Dr Lucas: Lecture 1-3 Flashcards
Types of muscles:
- Striated
- Skeletal (actively control/voluntary/muscle attached to the skeleton, cylinder shaped, multinucleanated)
- Cardiac (heart muscle, branched, uninucleated) - Smooth
- Single or multi unit (wether or not the cells are connected to eachother, uninucleated, spindle shape)
Muscle cell synonyms (2)
- muscle fibre
- Myocyte
Skeletal muscle cell deconstruction of unit (4):
- Muscle cell/Muscle fibre/Myocyte
- Multinucleate (fusion of precursors, facilitate cell function)
- Strands of protein called myofibril
- Sarcomere: subunit of myofibril (for contration)
However, unlike cardiac and smooth muscle fibers, skeletal muscles are —–, meaning that ——
- multinucleated
- each cell possesses more than one nucleus
M-Line
- the fine vertical line in the center of the sarcomere, which links myosin (thick) filaments to each other in a lattice-like arrangement. The protein myomesin anchors the myosin filaments to the M line.
A-band
- The length of a myosin within a sarcomere
I band
composed of thin actin filaments and proteins that bind actin and they are bisected by the Z line
H-zone
a zone of thick filaments that has no actin. Within the H-Zone is a thin M line
Z-line
Z-lines define the boundaries of the sarcomere and anchor thin, titin, and nebulin filaments
The thick filament is anchored by
titen and M-line
There are only thin filaments at
the I-band
There are only thick filaments at
the H-zone
Myofibrils hthick to thin ratio:
2 thin to 1 thick filament in vertebrates
Thick filaments are made of —–
Myosin heavy and light chains
Describe the structure of a myosin heavy chain:
Myosin filament organization
Tails form the body of the filament and the heads stick out. Myosin heads spiral in 3 rows arounf the thich filament shaped like a brush bar in a vaccum.
Bare Zone
No myosin heads in center of thick filament
Thin filament structure
Actin molecules combone to make 2 strands of f-actin which has tropomyosin and troponin blocking the binding sites
In F-actin, myosin binding site is:
alwats avaliable
Hierarchical structure of muscle:
Smallest to larges
- Sarcomere
- myofribrils
- Muscle fibre (many myofibril packed inside one cell)
- Mucle Fassicle (a bunch of muscle fibres)
- Muscle (a bunch of muscle fassicles)
Role of myosin light chain:
RLC and ELC
- Regulatory light chain is at the neck (bend part) and undergoes phosphorylation to help change the activity of myosin.
- The Essential light chain is more structually stabilizing the myosin head and neck and is right under the head budge part.
I band, A band and H band 3-D cross section
Explain the cross bridge cycle steps (6)
- ATP is bound to the myosin head making it into a bent position.
- ATPase split ATP into ADP and Pi. This releases energy and charge spring in myosin head (pull back from bent position).
- Nothing change in the molecule. Weak bond forms between actin and myosin, can dissociate easily and is reversible.
- The phosphate group leaves myosin and this will cause the head to snap back to bent position and release energy.The bond changes to a strong bond between actin and myosin (irreversible) as phosphate group leaves. The head snaping back to bent will pull on actin and move the thin filament causing the power stroke/muscle force.
- ADP spontaneously leave myosin.
- New ATP comes in and binds to myosin head releasing strong bond
How does calcium interact with troponin to control cross bridge?
Troponin had 3 subparts:
I subpart: anchor rest of troponin onto thin filament
C subpart: Bind to Ca2+
T subpart: Unit of troponin that binds to tropomyosin
Binding to calcium changes troponin conformation and lift tropomyosin off the binding site.
Sarcomere lengths tension curve (General)
Sarcomere lengths tension curve: Point 1
- The sarcomere is really long and there is no force produced because thin and thick filament doesnt overlap
- There is no cross bridges as the myosin head which would link up with the thin filament are too far away from the thin filaments to form cross bridges
Sarcomere lengths tension curve: Point 2
- some cross bridge overlap between thin filaments but not all of the heads.
- More force produced
Sarcomere lengths tension curve: Point 3
- Overlap of all myosin head making all crossbridges
Sarcomere lengths tension curve: Point 4
- Thin filament extends to the bare zone so theres no more crossbridges to recruit.
- Sarcomere gets shorter and our force stays the same.
- About to touch but same amount of crossbridges and force as point 3.
Sarcomere lengths tension curve: Point 5
- Thin filament overlap.
- Harder to form crossbridges (thin filament in way)
- Less force produced
- Myosin head will not bind to a thin filament from opposite side of sarcomere because of orientation
Sarcomere lengths tension curve: Point 6
- Z lines are right up against edge of thick filament
- A-band compression crush thick filament producing less force
In the length tension curve, there is no H-zone at step:
Four to five
Electrical synapse (7)
Mechanism + direction + SPEED + always + AP + no
- Direct contact between excitable cells (neuron + muscle or 2 smooth muscle) cytosplasmic continuity
- Linked by channels called connexons (span 2 cells)
- Bidirectional (either direction for ion)
- Very fast (no delay)
- Always transmit signal
- Not selective about what ions are passed (pass Na+ ions to make AP continuation, if you have other ions around these can get passed)
- No fine tuning of signal
Chemical synapse (7)
No + use + variety + direction + speed + modulate signal + go wrong
- No cytoplasmic continuity
- Use chemical intermediate to cross space (cleft) between cells
- Variety in type based on neurotransmitters and receptors
- Unidirectional (in one direction)
- Slow (relative to electrical synpase)
- Can modulate signal and response (by changing the amount of NT, response to receptor)
- More places for things to go wrong
Neuromuscular junction structure:
axon terminal (3), sarcolema (3), SNARES (1)
Presynaptic axon terminal:
- has schwann cell for physical and trophic support
- contains V-gated Ca2+ channels to let Ca2+ into axon terminal
- Has an active zone where whole cluster of vesicle i is neat a particular portion of the membrane
Sarcolema/Skeletal fibre:
- Contains V-gated Na+ channel that lets sodium into the cell in sarcolema away from the junctional fold and deep in them
- contains ligand (ACh) gated ion channel to allow Na+ into the cell
- Directly opposite from active zone we have a big junctional fold
SNARES: attach to membrane On vessicles, axon terminal membrane in active zone
Process for stimulating muscle at the neuromusclar junction (6)
- AP opens V-gated Ca2+ channel allowing Ca2+ into axon terminal
- SNARES link up (axon terminal and vessicle) due to Ca2+
- Exocytosis (fuse to active zone)
- Diffusion of NT (ACh)
- ACh binds to AChRs (ligand gated Na+ channels), Na+ enters fiber. This causes flicker of slightly depolarization of the cell near ion channel (EPSP).
- EPSP depolarize membrane strong enough to open V-gated Na+ channels (nearby to open and AP spread from NMJ).
Excitation-contraction coupling controls Ca2+ inside muscle cells steps (7)
- Excitation comming down axon terminal
- Vessicle with ACh to be released
- ACH binds at NMJ
- AP travel away from NMJ along sarcolema
- AP travel down into our T-tubule causing voltage-sensitive DHPR to change shape (acts more as a sensor)
- Physically link to ryanodine receptor and cause it to change shape as well
- Open Ca2+ channel, Ca2+ diffuse to cytoplasm
Ending contraction mechanism (2)
- Stop the signal at the NMJ by having enzyme break down ACh (AChE)
- Remove Ca2+ from the cytosplasm via an ATP-dependent pump in the SR membrane that constantly moves Ca2+ back into SR. The pump is always running, when we release Ca2+ we release so much that pump is overwhlemed and it takes time to catch up, while it catch up, contraction occur.
Explain latency: delay between muscle excitation and subsequent events (2):
+ Explain how graph looks like too
- Stuff takes time! Excitation, then Ca2+ release then force then shortening takes time.
- There is a delay rise in force
