Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
97 Cards in this Set
- Front
- Back
|
what is a muscle fiber?
|
a muscle cell
|
|
|
what does a typical muscle cell look like?
|
big and multinucleated
|
|
|
where does the alpha-motor neuron originate?
|
in the spinal cord
|
|
|
what are the compotents of the alpha-motor neuron
|
soma (cell body)
dendrites axon myelin and nodes of Ranvier branches motor end plate and synapse |
|
|
what is the job of the alpha-motor neuron?
|
it propagates the action potential
|
|
|
what are the components of the neuromuscular junction?
|
motor end plate
post-synaptic membrane |
|
|
what makes up the motor end plate?
|
ACh vesicles
pre-synaptic membrane (which works by a secretory vesicle process) |
|
|
what are the components of the post-synaptic membrane?
|
junctional folds
ACh receptors Na+/K+ channels (ion channels) |
|
|
what do the ion channels in the post-synaptic membrane do?
|
cause depolarization, which spreads from the initial point
|
|
|
what does an action potential do?
|
opens gates leading to depolarization, dep. spreads
|
|
|
what is the weird word Eng uses for the motor end plate?
|
bouton
|
|
|
how is the speed of conduction increased?
|
saltatory conduction via nodes of Ranvier
|
|
|
what is myelin?
|
a lipophilic structure laid down by schwann cells; it doesn't allow for leakage
|
|
|
what is a motor unit?
|
the alpha-motor neuron and all of the fibers that it innervates
|
|
|
what are the 3 types of motor units?
|
slow
fast intermediate |
|
|
what are slow, small fibers?
|
dark due to lots of myoglobin which store O2 so the cell can use it to make E, have more mito, smaller peak
|
|
|
what are fast, big fibers?
|
light, larger in diameter, can produce a higher peak tensile strength, doesn't use mito or glycolysis, max tension quickly
|
|
|
why are there different types of fibers?
|
due to different ATPases
|
|
|
what are the characteristics of fibers?
|
a single fiber vs. a motor unit
functional unit of the motor unit |
|
|
how do nerves and muscles communicate?
|
by the propagation of the action potential
|
|
|
what is the mechanism of electrochemical communication with the muscle fiber? 6 steps
|
mobilization of ACh vesicles
fusion with pre-syn membrane ACh release into synapse ACh binds to ACh-R generation of the muscle fiber action potential degradation of ACh |
|
|
what is Curarae?
|
a paralytic
inhibits ACh release no contraction occurs |
|
|
what are OP's?
|
nerve agents, pesticides
block AChE and lead to constant depolarization |
|
|
what is Myasthenia Gravis?
|
autoimmune disease where the body kills its own ACh receptors
signs: relaxed muscles, breathing tube paralysis, mega-esophagus, paralyzed |
|
|
what is tetany?
|
continuous contraction
|
|
|
how is force regulated?
|
motor unit recruitment
rate coding |
|
|
what is motor unit recruitment?
|
the number and size of motor units
more cells and more motor units lead to greater strength |
|
|
when are small motor units recruited?
|
at low force outputs
|
|
|
what happens as force output increases?
|
progressively larger motor units are activated
|
|
|
when might all units be recruited?
|
at high force output
|
|
|
what is rate coding?
|
the frequency of stimulation
|
|
|
what is a twitch?
|
a single stimulus
|
|
|
what happens when there are multiple stimuli delivered at low frequency?
|
twitches sum and an unfused tetanus occurs
|
|
|
what happens when there are multiple stimuli at high frequencies?
|
a fused tetanus (maximal F) occurs
-the faster the axon fires, the higher the F -fast=few mito, low O2 |
|
|
is there a close association between stimulation frequency and force output?
|
yes
|
|
|
what are graded voluntary contractions?
|
don't know
|
|
|
what happens when force is low? (GVC)
|
small units are activated
individual activation frequencies begin to increase |
|
|
what happens as force increases? (GVC)
|
activation frequencies continue to increase until a plateau is reached
larger units are recruited activation frequencies increase |
|
|
when does the process of graded voluntary contractions stop?
|
when all units are activated at their maximal frequencies
|
|
|
what are the parts of the muscle membrane structure?
|
sarcolemma
T-tubule SR |
|
|
what is the sarcolemma?
|
muscle membrane that functions as most cell membranes and contains myoplasm or sarcoplasm
|
|
|
what is the transverse tubular network? (T-tubule)
|
invagination of the sarcolemma, extention of the sarcolemma
|
|
|
what is the fuction of the T-tubules?
|
transports excitation into the interior of the fiber
transports extracellular fluid into the interior of the fiber |
|
|
what is the SR?
|
highly specilized ER which stores and releases Ca++
|
|
|
what happens at the terminal cisternae of the SR?
|
Ca++ is released through channels
|
|
|
what happens at the longitudinal region of the SR?
|
Ca++ is sequestered, contains Ca++ ATPase (Ca++ pump, which pumps out of sarcoplasm and into ER)
|
|
|
how many muscle filaments are in each muscle cell?
|
100's or 1000's packed side by side and surrounded by SR
|
|
|
does every cell have a motor endplate in the middle of the cell?
|
yes
|
|
|
what are the 2 types of filaments in myofibrils?
|
actin-thin
myosin-thick |
|
|
do the T-tubules and TC merge?
|
no
|
|
|
what are the components of the contractile apparatus?
|
myofibrils
thin myofilaments thick filaments cytoskeletal proteins |
|
|
how do myofibrils appear?
|
striations
|
|
|
what does the Z-line define?
|
the sarcomere
|
|
|
what is a thin myofilament
|
actin which is the backbone of the thin filament; myosin binding site
|
|
|
how many subunits does troponin have and what do they do?
|
3 subunits
C-binds calcium (causes a physical change of C which changes other subunit configuration; I no longer inhibits ATPases, T pulls on Tropomyosin and changes it's physical force which leaves myosin heads accessible) I-inhibits ATPases T-binds tropomysin |
|
|
what is a thin myofilament made of?
|
actin
troponin subunits tropomyosin |
|
|
what is tropomyosin?
|
thin linear molecule that is bound to the T subunit of troponin
|
|
|
what happens when the myosin head is accessible?
|
ADP bound myosin heads bind to actin
head flexes filaments move ADP leaves ATP comes in breaks bond ATPase cleaves ATP to ADP re-cocks |
|
|
what is needed for the head to release?
|
ATP
|
|
|
what is necessary for contraction?
|
depolarization
|
|
|
where is the ATPase activity?
|
on the light chain
|
|
|
what constitutes a thick myofilament?
|
myosin heavy chain (MHC)
myosin light chain (MLC) myosin ATPase actin binding site |
|
|
where does actin bind?
|
on the light chain
|
|
|
where are light chains found?
|
only on the head
|
|
|
what is the sliding filament theory?
|
heads bind to thin filaments
head releases, shifting thin & thick filaments thin filament is released |
|
|
what causes the mechanical event involved in the contractile apparatus?
|
an electrical event
|
|
|
what is necessary to pump Ca++ back into TC?
|
ATP
|
|
|
outline the overview of the contraction process
|
initiated at NM junction
sarcolemma AP spreads to T-tubules Ca++ released into myoplasm Ca++ binds to C subunit of troponin Relaxation |
|
|
where is the contraction process initiated?
|
at the NM junction
|
|
|
what does the sarcolemmal action potential do when it spreads to the T-tubules?
|
activates a voltage sensor located in T-tubular membrane which opens the release channels of the SR TC
|
|
|
what happens when Ca++ binds to the C subunit of troponin?
|
causes a conformational change in the thin filament
myosin x-bridges shift from weak binding to strong binding sites ATP is hydrolyzed and F is produced if there is adequate ATP and Ca++, myosin X-bridges cycle b/t weak and strong binding states and produce F |
|
|
what happens in the relaxation step of muscle fiber contraction?
|
SR Ca++ release channels close
myoplasmic Ca++ is re-sequestered by the longitudinal SR via Ca++ ATPase Ca++ dissociated from troponin myosin X-bridges remain in the weak binding state |
|
|
what is the only source of E for contraction?
|
ATP
|
|
|
what are the 2 major ATPases that account for the vast majority of E consumed during activity?
|
myosin ATPase
Ca++ ATPase |
|
|
what does myosin ATPase need E for?
|
force production (2/3 of total)
active contraction |
|
|
what does Ca++ ATPase need E for?
|
Ca++ transport (1/3 of total)
maintains pump |
|
|
what is rigor mortis due to?
|
total lack of ATP
|
|
|
what is needed for contraction?
|
ATP and Ca++
|
|
|
is it true that the more Ca++ you have available the stronger the F can be?
|
yes
|
|
|
how is force production regulated by Ca++?
|
-force production by contractile apparatus is dependent on myoplasmic [Ca++]
-sigmoidal relation between F and [Ca++] -[Ca++] is regulated by SR |
|
|
what is the concentration of Ca++ at rest?
|
0.5uM
|
|
|
what is the concentration of Ca++ during tetanic contraction?
|
10uM
|
|
|
how is [Ca++] regulated by the SR?
|
release rate
uptake rate |
|
|
at rest, what state are the myosin crossbridges in?
|
weak binding state
|
|
|
what happens to myosin crossbridges at rest?
|
they attach and detach from actin very rapidly, with low affinity
ATP is hydrolyzed to ADP and Pi by the myosin ATPase |
|
|
what remains bound to the head when ATP is hydrolyzed?
|
ADP
Pi |
|
|
is force produced at rest (low Ca++)
|
no
|
|
|
what happens during contraction (high Ca++)
|
Ca++ binds to troponin
troponin I inhibition is removed Pi is released from myosin head X-bridges move to the strong binding site |
|
|
what happens at the strong binding site?
|
-E is utilized and the myosin head contracts (produces F)
-ADP is released from the myosin head -new ATP attaches to the myosin head and the rigor bond is broken -X-bridges move back to the weak binding state |
|
|
with adequate ATP and Ca++, what happens to crossbridges?
|
they cycle continually between the 2 states
|
|
|
what is the force of a contraction dependent on?
|
the number of cycling crossbridges
force per crossbridge rates of crossbridge cycling |
|
|
what are some changes which skeletal muscle makes to adapt under different circumstances?
|
strength and fatiguability
|
|
|
can weakness develop without noticible changes in muscle size?
|
yes
force per unit muscle declines |
|
|
what happens when weakeness develops without noticible changes in muscle size?
|
likely that one or more of the steps in the contraction process is impaired
|
|
|
what are the major steps of the contraction process?
|
1. initiation of the contraction in the motor cortex
2. activation of the motor neuron 3. propagation of the AP 4. NM communication 5. initiation of the sarcolemma AP 6. SR Ca++ release 7. Ca++ binding to troponin 8. X-bridge cycling and force generation 9. SR Ca++ uptake |
|
|
what can happen in the case of a spinal cord injury?
|
inibility to activate the motor unit and paralysis
|
|
|
what happens when the communication b/t the motor cortex and the motor neuron is blocked?
|
severe weakness occurs
|
