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140 Cards in this Set
- Front
- Back
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skeletal muscles
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connect to bones and are used for complex cordination
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smooth muscles
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surround internal organs such as large intestine, uterus, large blood vessels
contract slowly and maintain tension for long periods of time |
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cardiac
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striated muscle of the heart
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muscle are protiens so they are energy______
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expensive
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microtubule function
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-move subcellular components
-use motor protiens like kinesin and dynein -have positive and negative end -assembled from tubulin dimers (form sheet then roll up) - |
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MTOC
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microtubule organization center
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micro tubules Dynamic Instability
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is a balance between growth and shrinking aka treadmilling
-grow at positive end and shrink at neg end |
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factors affecting dynamic instability are
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-local concentration of tubulin (inc tubulin=grow)
-microtubule associated protiens (MAPS) -Temperature -some chemicals can disrupt the dynamics |
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Micro tubule associated protiens
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- can stabilize or instabilize MTs
- capping protiens are a example, they prevent shrinkage |
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direction of movement along microtubules is determined by
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polarity and the type of motor protien
-kinesin moves in the + direction (move NT towards the Synapse) -dynein moves in the - direction (move empty vesicle back to be refilled) |
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Movement along a MT is fueled by ATP and the rate of movement along MT is determined by
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the ATPase domain of the motor protien and regulatory protiens (hydrolyze ATP to enable movement)
-dynein is larger then kinesin so moves 5x faster |
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cilia and flagella are composed of
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-MT that are arranged into axoneme (9 doublets on outside 1 in center)
-movement is result of asymmetrical movenment of dynein |
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physiological function cytokinesis
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development and growth
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physiological function axon structure
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MT support the long axons
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physiological function vesicle transport
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hormones and cell signalling, carry the vesicles
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pigment dispersion
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adaptive coloration, move pigment granules around cell
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flagellar movement
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reproduction,sperm swim
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ciliary movement
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respiration, digestion. propel mucus ect
In digestion cilia inc SA |
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Microfilaments
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-other type of cytoskeleton fiber
-polymers composed of the protien actin -often use the motor protien myosin (ATPase) -found in eukaryotes |
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movements of microfilaments arrive from
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-actin polymerization
-sliding filament model using myosin which is more common |
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mircrofilament structure and function
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-polymers of g-actin called f-actin
-spontaneous growth - treadmilling when length is constant -capping protien inc length by stabilizing the - end |
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microfilament arrangement
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they can be attached to membranes and crosslinked together
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skeletal muscles are
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-multinucleated
-contract in response to a electrical signal (depolarization) -the signal is generated at the NMJ |
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Transverse tubules (t tubules)
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-specialized invaginations that allow AP to penetrate deep into tissue very quickly
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one neuron can innervate several muscle fibers but
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each muscle fiber has its own threshold and is only innervated by one neuron
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NMJ vesicles have
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very high concentration of NT
-excess NT is released to make sure the depolarization is strong enough to produce a AP (steady margin) |
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motor unit
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a motor neuron plus complement muscle fibers
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nerve terminals of motor neurons contain
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lots of mitochondria and vesicles and voltage gated Ca2+ channels
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in nACHR there are 2 alpha subunits in the channel. To open the channel
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Two molecules of ACH are needed. Each one binds to a Alpha subunit
one vessicle contains enough NT to open 3000 receptors so min of 6000 ACH per vessicle |
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Na+/K+ ATPase pump in striated muscle
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is used to re establish electrochemical gradients of sodium and potassium
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ca2+ ATPase
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uses energy from atp to remove 2 CA2+ from inside to outside of the cell to insure internal concentrations maintain low
-if didnt have we would have constant contraction |
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Na+/Ca+ antiporter
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remove calcium from inside cell and uses energy of cotransport of 3 sodium for 1 calcium
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Muscle Ca2+ ATPase pump
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found highly concentrated in SR
-pumps two calcium into sr |
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muscle cells have many the same channels as
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neurons
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muscle cell leak channels
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-have K+ leak channels
-have Cl- leak channels which helps to repolarize the membrane after a AP |
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Muscles have voltage gated....
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K+ channels (delayed rectifier K+ which is important during the AP)
Na+ channels (important to get a AP) Ca2+ channels (needed for muscle to contract and to release NT, high threshold Ca2+ channels) |
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muscle cell
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muscle fiber
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myofibrils
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main intracellular structure in striated muscles, bundles of contractile and elastic fibers
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sarcolemma
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cell membrane of muscle cell
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cytoplasm
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sacroplasm
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sacroplasmic reticulum
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wraps around each myofibril like a piece of lace and release/sequester Ca2+ ions
-regulate cytosolic calcium levels in skeletal muscles -terminal cisternae increase storage |
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myofibril
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a long bundle of actin, myosin and associated protiens in a muscle cell
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transverse (T) tubules
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invaginations of the plasma membrane , enter myofibrils at the z disks where they come in close contact with the terminal cisternae of the SR
-enhance action potential penetration |
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Terminal Cisternae
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store Ca2+ ions and connect the lacelike network of SR tubules that overlie the A band
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Triads
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junction between T tubules and SR
-voltage gated Ca2+ channels are concentrated in t tubules at the triads |
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to get ca2+ back to resting concentration
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-after ap passed voltage gated channels ca channels close
-ca is recycled back into the Sr through ca ATPase -ca binds to calsequesterin =high affinity for ca and helps store it in the SR |
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general sequence of events
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-resting concentration of calcium 0.1 micro molar
-AP propergation along sarcolemma and into T tubules -depolarization and vgated channels at triad junctions open -ca enters cytosol through ca release channels in SR -inc in cytosolic ca -diffusion and binding of ca to Troponin C -contraction events |
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release of ca from stores is mediated by
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ryanodine receptors (RYRs) in skeletal muscles
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voltage sensing dihydropyridine DHP receptors in the plasma membrane...
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are in contact with RYRs
-in response to chnage in voltage undergo comformational chnage -which produces a conformational chnage in associated RYRs and causes them to open so they let ca exit into cytosol |
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some channels are not voltage gated but instead they are
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opened soley by a influx of ca
-the ca release channel in the SR of most muscles is a Ca activated Ca channel -open at low concentration Ca but inhibited at high (as it is released it inhibits the release of more) |
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depolarization induced calcium release in muscles
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EXCITION: depolarization of the plasma membrane (sarcolemma) opens the DHPR while CA2+ enters the cell it is the changes in DHPR structure that trigger the opening of RyR
CALCIUM RELEASE: RyR opening allows Ca to escape the SR. The elevated cytoplasmic [Ca] triggers actino-myosin ATPases RELAXATION: after repolarization , ion pumps begin returning Ca to resting location, outside the cell and in the SR (SERCA= Ca ATPases that move Ca back into SR) |
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Ca+ induced Ca2+ release
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EXCITATION: depolarization of PM (sarcolemma) opens DHPR and allows Ca to enter cell
Calcium Release: elevated [Ca] triggers opening of RyR allowing Ca to escape the SR. The elevated cytoplasmic [ca] triggers actino-myosin ATPase Relaxation: After repolarization, ion pumps begin returning Ca2+ to resting locations, outside the cell and in the SR |
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at maximum contraction you have recruited all muscle fibers and cannot recruit more you get this at
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high myoplasmic [ca]
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muscle fatigue
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run out of calcium or ATP
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skeletal muscles is made up of bundles of muscle cells (myofibers) and each cell contains myofibrils that are composed of repeated units of myosin and actin called
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sacromeres
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thick and think filaments are arranged into
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sacromeres and are repeated in paralel and in series
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sacromeres feature
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z disk
a band i band m lines tropomodulin (cap) nebulin (stabilizing) |
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Z discs
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-at the end of the sacromere
-attachment sites for the plus ends of actin filaments (thin filaments) |
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M line
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-midline
-location of protiens that link adjacent myosin II filaments (thick filaments) to another |
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dark bands( A Bands)
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- mark the location of the thick filaments
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Light bands (I bands)
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-contain only thin filaments and therefore have lower density of protien
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myofibril
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a single continuous stretch of interconnected sacromeres
-run the length of muscle cell -myofibrils in parallel = more force |
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myosin
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is a ATPase
-motor protien used by actin -sliding filament model -converts the Energy released (ATP to mechanical) -simple structure tail neck head |
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Actin
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-capped by tropomodulin (-) and capZ (+) to stabilize
-form long chains called F-actin -in skeletal muscles 2 F-actin actin polymers twist together -surrounded by troponin and tropomyosin |
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pulling yourself along a rope analogy
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actin is the rope
myosin is your arm |
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two process of the sliding filament model
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chemical : myosin binds to actin (cross bridge)
structural: myosin bends (power stroke) |
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cross bridge cycle
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-formation of cross bridge, power stroke, and release
-need ATP to attach and release no ATP leads to riger mortis |
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sliding filament model
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-myosin is bound to actin in the absence of ATP and this is the rigor state
-ATP binds to the myosin causing the head to dissociate from the actin -ATP is then hydrolyzed cause a conformational change in the myosin head to move to a new position and bind to actin (pivots and binds to new actin subunit) -Pi is released cause the myosin head to chnage conformation again and its this movement that moves the actin (head pivots and moves actin (power stroke)) -ADP is released |
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Calcium allows myosin to bind to actin because
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-ca binds to troponin C (TnC)
-reorganization of troponin-tropomyosin -expose myosin binding site on actin |
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Step by Step myosin binding to actin
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1.calcium levels increase in cytosol
2. calcium binds to troponin C 3. Troponin-calcium complex pulls tropomyosin away from g actin binding site 4.myosin binds to actin and completes power stroke (see previous) 5.filament moves |
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contractile force depends on
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-scaromere length (distance between z disks)
-number of myofibrils -number of cell recruitment -alignment is important, optimal overlap for maximal contraction |
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isotonic contraction
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enough force to move load before muscle relaxes
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isometric contraction
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not enough force to move load before muscle relaxes
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cardiac myopathy
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enlargement of heart
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recruitment calcium
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increase calcium and inc NT and Ca to cause contraction
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regulation of contraction
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-excitation-contraction coupling
-depolarization of muscle membrane (sacrolemma) -elevation of intracellular calcium -contraction -relaxation when sarcolemma repolarizes and calcium returns to resting levels |
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skeletal muscles have a latent period between stimulus and contraction
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cardiac muscle does not AP last into contraction
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smooth muscle depolarization lasts long time
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cardiac is a lttle longer then skeletal
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causes of depolarization
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Myogenic and neurogenic
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Myogenic
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doesnt need a AP persay (spontaneous)
-pacemaker cells in heart: have unstable membrane resting potential so constantly depolarize, they depolarize the fastest |
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neurogenic depolarization
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-excited by neurotransmitters (ACH)
-have multiple (tonic) or single (twitch) innervation sites |
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relaxation of skeletal muscle
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-repolarization
-reestablish ca gradients -extracellular : ca ATPase, Na/ca exchanger (NaCAX) in reverse -Intracellular : Ca ATPase (SERCA), Parvalbumin |
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parvalbumin
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-is a cytosolic calcium buffer
-binds to calcium and inhibits it |
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The Z disk
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-responsible for anchoring actin filaments
-actin filaments are capped at both ends so will not depolymerize -titin-nubulin filament system stabilizes the alignment of thick and thin filaments -Thick filaments are connected at both ends to Z disks through titin -nebulin is associated with a thin filament from its + end at the z disk to the other end. |
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titin
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-each titin molecule is closely associated with a myosin thick filament
-the rest of the titin is elastic and chnages in length as sacromere relaxes and contracts |
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nebulin
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-exactly the length of the actin
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skeletal metabolism
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-muscles require lots of atp
-atp met by glycolysis or respiration -skeletal muscles have large glycogen stores -creatine phosphate+adp= creatine + ATP -lots of mitochondria, red color myofibrils because of myoglobin (stores o2) and large blood flow |
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break down of glycogen stores can be stimulated by
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ca 2+ and epinephrine
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@ beginning of exersize
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anaerobic, so get latic acid accumulation b/c blood vessels not dilated enough
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asynchronous insect flight muscles
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-due to stretch activation
-one ap causes continuous release of ca, muscle contracts several times, Ca is released due to mechanical change -contracted = ca insensitive -stretched = ca sensitive |
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heater organs
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modified muscles by eye use futile cycles, get heat from ATP hydrolysis
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electric shock organs
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modified muscles
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smooth muscles
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-spindle shaped with single nucleus
-packed with thick and thin filaments but not in organized fashion -smooth regular contractions -prolonged contractions -contribute to many systems -accessory protiens keep structurally intact |
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Key differences of smooth muscles from skeletal muscle is
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-lack sacromeres (no striations)
-no t tubules -minimal SR -Gap junctions -contract in all dimensions -more complex regulation |
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-smooth muscles have
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multiple receptors and activation mechanisms
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-smooth muscles can be activated by
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NT, Hormones, neighbouring cells which can release paracrine substances like Nitric oxide
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overall goal of smooth muscles is always the same
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chnage cytosolic ca to change degree of contraction
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in smooth muscle SR is sparse so
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Ca needed enters through plasma membrane ca channel
-changes in cytosolic ca level occurs very slow |
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innervation of smooth muscle cells is from
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autonomic nervous system
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many smooth muscle cells have the ability to
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spontaneously activate-unstable resting potential
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filaments in smooth muscles are gathered into loose bodies which are attached to
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dense bodies in the cytosol
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dense bodies
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serve same function as Z disks
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other end of filaments is attached to
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attachment plaque which is rich in actin binding protien like a Z disk and contains vinculin
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vinculin
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is an integral membrane protien in the plaque
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smooth muscle is not controlled by the bind of Ca2+ to the troponin complex like in cardiac and skeletal muscle
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instead Ca control of myosin
-ca binds to calmodulin and this complex is what controls the contraction -troponin is not in smooth muscle cells but tropomyosin is |
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calmodulin
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intracellular second messager that binds to calcium
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caldesmon
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regulatory protien on smooth muscle actin
-binds to actin and prevents myosin from binding actin |
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steps in smooth muscle contraction (5)
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1. intracellular calcium increase and ca is released from the SR
2. calcium binds to calmodulin (CaM) 3.Ca-CaM complex activates MLCK (myosin light chain kinase) 4.MLCK phosporylates light chains myosin heads and increases myosin ATPase activity 5.active myosin crossbridge slides along actin and creates tension |
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steps in smooth muscle relaxation (4)
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1. Free Ca in cytosol dec when Ca is pumped back into SR (if released from SR) or out of cell
2. Ca unbinds from calmodulin 3. myosin phosphatase removes phosphate from myosin which decreases myosin ATPase 4. less myosin ATPase activity results in decreased muscle tension |
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regulation of smooth muscle contraction
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-mainly through chnages in resting membrane potential
-gprotien mediated cascades that have nothing to do with membrane potential can release Ca from internal stores |
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norepinephrine and epinephrine effects on smooth muscles
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-effect depends on type of receptor
-Epi bound to beta-adrenergic receptors on intestinal = relax -Epi bound to alpha 2-adrenergic receptors on SM blood vessel cells lining intestine, kidney,skin -causes arteries to constrict, reducing circulation to organs |
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ACH and NO
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-ach released by autonomic nerves causes walls of blood vessels to relax
-act indirectly by inducing nearby endothelial cells to make and release NO which signals underlying smooth muscle cells to relax -No diffuses through tissue and activates guanylate cyclase in nearby smooth muscles -rise in cGMP leads to relaxation of muscle, vasodilation |
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Nitric oxide
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potent vasodilater
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increased cGMP activates a kinase that leads to
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-inhabition of calcium influx
-decreased calmodulin-ca stimulation of MLCK -decreases phophorylation of myosin light chains |
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vigara
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inhibits cGMP phosphodiesterase
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Nitroglycerine
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converted to NO
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heart contains
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-pacemaker cells
-contraction is not neuronally driven but self driven -not multinucleated like muscle cells -cardiac muscle cells linked by gap junctions |
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pacemaker cells
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in frog = sinus vinosus
in human= sinus node some pacemaker cells in atrium but not the driving force of contraction |
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many different types of cardiac muscle cells
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pacemaker cells in sinoatrial node
atrial and ventricle cells that produce contraction |
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action potential is quite different in cardiac muscle because
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voltage gated calcium channels play a much larger role
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pumps and transporters of cardiac muscle
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na/k atpase pump, establish electrochemical gradients
ca ATPase pump-remove 2 ca na/ca antiporter remove ca from inside of cell |
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channels in cardiac muscles
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leak channels (k+)
voltage gated na voltage gated K (delayed rectifier) voltage gated ca high voltage gated ca channels=DHP or L channel |
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action potential in ventricular and atrial cardiac cells
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-resting potential due to K (leak channels and inward rectifier channel that is open at rest)
-rising phase is set by cadiac voltage gated Na channels which then start to inactivate -open delay rectifier K channels and voltage gated ca -long plateau is balnce between open ca channel and open k channels -voltage gated ca channel inactivates but k remains open so cell will repolarize -then voltage gated k channels close and na channels become inactive to closed state -long plateau allows ca to elevate enough to generate contraction |
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ap in sinoarterial cells
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-spontaniously fire AP
-ap then propagated through gap junctions to aterial cells then ventricle cells |
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sinoartial cells
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-do not have a stable rest
-ap driven by voltage gated ca channels -rising phase due to opening of voltage gated ca channel -as ca channel inactivates the membrane is repolarized by delayed rectifier k+ channel -spontaneously depolarize once K+ channel clooses due to funny channel |
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funny channel
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activated by hyperpolarization
-channel opens and allows na+ to flow into the cell -cAMP can have dramatic effects on the channel and shift its activation threshold |
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sinus node>atria>boundry which ensures delay between activation of A and V...
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AV node is located in the boundry and provides the only conducting path from atria to ventricles
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proppagation from av node is provided by
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bundle of His which seperates further down into right and left bundles which then split into purkinje fibers which connect to innerwalls of ventricles
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signal propagates from innerwalls of ventricles to outer walls through
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gap junctions
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P wave
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impulse generated at sinoatrial node and spreads across atrium causing them to contract.
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Delay
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fibro fatty atrioventricular groove insulates the ventricles from arterial impulse
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QRS wave
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impulse down AV bundle, its branches and purkinje fibers, stimulates the ventricles to contract
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T wave
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repolarization of ventricles
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increasing heart rate
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Epinephrine and norepinephrine
Released from the sympathetic nervous system Epinephrine and norepinephrine are synthesized and released into the blood by the adrenal medulla, an endocrine organ Epinephrine and the related norepinephrine are all synthesized from tyrosine and contain the catechol moiety; hence they are referred to as catecholamines Nerves that synthesize and use epinephrine or norepinephrine are termed adrenergic Adrenergic receptors: bind epinephrine and norepinephrine. Because different receptors are linked to different G proteins, the activation leads to different signal transduction cascades More Na+ and Ca2+ channels open Rate of depolarization and action potentials increase |
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increasing heart rate cont.
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Epinephrine and norepinephrine cont….
In sinoatrial cells: norepinephrine binds to the b-adrenergic receptor which is a G protein associated membrane receptor This triggers a signal transduction cascade outlined below that activates the G protein (Gs - stimulates) that activates adenylate cyclase to produce cAMP. Beta-blockers: Drugs which are used to slow heart contractions in the treatment of cardiac arrhythmia and angina, are beta1-adrenergic receptor antagonists They bind the beta1-adrenergic receptor to block the receptor and thus slow heart contraction Cardiac muscle cells possess beta1 adenergic receptors |
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decreasing heartrate
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Acetylcholine: released from parasympathetic nervous system
Muscarinic acetylcholine receptor: a G protein associated receptor. The G protein activated in this case is a Gi subunit that inhibits adenylate cyclase More K+ channels open Pacemaker cells hyperpolarize Time for depolarization takes longer |
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modulating the funny channel
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Binding of hormone (e.g., epinephrine, glucagon) to a Gs protein coupled receptor
Gs protein relays the hormone signal to the effector protein, ie adenylyl cyclase Gs cycles between an inactive form with bound GDP and an active form with bound GTP Dissociation of the active form yields the Gsalpha · GTP complex, which directly activates adenylyl cyclase The increase in cAMP physically binds to the funny channel and makes the channel open more easily Funny channel will open sooner during the repolarization stage of the sinoatrial action potential and a second action potential will be triggered sooner Increase heart rate. |
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modulation of ca channel
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Epinephrine:
Causes an increase in cAMP that stimulates PKA (protein kinase A) which in turn phosphorylates the voltage-gated Ca2+ channel (L channel) Results in a protein conformational change that enhances the channels activity This new conformation of Ca2+ channel opens more readily (i.e. less time between action potentials) and opens for longer (i.e. more Ca2+ flow into the cell = greater [Ca2+] intracellular = greater contraction). Stimulates glycogen breakdown in skeletal muscles Caffeine (mmmmhhh): Blocks the activty of phosphodiesterases. Phosphodiesterases break down cyclic nucleotides. cAMP levels remain elevated and thus the funny channel continues to open more readily. Affects the Ca2+ release channel or ryanodine receptor such that more Ca2+ is released through the channel. Therefore heart contractions are stronger in the presence of caffeine as well |
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modulating the funny channel
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Acetylcholine works to block any rise in cAMP and reduces cAMP levels in the cell
Therefore the funny channel will now not open so readily and the slow depolarziation of the membrane will occur later thus resulting in a longer time to generate a second action potential. -anytime slow something down=open more k+ channels |
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modulating k+ channels
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Acetylcholine-induced opening of K+ channels in the heart muscle plasma membrane
Binding of ACH by muscarinic ACH receptors triggers activation of a transducing G protein by catalyzing exchange of GTP for GDP on the alpha subunit The released beta/gamma subunit then binds to and opens a K+ channel The increase in K+ permeability hyperpolarizes the membrane, which reduces the frequency of heart muscle contraction Activation is terminated when the GTP bound alpha subunit is hydrolyzed to GDP and Galpha · GDP recombines with Gbeta/gamma. |
