Anatomy Final Lecture New Material
What components in the CNS and PNS myelinate axons?
- schwann cells are only found in the PNS and allows for myelination - oligodendrocytes in CNS myelinate axons to speed up AP
Know all the steps of head -cycling, their names if mentioned and what is accomplished at each step as per class lecture.
1) Exposure of the active sites ○ 2) Cross-bridge formation ○ 3) Power stroke ○ 4) Cross-bridge release ○ 5) Hydrolysis of ATP ○ 6) Recovery stroke
How many pairs of cranial nerves?
12
How many pairs of spinal cord nerves
31
Where does an axon originate from and what does it do?
A single axon arises from a cone-shaped area of the neuron cell body called the axon hillock Initial segment - the beginning of the actual axon Project away from the cell body (anterograde) vs protection towards the cell body (retrograde)
What is an action Potential Down a Neuron?
A travelling wave of charge that travels down the axon, and initiates the activation of the synapse (NMJ)
Describe the key shape of an action potential.
A wave that goes up, stops, then goes back down ■ Depolarize to -55 mV with graded potentials, action potential is produced, wave goes up (depolarization caused by V-gated Na+ channels), wave stops at +30 mV (V-gated Na+ channels close but V-gated K+ channels not open yet), wave goes down to -85 mV (repolarization caused by V-gated K+ channels)
What happens at the recovery stroke step of head cycling?
ADP is used to return myosin heads to the high energy position ■ Can repeat the whole cycle if the neuron released multiple APs since the calcium is gone (Ca pump in terminal cisterns sucked it up)
How does the AP interact with the T-tubules?
AP reaches the inside of the cell through T tubules. It activates the V-gated Ca++ channels in the terminal cisternae (located on each side of a T tubule) to open and release its Ca++. This causes the Ca++ levels in the sarcoplasm to rise. Calcium binds to the troponin complex, causing the troponin complex to change conformation and pull tropomyosin away from the actin. This exposes the myosin head binding sites. The myosin heads bind to the myosin head binding sites (cross bridge formation).
About how long does an action potential last on a given location of sarcolemma?
About 1 ms
What does Acetylcholine Gated Sodium Channel do and what binds to it?
Acetylcholine will bind to this channel and allow Sodium to be released from a more concentrated area outside to a less concentrated area inside of the muscle cell membrane → Positive charge IN This action DEPOLARIZES the membrane & fully ACTIVATES the synapse and triggers ACTION POTENTIAL down the sarcolemma
Once an action potential is initiated, what are its characteristics?
Action potentials: are all or none (digital) events, very fast, exclusive to excitable cells, once they start they will self-propagate all the way down to the end of the cell without decrement, cannot summate (twitches induced by action potentials can summate though....)
What are the components of the peripheral nervous system?
All 31 pairs of spinal nerves and 12 pairs of cranial nerves Ganglia (ganglion): relay stations to the CNS Receptors Plexuses
Does the AP "move"?
An AP does NOT "move." An AP causes an area of the plasma membrane next to it to create another AP, which then causes an area of the plasma membrane next to it to create another AP.....
How is an action potential channeled into the cell and how does it also keep going down the sarcolemma after encountering such a channel?
An AP is channeled into the cell through T tubules The terminal cisternae are excitable by an AP moving next to them down t tubule and voltage gated calcium channel open and allow calcium to move down into the sarcoplasm ○ Some of the AP can go down the T tubule and some of the AP can continue down the sarcolemma to the next T tubule Calcium spikes in the sarcoplasm because concentration gradient of calcium is more concentrated in terminal cisternae and moves down gradient (10 fold increase in sarcoplasm)
How do calcium pumps and voltage activated calcium channels of the terminal cisterns work together to modulate sarcoplasmic calcium ion concentrations during and after an action potential is conducted down a T-tubule?
An action potential activates the V-gated Ca++ channels to release Ca++ into the sarcoplasm, and Ca++ pumps (always on) bring in Ca++ back into the terminal cisterns When action potentials stop, Ca++ pumps take in Ca++ so the Ca++ levels in the sarcoplasm drop (the pumps require ATP and get energy to pump against concentration gradient through ATP hydrolysis) which allow muscles to rest. Troponin drags tropomyosin back over the myosin head binding sites (so myosin can no longer bind), and titins push the Z discs back to the resting positions (muscles relax).
Pharmacologically, what is an antagonist and how does curare mode of action fit the definition of an antagonist?
Antagonist: inhibit natural neurotransmitter from being activated Curare binds to Ach receptor sites, preventing the natural neurotransmitter (Ach) from being activated
What happens during the release of acetycholine?
As the acetylcholine is released, it passively diffuses across the axon terminal into the synaptic cleft As the acetylcholine is being deposited in higher concentrations near the end of the axon, it will move towards the Motor End Plate, where it is less concentrated (passive diffusion)
Specifically, how and when is the energy in ATP imparted to the cycle?
At the cross-bridge release step, the myosin heads let go of the myosin head binding sites and bind to ATP
How is it possible that calcium that spiked so quickly can also diminish so quickly before another head cycling is allowed? Specifically, what causes this?
Because the Ca++ pumps in the terminal cisterns remove Ca++ from the sarcoplasm. They have reestablished baseline positions!
What is BOTOX ® and what is its medical usage(s)?
Botox is botulinum toxin and is used to lightly paralyze facial muscles to get rid of frown lines and wrinkles Medical usage: injections of botox can be used to treat TMJ (temporomandibular joint) pain and bruxism for up to 4 months at a time Botox prevents the release of neurotransmitters that stimulate skeletal muscle contraction, which allow muscles of the face and jaw to relax. The relaxation of these muscles can relieve pain caused by TMJ disorders. Patients need to receive injections regularly to continue the benefits of botox therapy.
What is (are) the components of the central nervous system?
Brain and spinal cord
Know the initialisms CNS and PNS and what they stand for?
CNS - central nervous system PNS - peripheral nervous system
What happens at the exposure of the active sites step in head cycling?
Ca binds to troponins→ tropomyosins move→ myosin head binding sites are exposed ■Myosin heads are in the high energy position (upright)
Head- cycling events/mechanics What initiates cross bridge formation?
Ca++ binds to troponins & they move the tropomyosins that block myosin head binding sites, leaving the myosin head binding sites exposed
What reacts to acetylcholine?
Ca2+ fuses to synaptic vesicles containing the neurotransmitter, Acetylcholine Then, the exocytosis of these synaptic vesicles begins as the vesicles fuse to the cell membrane and inject Acetylcholine into the Synaptic Cleft
How does calcium interact with the myofilaments?
Calcium allows the myosin myofilament to bind to the actin myofilament ■ Calcium binds to the troponin complex, which pulls the tropomyosin away from the actin (thin myofilament) and leaves the myosin head binding sites exposed. Myosin can now bind to actin (cross bridge formation).
What "pump" is embedded within the membrane of the terminal cisterns and what role does it play in the regulation of sarcoplasmic calcium?
Calcium pump that vacuums the calcium from the sarcoplasm and back into the terminal cisterns
What other cytoplasmically soluble factor (besides ATP) is necessary for head cycling progress to the recovery stroke? (Hint: initiation of head-cycling).
Calcium- without calcium you cannot move forward with contraction/twitch
How might acetylcholinesterase inhibitors that are less potent be used for the good?
Causes compensatory physiological change More "bullets" because there are less "targets" (hits less targets more efficiently) You can boost acetylcholine levels even though you have less receptors Used to treat myasthenia gravis
What is clostridium botulinum and how is the poison it produces (botulinum toxin) relevant to the NMJ (what effect does it have on NMJ physiology?)
Clostridium botulinum: bacteria in food that produces botulinum toxin which causes botulism Botulinum toxin: paralytic neuromuscular toxin at the level of the synapse, most toxic chemical on earth Effect on NMJ physiology: neuron cannot release acetylcholine or releases less ach than usual Clostridium botulinum: Interferes with proteins that allow the mating of the vesicle with the inner surface of the axon terminal and blocks exocytosis (vesicles can't dock and open) Results in an excited neuron that can't release any acetylcholine or a lot less acetylcholine than normal → muscle weakness
What are the trigger zones?
Combination of the axon hillock and the initial segment. anatomical name = axon hillock
What happens at the power stroke step of head cycling?
Energy from the myosin head is used to move the myosin heads, they pull the thin filaments towards the center of the sarcomere (dragging the Z discs with them) -take the first baby step in shortening the sarcomere. Potential energy is converted to kinetic energy (energy of motion) ■ Myosin heads are in the low energy position
What allows the initial upswing (depolarization) and when, how and why does it end?
Depolarization is caused by the V-gated sodium channels opening and letting sodium into the cell, thus making the inside of the cell more positive (membrane potential becomes positive) ○It ends when the V-gated sodium channels close after ½ ms
What is sympathetic/parasympathetic tone? Based on the difference in this autonomic response, how might your somatic responses differ?
During period of stress, parasympathetic tone will move towards the sympathetic tone We don't have conscious control but emotions do play a role in which one is activated - producing stress hormones - riding wave of stress until exams are all over May become tense, heart rate may strike due to stress, may start shaking leg from anxiousness Somatic response is either fight or flight in sympathetic nervous system
Will fatigue eventually set in? What will be the result when this fatigue happens?
Eventually, the muscle will fatigue and the muscle will relax. If you push your muscle hard, it can have PH changes that become more acidic, producing lactic acid; sarcoplasm puts a damper on the ability of Ca voltage gates to function, so Ca levels go down. When Ca gets low, muscle is not harmed, but needs rest, which results in the muscle relaxing
What are dendrites, what do they do and what are dendritic spines?
Extensions of the cell body and receive information from other neurons or from sensory receptors. Dendritic spines: small extensions at the end of dendrites that help axons, of other neurons, connect with the dendrite. Dendrites generate small electrical currents, which are conducted towards the neuron cell body
What are voltage-Gated Calcium Channels and when do they occur?
Once the action potential reaches the end of the axon, it passes through a large number of Voltage-Gated Calcium channels The wave-like change in voltage from the action potential opens these channels INCREASING Ca2+ levels inside of the cell
During complete tetanus,...is ATP being expended....must calcium remain high....must the controlling neuron keep firing?
In complete tetanus, the sarcomeres do NOT continue to shorten since they are maximally contracted. Myosin head cycling still occurs to hold the thin filament in position: the myosin heads "paw" at the thin filament (bind and unbind). ATP is required for the myosin heads to be able to unbind from the myosin head binding sites. To have myosin head cycling still occurring, need the neuron to keep firing so that continuous action potentials occur, and for Ca levels to remain high so that the myosin head binding sites remain open (Ca binds to troponin→ troponin moves tropomyosin→ myosin head binding sites are exposed→ myosin heads can now bind!).
What is the role of the sodium/potassium pump in allowing an AP?
In the afterpotential portion of the wave, there could be leftover Na inside the cell and K outside the cell. The sodium potassium pump removes these leftover ions to reestablish the resting membrane potential so that another action potential can be created. 3 Na+ out of cell and 2 k+ into cell.
Given the range between individual twitches, varying degrees of intermediate tetanus, and full-blown tetanus, which of these do we keep our muscle fibers in most of the time to do most productive movements throughout the day?
Intermediate tetanus
Nevertheless, can botulinum toxin be prepared in a way that in certain contexts- makes it a useful medical drug? If so, how so? I can think of two ways.
It can be used as a medical drug in tiny amounts 1) When you have spastic paralysis/uncontrolled spasm of muscles in arm that continuously contracts, you can inject very small amount of toxin into the arm so that the muscle can relax, get relief, and reduce pain Diminish the ability of the synapse to work by blocking Ach from getting released → paralytic effect 2) Plastic surgeons can use a very tiny amount of botulinum toxin in the face to make you look younger A)Paralyzes certain face muscles to reduce frown lines B)However, give too much and you prevent the ability to make facial expressions, as face muscles are paralyzed
What effect might you expect a powerful acetylcholinesterase inhibitor have on neuromuscular physiology?
It could cause permanent contraction of the muscle (permanently excited synapse). → convulsions
How toxic is botulinum toxin compared to other chemical toxins?
It has a very low LD50 (lower LD50=increased toxicity), which means only a tiny mass per kg is necessary to kill humans
How is it a "rolling wave of depolarization/repolarization"?
It is a self-propagating chain reaction: an AP depolarizes an area of the plasma membrane, which causes an AP next to that AP, which then causes an AP next to that AP..... Waveform because once AP is initiated, it will continue and reach the end.
What does an AP moving down the t-tubules induce in the terminal cisterns?
It opens the V-gated Ca++ channels in the terminal cisterns and Ca++ flows into the sarcoplasm
Specifically, what ion and ion channel orchestrates the repolarization?
K+ and the V-gated potassium ion channel cause the repolarization
For a force-tension myogram, what are the phases of muscle twitches?
Lag, Contraction, and Relaxation When a fiber gets stimulated at time 0, the moment that AP starts travelling down the sarcolemma is due to excitation of NMJ Once an AP is activated, there is a delay or lag period (latent period when you get a twitch of 5ms) What causes the delay? AP occurs very fast, but part of the time is getting the AP to the end of a muscle (takes time for channels to open and calcium release into sarcolemma etc..) At first formation, cross bridge formation takes place, but has not pulled yet (non tension) After you make contact, the % of tension goes all the way to 100% which is the power stroke (Contraction) Slope of the line is at 0 at top, ATP attaches and causes cross-bridge release at 30ms and thin filament is no longer being held; tight strings relax which push z disks to original position (relaxation)
Why do you think there is always a latent or lag period for a twitch? Specifically, what events comprise the latent period and in what order do they occur?
Latent period is excitation-contraction coupling time. This is the amount of time the action potential takes to make a contraction. The events are those that lead up to cross bridge formation... so the calcium bind
What is myasthenia gravis, what type of disease is it, and what goes wrong when one has this disease?
Myasthenia gravis: autoimmune disease where you produce immune reaction to motor end plate (acetylcholine gated ion channels) In myIasthenia gravis the immune system does not like the acetylcholine gated ion channels and makes antibodies against it The T cells that make antibodies bind to the acetylcholine-gated ions channels which prevents acetylcholine from binding The Antibodies bind to and coat surface of each gated ion channels and block them from accepting acetylcholine when wanting to move muscles The Ach cannot get to ach gated ion channels → no depolarization occurs → weakens muscle
What is a myogram? Is there more than one type?
Myogram is graph/record of muscle activity Two types: myogram Force-Tension myogram
Do myosin heads cycle synchronously or asynchronously? Functionally, why is this important?
Myosin head movements are asynchronous - some myosin heads hold onto myosin heads binding site to complete the power stroke while others are releasing and rocking the myosin head (mixed population in sarcomere which allows for continual shortening and contraction) They cycle asynchronously for contraction. If all the heads powerstroke and let go at the same time, then there would be no point bc you're back where you started. Some myosin heads swing ahead and contract while others hold on to the actin (they take turns) to keep constant continuous contraction. Ex: climbing a rope
In repeated head-cycling, what has to continue happening to keep sarcoplasmic calcium levels high? (Hint: What would keep v-activated calcium channels of the terminal cisterns flickering open in rapid succession; what would keep a train of action potentials moving down the sarcolemma, etc, etc all the way to the behavior of the controlling neuron)?
Neuron needs to fire multiple action potentials Need constant calcium and depolarization to reach threshold The Na+ entering the cell depolarizes the sarcolemma which then will cause the voltage-gated Na+ channels to open, initiating an action potential that spreads out from the neuromuscular junction. The action potential not only travels across the sarcolemma, but also down the T tubules.
On the other hand, are all acetylcholinesterase inhibitors equally potent and therefore terribly poisonous?
No, some that are a lot weaker than sarin are helpful, such as neostigmine. Neostigmine stops acetylcholinesterase from inhibiting acetylcholine, which increases the levels of acetylcholine.
Why is the presence and activity of acetylcholinesterase every bit as important as acetylcholine release in the first place? I spoke of a class of drugs called acetylcholinesterase inhibitors
One action potential releases one puff of acetylcholine (lets sodium come in & depolarize membrane) and, without acetylcholinesterase, it can cause a maximal, permanent contraction (keeping ligand gated sodium channels open way too long). Creates convulsions if no acetylcholinesterase is able to hydrolyze acetylcholine Acetylcholinesterase inhibitors = inhibit the inhibitor
What is the "resting and digesting" part of the nervous system, what affects its activity and what effect does it have on physiology
Parasympathetic nervous system Decrease heart rate Decrease breathing rate Stores glucose Digestion active Conserves energy and promotes housekeeping during rest
What is a soma (Cell body) and what does it do?
Perform the typical function of a cell, such as protein synthesis and packaging proteins in vesicles. Nissl bodies represent the rough ER and the abundance of these nissl bodies reflects the significant amount of protein synthesis neurons perform. Between the soma and base of axon is the launching pad for action potential called the trigger zone (axon hillock)
What is curare, where does it come from and who first discovered a use for it? What was that use?
Plant toxin antagonist used by indigenous people of South America in poison arrows. If injected into the bloodstream, it circulates very fast and blocks acetylcholine by binding to the acetylcholine gated ion channels Competitive inhibitor of acetylcholine = outcompetes acetylcholine Like botulinum toxin, it disrupts the ability of neurotransmitters to communicate with the cell Richard Evans Schultes discovered Modern use is a muscle relaxant (no muscle tone, but also no effect on CNS) First drug type used in surgery- risky, but gave ideas for the use of other types of drugs
What part of the head cycling accounts for the increase in tension throughout the contraction period?
Power Stroke
What then causes the repolarization?
Repolarization is caused by the V-gated potassium channels opening and letting potassium out of the cell, thus returning the membrane potential to its resting value
Is rigor mortis regulated?
Rigor mortis is unregulated: when you die, you still have aerobically produced ATP that is in the cell at the moment of death which allow for head attachment to take place. When you are dead, there is no more control of this ATP; there is a leakage of calcium into the cell, but its not regulated so you can start head attachment and pulling without release from ATP (can contract certain muscles and cause rigidity)
What is rigor mortis, what does it mean and when does it happen?
Rigor mortis: the development of rigid muscles several hours after death- similar to physiological contracture. body is stiff and rigid ■ Occurs after you die; goes away after 24 hrs ■ Eventually run out of ATP so myosin heads cannot detach from the thin filament (muscles are rigid since the thin filaments are locked to the thick filaments)
The T-tubules are effectively involutions of what?
Sarcolemma
What is sarin and why is it so terrible?
Sarin is a poisonous gas - and acetylcholinesterase inhibitor - which causes convulsions and a torturous death, because a person who inhales it cannot relax the breathing organs. It also causes uncontrolled urination, foaming at the mouth, etc.
How does the creation of multiple head-cycling's (one after the other) change the geometry of the sarcomere?
Shortens it: pulls the thin filaments & Z discs toward the center of sarcomere I band almost disappear in length, the H zone completely disappears during max contraction (tetanus)
And afterwards, what happens to the calcium concentration in the sarcoplasm?
The calcium concentration in the sarcoplasm increases
What is summation and how does it apply to twitches?
Summation - amount of force in an individual muscle fiber If there are many action potentials applied at a high frequency, twitches can merge into higher force contraction aka twitches can summate. Summation is repeated twitch contractions, where the previous twitch has not relaxed completely before another AP is fired
How does summation occur?
Summation occurs when a second stimulus is applied before a previous stimulus has disappeared resulting in an even larger depolarization (4-5) in picture
What are myelin axons?
Surrounds one axon - protects and electrically insulates each axon. This helps axons conduct electrical signals more rapidly than unmyelinated axons
What is another term for cisterns?
Terminal cisternae
Describe how the v-gated sodium channels and the v-gated potassium channels work in tandem to construct an action potential
The V-gated sodium channels flicker open first and let Na+ into the cell, thereby depolarizing it (front half of the wave). The wave peaks at +30 mV when the Na+ channels close and before the K+ channels open. Immediately after the V-gated sodium channels close, the V-gated potassium channels open and let potassium out of the cell which repolarizes it (back half of the wave). ■ The V-gate sodium channels open first bc they are more sensitive
Why do you think it is important that the v-gated sodium channels activate at an offset in time compared to the v-gated potassium channels?
The V-gated sodium channels need to open first to make the inside of the cell more positive so the cell depolarizes ○ Opening the V-gated potassium channels (which make the inside of the cell more negative) at the same time as the V-gated sodium channels would counteract the effect of the V-gated sodium channels and no action potential would be initiated Dr: Cohn review If not offset, you would have depolarizing and then without finishing you would have repolarizing which will cancel each other out You will never have a wave and then will never be able to transmit an action potential V gated sodium channels react first... potassium channels react just when V gated sodium channels deactivate
Explain --based on your newly acquired detailed knowledge of the physiology of head cycling at the molecular level --what accounts for the development of rigor mortis after death?
The absence of ATP accounts for the occurrence of rigor mortis- w/out ATP, the myosin heads can't release and the muscles remain very rigid for hours.
Head- cycling events/mechanics (continued)- What effect would this "vacuuming up of calcium back into the sarcoplasmic reticulum" have on the possibility of a subsequent head cycling?
The lack of calcium prevents a subsequent head cycling from occurring Calcium is needed so that the myosin head binding sites are exposed and myosin can bind
What is the motor end plate and what does it contain?
The motor end-plate is the postsynaptic region of a muscle cell that is activated by Acetylcholine -The motor end-plate is the part of the sarcolemma where there are Acetylcholine Gated Sodium (Ligand) Channels
Going back to head-cycling, what parts of the head cycling account for the moment at the end of the latent period but before the contraction period?
The exposure of myosin active site
Exactly how do the myofilaments slide past one another and how does this lead to the shortening of the sarcomere from repeated head cycling
The myosin heads in the power stroke pull the thin filaments towards the center of the sarcomere (dragging the Z discs along with them)
How does the activation of the voltage (v) -gated sodium channels and v-gated potassium channels function like "a cascade of falling dominoes'? Specifically, what role do the v-gated sodium channels play in orchestrating the action potential (AP)? Specifically, what role does the v-gated potassium channels play in producing the action potential (AP)?
The sodium and potassium voltage gated channels are originally closed when the cell is at rest (not excited) Note: resting membrane potential is governed by potassium ions leaking out of the cell which is counterbalanced by the electrical gradient) When the synapse is activated, some depolarization from synapse comes and depolarizes membrane to the threshold potential for sodium gated channels (-55mv). Voltage gated sodium channels open which depolarizes the membrane from -85 to about +30mv - gate closes about ½ ms later. Then potassium channel which initiates repolarization creates the AP wave (if channels stay open hyperpolarizaton can take place which goes below -85mv)
How has a resting sarcomere changed after multiple head-cyclings until a sarcomere is maximally contracted?
The thin filaments are pulled very close to the edge of the thick filaments (the titins are maximally compressed) so the sarcomere cannot be shortened any further
What is acetylcholinesterase and what does it do? What is it necessary for?
This is an enzyme that uses water to break down Acetylcholine into its 2 parts: acetic acid & choline Allows Acetylcholine to bind, but nothing more as it breaks it down It's function is necessary to prevent constant muscle contraction
How are the myosin heads behaving (what is their position and orientation) at the apex (highest point) of a twitch?
This is right at the end of the power stroke when they are in an upright position, and it is at the stage after ATP is released and binds to the myosin heads, causing the heads to detach from the thin filament
In the absence of reformation of a cross-bridge for a subsequent head-cycling, what do you think leads to the "pushing back" of the z-disks to the relaxed position (Hint: A really big protein with "spring like" properties).
Titin pushes the z-disk back into the relaxed state
What limits the extent of contraction of a sarcomere?
Titins and thick filaments (thick filaments or A bands stay the same length, while thin filament shortens) ■ Thin filaments get pulled to the center, spring (titin) becomes maximally compressed and thick filaments cannot shorten at all ■ When the sarcomere is 2/3 shortened it cannot shorten any more
What is necessary to induce two or more head-cycling's one right after another?
To have multiple head cyclings, multiple action potentials are necessary (keeps calcium high in sarcoplasm which causes repeating head cycling) ■ Causes overlapping puffs of ACh in the synapse→ causes multiple sequential action potentials down the sarcolemma→ causes overlapping puffs of Ca++
Are individual twitches digital events? What does "digital" mean in this context?
Twitches are digital events → they either don't happen or happen all the way. They don't allow for smooth movements You either create a head cycling at full twitch, or you will not
What are the two significant types of summation?
Two types of summation: Spatial summation: depolarization happening at the same time in different locations of the axon (S in spatial for same time) Temporal summation: addition of single stimuli over a short period of time (one fired after another that is strong enough to reach threshold)
During muscle contraction, is the typical fiber more apt to fatigue via running low on ATP first, or running low on sarcoplasmic calcium first? Given your answer, what are the ramifications of this?
Typical fiber will fatigue via running low on sarcoplasmic calcium first Ca+ gets low = muscle is not harmed, run out of atp = damage or ruin to muscle Running out of ATP is rare, but if it happens, myosin heads can stick to thin filaments which can cause muscles to seize up which is painful and damaging
Under what circumstances might an electromyogram be the only option and why?
When you want to measure muscle activity of living human non-invasively
In the absence of another action potential (AP) that causes an immediate subsequent burst of calcium, what happens to the re-charged myosin heads in high energy position? Do these heads reform cross-bridges or no? Explain how your answer leads to relaxation. (Hint: if you know the steps of how calcium allows filament sliding, then think of these steps occurring in the reverse).
Without another AP, the myosin heads do NOT reform cross-bridges. This is because Ca is no longer being released from the terminal cisterns and is instead being sucked back up by the Ca pumps in terminal cisterns. Lack of Ca causes the troponins to return to their original conformation and drag tropomyosin back over the myosin head binding sites, so myosin heads can no longer bind to the thin filament. Since cross-bridges cannot reform, the muscle relaxes.
Might a mild acetylcholinesterase inhibitor be useful as a component of treatment for myasthenia gravis? If so, Explain
Yes, a mild acetylcholinesterase inhibitor: causes levels of ach to increase and stay in synapse. Lots of bullets for a limited number of targets. Bullets keep firing on the targets then ion channels can stay open. This is compensation for having less receptors
Can the degree of rigor mortis be measured by experts? If so, might this be useful under certain circumstances? Explain.
Yes, after someone dies the mortician on the scene can determine how long one has been dead based on a number of factors. ○ Yes, since rigor mortis goes away ~24 hrs after death it can be used to determine time of death
What is the difference between various amounts of intermediate tetanus vs. full blown tetanus?
You normally are in intermediate tetanus (more than twitches but not full tetanus) throughout the day because you don't want to always be moving maximally and individual twitches wouldn't work so the somewhere in between is intermediate tetanus to accomplish movement that is more than twitches but less than max tetanus (fully contracted muscle)
What happens at the hydrolysis step of head cycling?
myosin head hydrolyses the ATP (with ATPase) that it's bound to and releases energy. Conducts a hydrolysis reaction! Hydrolysis of ATP, when you hydrolyze ATP, you release a bunch of energy. That energy can be harvested to do work! Can eventually be recocked into the higher energy position! Heat is released! ■ Myosin heads are in the low energy position
What happens at the cross-bridge formation step of head cycling?
myosin heads bind to the myosin head binding site ■ Myosin head s still in the high energy position
What happens at the cross-bridge release step of head cycling?
myosin heads unbind from the myosin head binding sites so that they can bind to ATP (need ATP to release)-once in a relaxed position, myosin HEADS love getting on that ATP. IT CAN't have both, it must only pick one contestant. This is cross-bridge RELEASE in its finest form! ■ Myosin heads are in the low energy position
What is the "fight or flight" part of the nervous system, what affects its activity and what effect does it have on physiology?
sympathetic nervous system Increase heart rate Increase breathing rate Releases glucose Smooth muscle of digestive system immediately inhibited Blood pressure goes up Eyes dilate We sweat Release adrenaline
What effect does depolarization have on the sarcolemma that borders the motor end plate? What two sarcolemma transmembrane proteins allow this to take place?
○ Depolarization activates the voltage-gated sodium channels and the voltage-gated potassium channels on the sarcolemma that borders the motor end plate, which then create an action potential that self-propagates down the entire length of the muscle cell