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what makes animals diff from other organisms?
animals can move very rapidly--microtubule and microfilaments of cytoskeleton make this possible
microfilaments used in muscle contraction
-both are long polymers of proteins
most abundant microfilament in cell
which microfilament is seen in all animals that move rapidly?
diff between skeletal and cardiac muscle
-cardiac muscle has gap junctions and electrical synapses between cells but skeletal muscles dont (behave on their own and not connected to neighbors).
-skeletal muscles have action potentials similar to nerve action potential. skeletal muscle will have brief action potentials like nerve but cardiac action potentials longer
-generating force that makes 2 ends come together
-when do this, muscle shortens
-ex) try to lift something heavy but object doesn't move--muscle is contracting, but not shortening.
contraction does not equal shortening
. but if actually lift object, then muscle is contracting and shortening
-ex)if lowering arm slowly but holding a weight, then contracting biceps, but lengthening them.
how do skeletal muscles connect to bones?
insertion and origin
insertion=end of muscle that moves more than other one.
-each muscle has many bundles (Fascicle) of muscle cells.
-fascicles surrounded by connective tissue.
-a muscle fiber is a long big cell (fiber=cell)
-during embryonic development, fiber comes from fusion of many precursor cells. so get giant cell w/ multiple nuclei
-in the cell there are microfilaments (dark green and purple stuff)--polymers of actin and myosin.
-microfilaments are arranged into bundles called myofibrils.
-so muscle fiber is a bundle of many myofibrils surrounded by plasma membrane.
one repeating unit
location of nuclei of muscle cells
nuclei are on the outside just underneath plasma membrane and inside is just myofibrils
-include skeletal and cardiac muscles
-fibers lined up and make striated patterns
-smooth muscle not striated b/c fibrils not organized like this
Z lines/ Z disk
-dark vertical lines (in black and white pic) are Z lines/Z discs b/c they are discs that go through whole thing.
-Z lines are points of attachment of microfilament composed of actin and they extend out from the disc toward middle of sarcomere.
thin filaments and thick filaments
-actin microfilaments that extend from Z line are thinner than the other filaments (pink ones), these are called thin filaments.
-pink ones are polymers of myosin. these are thick filaments.
-contract muscle by stimulating its nerve
-Z lines came closer together when contract
-'A' band did not differ in length though (purple things in relax pic and contracted fiber same).
-actin (orange line) and thick filaments (purple) both don't change length when contract. but the reason why Z lines get closer is b/c filaments are sliding over each other
what's the force that's making filaments slide over each other?
ans: crossbridge cycling
structure of thick filament and thin filament
-this is only cross section, but each thick filament has 6 thin filaments around it (hexagon)
-thick filament subunit is myosin. myosin is made of 2 subunits that have tail that wrap around each other in double helix (so doesn't actually look like one strand that is shown). on the end is the head
-cylinder part consists of the tails of many myosin polymerized side by side and the heads are sticking out. like pack of spagetti.
-heads arranged so that they point to the 6 thin filaments around thick filament
-heads are polarized on each side (heads on the right side stick out to the right and heads on left side stick out to the left
-thin filaments are polymers of actin--each circle is a globular actin (G-actin). they polymerize into F actin (fibrous actin--entire strnad is an F actin filament). double helix.
-each of the G actin monomers have a spot where myosin head can bind to
-myosin head will bind and head undergoes conformational change so it will ratchet itself and generate force that makes thick filament and thin filament slide over each other. after that, head attaches to another actin and another conformtational change to head and cause another slide. this happens over again in a cycle. if the muscle can shorten, then it will shorten and if can't shorten, then the force will just build up in the muscle
-piece that connects the tail and the head of myosin
1. head not attached to actin and neck is at bent b/c has ATP bound to myosin head.
binding of ATP inhibits binding of myosin head to actin
. ignore the low energy configuration--magnesium ions (Mg+2) necessary as a cofactor for this process too
2. myosin is an ATPase (hydrolyze ATP to ADP and phosphate). ADP and phosphate are still bound (but separately). b/c they are not ATP even though they are still bound, it changes conformation of the protein. the angle of the head changed (angle of the neck didn't change).
3. ADP is not ATP. ATP inhibits binding but ADP doesn't. so head binds to actin. note: ADP and phosphate not released yet. the binding forms the cross-bridge between thick and thin filament
4. ADP and phosphate released--causes myosin to swing back to formation of first step (except it's bound to actin). this movement called
. the filaments slide past each other. in this configuration, myosin head has high binding affinity for ATP. so ATP binds and gets from left hand step back to first step. when bind to ATP, ATP blocks affinity for myosin to actin and head detaches
contraction means cross-bridge cycling and force generation (not movement/shortening). shortening cause movement, but can have contraction w/out shortening
-hydrolysis step is slowest step
-this step determines how fast the whole thing goes.
-goes about 7-8 times per second depending on the type of myosin
structure of muscle fiber
-tubes inside the big tube is myofirbil
-there are mitochondria between myofirbils
-tubular invagination of plasma membrane surrounds myofibirls.
-plasma membrane goes deep into middle of cell and forms rings around each myofibril.
-runs transversely to the long axis of muscle fiber so called T tubule (transverse tubule).
-lumen of tubule is continuous w/ extracellular fluid.
-T tubule is continuous w/ plasma membrane
-T tubule wraps around where Z lines are
sarcoplasmic reticulum and calcium sequesteration
-Smooth ER (a flattened sac of membrane) of muscle fiber is blue stuff that wraps around each myofibril.
-this is called sarcoplasmic reticulum
-smooth ER/SR pumps calcium into its lumen w/ ATP. there are calcium pumps (calcium ATPases) in membrane of smooth ER/SR. ("hide the calcium" in the lumen--calcium sequesteration).
-this maintains low free Ca conc in cytoplasm.
-in smooth ER there is reservoir that can release Ca as a second messnger. this is done by IP3. IP3 binds to Ca channel in smooth ER membrane and release Ca.
-in muscle cells, sarcoplasmic reticulum pumps Ca inside its lumen to maintain low Ca in cytoplasm and releases Ca as second messenger to trigger muscle contraction. but doesn't use IP3 gated Ca channels.
- SR wraps around fiber in between Z lines (covers sarcomere in between Z lines).
-structure of an SR sac, T tubule, and another SR sac on other side is called a triad junction.
-this pic is triad junction.
-cytoplasm between T tubule and SR membrane
synapse between motor neuron from spinal cord/brain stem and action potential
-when muscle gets activated, contraction happens.
-pic: synapse between motor neuron from spinal cord/brain stem.
-action potential from spinal cord and goes down axon. this synapse is a chemical synapse called
-acetylcholine transmitter released here and binds to receptor on muscle fiber memrbane.
nicotinic acetylcholine receptor
. this is an ion channel (lets both Na and K to pass through).
-when muscle fiber at rest, it has negative resting potential. more Na outside and inside cell negative, so electronegative gradient for Na going into cell. K+ go out, but relatively little compared to Na coming in. so if add those 2 together, there is strong inward current. inward current goes into muscle fiber and flows out of membrane nearby and depolarizes membrane surrounding it.
-this triggers action potential b/c there are voltage-gated Na and K channels in muscle fiber membrane. so when action potential comes down, there is a large EPSP and action potential takes off (blue arrows).
action potential and T tubule
-T tubule membrane continuous w/ plasma membrane and lumen is continuous w/ extracellular space so resting potential exists across T tubule membrane.
-action potential also spread down T tubular membrane.
release of Ca+
-yellow protein in T tubule membrane evolved from an ion channel (but it's not an ion channel). it changes conformation w/ depolarization. depolarization comes from action potential that goes down T tubule. so when action potential pass through this part, polarity of membrane gets reversed (positive on negative side and vice versa). reversal changes conformation of yellow protein
-dotted lines are cytoplasmic proteins that link the voltage-sensitive protein in T tubule w/ calcium channel in SR membrane (blue thing).
-regular Ca channels need IP3 to open (IP3-gated Ca channels), but this one not gated by IP3. it's gated by pulling on cytoplasmic proteins (dotted lines).
-when conformational change of yellow protein occurs, cyoplasmic proteins get pulled and Ca channel opens.
-Ca that was sequestered in lumen of SR goes out into sarcoplasm and triggers contraction.
-Ca is second messenger that triggers crossbridge cycling.
-result of Ca+ release is force build up and muscle twitches.
-build up of force due to Ca conc rising and then force falls.
-falling phase longer than build up.
-falling phase due to lowering Ca conc b/c of green calcium ATPase (Ca pump) in SR membrane. this is what sequesters Ca. when Ca released, stays high in cytoplasm for short time b/c pump pumps it back in again.
-time of falling phase determined by rate at which Ca pumps pump Ca back in
tropomyosin (a protein) also part of thin filament.
-troponin is a complex of 3 proteins.
-it's attached to tropomyosin. one of the subunits is a Ca binding protein (binds to Ca ions).
thin filament control
-top pic: thin filament at rest (low conc of Ca--10^-8M Ca)
-bottom: thin filament when contracting (there is higher conc of Ca here so contract--10^-6M Ca here)
-when lower conc, most of troponin not binding to Ca and in top configuration. note: tropomyosin blocking indentation to which myosin can bind.
-at higher Ca conc, Ca binds to troponin and tropomyosin change conformation (tropomyosin moves to the side and myosin binding site on actin exposed). now can bind myosin as long as there's ATP and Mg present.
-one action potential coming down neuron will cause muscle fiber to twitch and this happens.
-as soon as Ca conc high, then stimulate Ca pumps in SR which starts to pump Ca back to lumen of SR.
what is needed for muscle contraction/cross-bridge cycling
-in order for muscle contraction (cross-bridge cycling) to occur, need enough ATP, Mg, and Ca
what is needed for muscle contraction/cross-bridge cycling in absence of tropomyosin or troponin (just have actin and myosin)
muscle contraction can just occur with just ATP and Mg, but can't stop the cross-bridge cycle
-motor unit is the basic functional unit of muscle contraction. motor unit defined as the single motor neuron and all the muscle fibers it contacts
-in pic: both axons myelinated
-when motor neuron 2 has an action potential, the 3 muscle fibers that are connected will twitch (behave as a unit, so called motor unit).
importance of distance of current spread of current
-as current spreads down axon ahead of action potential, the nodes ahead are depolarized
-the amount of current coming in one node is enough to depolarize the next 3 nodes to threshold--important when axon branches b/c the last node before this branch point needs to supply enough current for the next 2 nodes right after the branch.
how many muscle fibers are there in a motor unit?
-depends. if there were more muscle fibers in a muscle unit, then the force will be large.
-for muscles that have to create very fine movements/finely graded levels of force, then the motor units of those muscles are tiny (face/finger muscles)--they have fewer muscle fibers attached to one neuron.
muscle w/ smallest set of motor units
-muscle that is most finely controlled (have the tiniest set of motor units) is extraocular muscles that move the eye.
-there are 6 muscles that attach to the eye and steer it. in the extraocular muscles there are 1-2 fibers in each motor unit
muscle unit in arm/leg
-if a muscle doesn't have to generate small increments of force or be graded really finely, then it doesn't matter, especially if muscle must be strong and powerful (big muscles in leg and arm). these muscles generate large amounts of force.
-each motor unit has hundreds of muscle fibers (not finely controlled).
properties of muscle fibers
-there are more than one type of muscle fiber.
-properties of a muscle fiber depends on what genes are expressed in the fiber
-there's also more than one type of each of the molecules (especially myosin) mentioned.
there are many diff genes for myosin to make many diff myosin proteins
(all myosin and all have same function but differ in functionally significant ways).
properities of muscle fibers depend on how the muscle fiber is used
-ex) if lift weights, hypertrophy occurs--muscle cells get bigger (not more cells). the patterns of activity makes cells double/triple in size.
-are you doing big bursts of activity in short periods of time or equal amount of activity over longer period of time? that makes a diff in the way genes are expressed.
properties of muscle fibers in a single motor unit
-all of the muscle fibers in one motor unit have the same properties b/c they all experience the same activity. ex) maybe purple one works in high frequency short bursts and red one works at lower frequencies over long period of time. that would cause diff gene expression of the 2 muscles that would make them have diff properties.
motor unit types
-if measure each of these properties for individual motor units or fibers within a motor unit, then fall into 3 categories
-humans don't have IIb but have IIx
-duration of twitch
-speed determined by step that involves ATPase activity.
-slow means only get few cross-bridge cycles per second.
-if fast, then more cross-bridge cycles per sec.
-reason for diff b/c of diff myosin forms expressed by diff genes
myosin ATPase activity
-this explains contraction speed
-cross bridge cycling depends on ATPase activity.
-IIb and IIa have high levels of ATPase activity.
major pathway for ATP synthesis
-3, 6, and 7 go together.
-slow fibers get ATP from aerobic respiration.
-IIa also get from aerobic respiration, but IIb gets from glycolysis.
-glycolysis doesn't produce as much ATP as aerobic respiration, but it can operate in absence of O2.
-so if O2 limited, the 2b fibers can still keep going and type 1 stops.
ones that use aerobic respiration have lots of mito and glycolytic ones have few.
capillaries supply glucose, so there are lots of them in I and IIa but less in IIb
rate of fatigue
-IIa slow to fatigue b/c there are lots of capillaries bringing lots of blood and can make ATP all day and don't fatigue.
-also, pattern of activity importnant--they operate at low fequecies all the time.
-the fast ones run out of ATP faster so fatigue more rapidly (if run, then muscles fatigue more rapidly and need more time to recover).
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