Strand that twists around f-actin and stabilizes it. In striated muscle, it "gets in the way" of myosin, but in smooth muscle it's always snugly in the grooves.
Prevents muscles from contracting without proper stimulation. Only present in striated muscle.
Groups/sections of thick and thin filaments. Only present in striated muscle.
Z-lines are the boundaries of sarcomeres (striated). Dense bodies are kind of like smooth muscle's version of z-lines, although the smooth muscle fibers still are NOT grouped into sarcomeres!
Skeletal and cardiac muscle.
How does the "rowing," AKA contraction, happen? How does it stop? (SKELETAL MUSCLE)
Start: Ca++ influx from SR (unusual "plunger" mechanism) binds to troponin, allowing contact between myosin heads and thin filaments. The actual bending of the head requires the binding and then hydrolizing of ATP.
Stop: Ca++ pumps rapidly lower the Ca++ concentration by sending the Ca++ back to the SR from whence it came.
Apparently some dumb shit thought "hey let's rename the ER. .umm. . . Wait for it, waaaaaait for it. . . . SR!!!!"
"But it's the exact same as the ER"
"no, but it's in muscle cells"
". . . . "
"fuck you it is Law"
Extensions of the plasma membrane that invaginate into the interior of the cell in skeletal and cardiac muscle.
How is Ca++ released from the SR in skeletal muscle?
AP travels down t-tubule, activating Ca++ "channels," but they DONT OPEN; instead they "plunge" an adjacent ryanodine channel, which releases the actual Ca++.
Ryanodine channels (striated only)
In skeletal muscle, release Ca++ in response to the "fake" Ca++ channel in skeletal muscle (plunger). In cardiac muscle, release Ca++ in response to "puff" of Ca++ that entered through L-type channel.
Temporal and spatial summation (skeletal only)
Methods of regulating skeletal muscle force.
Temporal: frequency of AP
Spatial: how many motor neurons are firing
Sinoatrial (SA) node
Located in right atrium; generates AP for cardiac muscle cells.
The gap junctions (transfer AP) and desmosomes ("spot welds"/glue) found between cardiac muscle cells.
Cardiac muscle cells' contraction mechanism
AP travels down t-tubules --> signals release of a little Ca++ via L-type channels --> Ca++ signals release of lots more Ca++ --> same mechanism as skeletal cells from here on
Allow the passage of Ca++ from the ECF to the cell.
How do β-adrenergic receptors regulate cardiac muscles?
β-adrenergic receptors --> G-protein --> adenylyl cyclase --> cAMP --> PKA --> PKA phosphorylates phospholamban --> phospholamban stimulates SR Ca++ pump (pumps more Ca++ into SR) --> SR has even more Ca++, so more Ca++ is released!
This allows the muscle to relax more quickly (allowing it to take advantage of an increased rate).
How does the "rowing," AKA contraction, happen? How does it stop? (SMOOTH MUSCLE)
Start: Ca++ activates calmodulin --> calmodulin activates myosin light chain kinase --> MLCK hydrolyzes ATP, phosphorylating the myosin heads and allowing them to "row."
Stop: Ca++ levels decrease, causing myosin light chain phosphotase to dephosphorylate the myosin.
How is Ca++ released from the SR in cardiac muscle?
A small "puff" of Ca++ enters through the L-type Ca++ channel and triggers a much larger release of Ca++ from SR via ryanodine channels. Then all of this Ca++ goes and moves aside troponin, like in skeletal cells, and crossbridging/rowing ensues.
How is Ca++ released from the SR in smooth muscle?
Normal g-protein pathway; IP3 releases Ca++ from the SR!
Which units are associated with which type of contractions in smooth muscle?
Multi unit (similar to skeletal) - tonic
Single unit (similar to cardiac) - phasic
Intervals of contractions.
The state of smooth muscle that can produce tension without crossbridging. Uses little to no ATP and is very slow.
When the myosin heads of the thick filament are in contact with the thin filament.
Basically, the "rowing."
What is asthma, and how do inhalers help?
Asthma is the hyper-responsiveness of airway smooth muscle.
Inhalers contain β-adrenergic stimulators.
*Remember, the β-adrenergic pathway leads to the activation of PKC. PKC then phosphorylates MLCK, lowering the sensiticity to Ca++ and relaxing the muscle.