A&P Exam 3

Vol: skeletal Invol: smooth and cardiac

Which types of muscle are voluntary? Which types of muscle are involuntary?

Jeff is experiencing dizziness, chest pain, shortness of breath, muscle cramping/spasms, fatigue

(exposed to Sarin) What symptoms is Jeff experiencing?

Muscles well adapted for anaerobic metabolism - less blood flow, less myoglobin, low glycogen stores, low mitochondria Muscles well adapted for aerobic metabolism - more blood flow, more myoglobin, high glycogen stores, high mitochondria

1. Humans and other animals have muscles that are specially adapted to specific uses. We have some muscles that work really well using anaerobic metabolism and others that work really well using aerobic metabolism. Based on what you know about the resources needed for each, predict how muscles that are well adapted for anaerobic metabolism differ from those adapted for aerobic metabolism. Would you expect that each type of muscle has the same amount of blood flow, myoglobin, glycogen stores, and mitochondria? Why or why not?

Aerobic respiration is favored when our activities are long in duration. This process of producing ATP is the most efficient. More ATP molecules are produced per molecule of glucose than during glycolysis alone. However, aerobic respiration also takes more time that just glycolysis. Thus, activities that utilize aerobic respiration also tend to be those that do not need to occur quickly, for example, the muscles in your back that maintain your posture. The processes that result in anaerobic respiration (glycolysis) are those that are shorter in duration and need to occur quickly. Glycolysis can produce ATP faster than aerobic respiration, but it burns through fuel more rapidly and also has a byproduct of lactic acid. One of the factors that may limit our body's ability to have enough oxygen in our muscles is the speed of the activity. It is difficult to deliver a lot of oxygen quickly to our muscles. This speed is limited by how quickly our heart can pump blood, i.e. our heart rate. Some muscles are also built for aerobic respiration. They contain a high concentration of myoglobin (see below). This protein can deliver oxygen from the capillaries in muscle to its mitochondria more quickly than diffusion alone, and it can also bind oxygen and store it in muscle for use when oxygen is not readily available from the circulatory system.

1. We are all capable of activities that result in either lactic acid fermentation or the citric acid cycle, depending on whether oxygen is available in the muscles. What factors might contribute to whether an activity you are participating in will favor the citric acid cycle or lactic acid fermentation in your muscles? That is, what types of activities would you expect to favor aerobic respiration and which ones would result in anaerobic respiration? What factors might limit our body's ability to have enough oxygen available in our muscles for aerobic respiration?

Sarin irreversibly binds to AChE in the synaptic cleft. The binding of sarin inactivates the enzyme. Thus, excess levels of Ach reach the muscle's sarcolemma (postsynaptic membrane).

1. What is the mechanism of action of sarin or a sarin-like chemical?

Acetylcholinesterase (AChE) breaks down acetylcholine (Ach) in the synaptic cleft. Break down of this neurotransmitter into choline and acetic acid stops the signal from nerve to muscle cells.

1. What is the role of AChE in the NMJ?

Since sarin is preventing the breakdown of AChE, the muscle cell's sarcolemma is exposed to more Ach. More Ach in the synaptic cleft causes more of this neurotransmitter to bind to its receptors in the postsynaptic membrane. Thus, more Na+-K+ channels are opened, more Na+ enters the cell and leads to a prolonged depolarization of the muscle sarcolemma.

2. How would exposure to a sarin-like poison affect the amounts of Na+ going into the muscle cell? Explain why.

dihydropyridine receptor

A L-type calcium channel in the muscle cell membrane, activated upon depolarization, couple depolarization signal to release of calcium

Fasicle

A group of muscle fibers is called a __________________

Acetycholine (ACh)

A neurotransmitter derived from choline; responsible for sending the excitatory signal in the neuromuscular junction

Acetylcholinesterase breaks apart ACh

After nervous stimulation stops, what prevents ACh in the synaptic cleft from continuing to stimulate contraction?

Acetylcholinesterase breaks apart the ACh

After nervous stimulation stops, what prevents ACh in the synaptic cleft from continuing to stimulate contraction?

depolarization

An electrical change which brings the relative charge of the inside of the cell more positive; necessary for transmission of electrical impulses within a cell, or from one cell to another

Z disc

Anchors the contractile filaments

If the muscles ran out of ATP, the myosin would not be able to release the actin. The inability of myosin to release actin would cause the muscles to remain contracted. Not having the ATP necessary to allow the myosin to release actin occurs during rigor mortis.

As you have described above, ATP is an essential part of the process of muscle contraction. What do you would expect would happen during muscle contraction if your muscles ran out of ATP to use in this process? Why do you think this would happen?

I bands

At the light microscope level, the light bands that make up striations consists of the _________.

· Free ATP floating around in the muscle, which is available for use immediately. · The creatine phosphate system, which donates a phosphate to "spent" ATP (ADP), which converts it back into ATP that is ready to use for more muscle contraction. · Glycolysis, where glucose, a 6-carbon sugar, is broken down into two separate 3-carbon sugars called pyruvate (the word glycolysis means the lysis of glucose, or the splitting of glucose). The breakdown of glucose into pyruvate produces a modest amount of ATP. · After glycolysis, the body will use pyruvate in one of two ways. One option, lactic acid fermentation, occurs when there is not enough oxygen available to support the citric acid cycle and produces lactic acid (called anaerobic respiration). When there is enough oxygen available for the citric acid cycle to occur, the body uses pyruvate to produce ATP, CO2, and H2O in the mitochondria (called aerobic respiration). You may recognize mitochondria as the "powerhouse of the cell". It has earned this moniker because of all the ATP it produces during this process. All of these processes provide ATP for the muscles to use to fuel activity. No muscle activity can occur if we run out of ATP (in fact, muscle tissue is damaged and dies if ATP runs out completely). Thus, it is essential that we have effective mechanisms to keep lots of ATP available in our muscles and, if our muscles use ATP faster than we can replace it, our muscles will be unable to do anything at all as they approach complete depletion of ATP.

Because ATP is so important to muscle contraction, your muscles have numerous mechanisms for providing ATP to fuel contraction, including:

Astrocytes

The concentration of ions in the chemical environment surrounding the neurons must be tightly regulated for neurons to function properly. Which of the following cells is most responsible for this regulation?

Fast glycolytic fibers

Exhaustion of glycogen storage within a muscle fiber would have the biggest effect on ________.

6

For each thick filament, how many thin filaments are arranged around it?

3

For each thin filament, how many thick filaments are arranged around it?

They could inject potassium into the ventricles of the brain.

How could the aliens raise the extracellular potassium concentration only in the brain and not systemically?

The increased calcium would bind to troponin, which would pull tropomyosin out of the way and expose the binding sites for myosin on the actin molecules. This exposure would allow myosin to bind to actin, which leads to muscle contraction. Thus, the muscles should be in a fully contracted state, as long as there is ATP available to support contraction.

How do these altered Ca2+ levels affect the position of the actin and myosin filaments? Why/how?

thick filaments occupy the center of sarcomeres where they partially overlap with thin filaments. The sliding of thick filaments past thin filaments is a highly regulated process that occurs in an ATP-dependent manner driving muscle contraction.

How does the anatomy of a thick filament fit with its function?

actin binding protein wraps around actin to prevent myosin from binding to keep muscles in relaxed state it is the regulator of muscle contraction

How does the anatomy of titin fit with its function?

Troponin (Tn) is the sarcomeric Ca2+ regulator for striated (skeletal and cardiac) muscle contraction. On binding Ca2+ Tn transmits information via structural changes throughout the actin-tropomyosin filaments, activating myosin ATPase activity and muscle contraction. The troponin complex is made up of three components8-10: the calcium binding subunit, troponin C (TnC); the inhibitory subunit, troponin I (TnI); and an elongated protein, troponin T (TnT), that binds both TnC and TnI and anchors the entire complex to tropomyosin.

How does the anatomy of troponin fit with its function?

If the neurons that possessed the voltage-gated Na+ channels that opened at more positive membrane potentials were inhibitory, then, because their activity would be reduced, they would stop regulating the activity of other neurons. Because their inhibitory affect would be removed, these other neurons could become more active than they should be, which would lead to seizures.

How does this lead to seizure activity in the brain?

Increasing the extracellular potassium concentration will decrease the movement of K+ out of the cell. This lack of movement of the K+ ions will bring the resting membrane potential towards the threshold for an action potential. Thus, the neuron will be more likely to produce an action potential.

How will increasing extracellular potassium affect the signaling capability of a neuron?

Initially, because the sodium channels are unable to inactivate and, therefore close, Na+ ions will continue to enter the cell. This influx of sodium will lead to a number of action potentials being generated. However, over time, the neuron will not be able to reestablish its resting membrane potential, so it cannot repolarize. Thus, it will not be able to produce another action potential.

How will preventing the inactivation of sodium channels affect the signaling capability of a neuron?

This change in the voltage-gated sodium channels would increase the membrane potential required to reach threshold. Thus, it is less likely that a neuron would produce an action potential.

How will the excitability of a neuron be affected by sodium channels that open at more positive membrane potentials?

Without voltage-gated sodium channels, a neuron will not be able to produce an action potential. The plasma membranes of dendrites and the cell body do not exhibit voltage-gated sodium channels, so, like these regions of the neuron, without the voltage-gated sodium channels, the axon will only be able to produce graded potentials. Sodium will be able to enter the neuron because of the opening of chemically gated channels, but without voltage-gated channels, action potentials cannot form.

How will the non-functional sodium channels affect the signaling capabilities of a neuron?

If the voltage-gated sodium channels open at a more negative membrane potential, the membrane will reach threshold more easily. This change in the ability to reach threshold makes the neuron more likely to produce an action potential. Batrachotoxin can lower the threshold of a neuron by 30 to 50 mV. This change in the threshold means that many neurons will be firing action potentials at the resting membrane potential.

How will the signaling of a neuron be affected if the voltage-gated sodium channels open at a more negative membrane potential?

A prolonged depolarization of the muscle's sarcolemma would lead to more action potentials firing, which would cause more Ca+2 to leave the sarcoplasmic reticulum (SR). The Ca+ rushes out faster than the Ca+2 can be pumped back in to the SR by pumps. Thus, the levels of Ca+2 in the SR would be dramatically decreased.

How would exposure to a sarin or sarin-like chemical affect Ca2+ levels inside the sarcoplasmic reticulum? Why?

Myosin would be able to bind to the exposed binding sites on thin filaments but it would not be able to detach

If a muscle fiber were to suddenly and permanently stop producing ATP, the fiber would no longer be able to actively transport calcium out of the cytoplasm (sarcoplasm) and the intracellular calcium concentration would rise. Which of the following would you expect to happen?

Motor end plate

Large and complex terminal formation by which an axon of a motor neuron establishes synaptic contact with a skeletal muscle fiber, transmitting neural impulses to a muscle.

A band

Length of the myosin filaments in one sarcomere

Neurons have stable, relatively unchanging internal environments.

Like all cells, the neurons' internal organization dictates its function. Neurons have relatively many mitochondria, an extensive network of rough endoplasmic reticulum and many clusters of ribosomes. These cellular features indicate all of the following EXCEPT ________.

ryanodine receptor

Located on the sarcoplasmic reticulum and once opened, allows Ca2+ flow from the sarcoplasmic reticulum into the sarcoplasm.

Microglia

Meningitis can be caused by infection of the central nervous system by bacteria. Which cells would be most responsible for removing the infection?

sarcoplasmic reticulum

Modified endoplasmic reticulum, stores and releases calcium

True

Muscles store glycogen.

Astrocytes, a type of neuroglial cell, usually take up excess potassium from the extracellular space. They have potassium channels in their membranes.

Which type of cell normally regulates levels of extracellular potassium in the CNS?

Parasympathetic division

Nerve impulses are sent to slow the heart's rate of contraction. The nerve fibers sending these signals will most likely belong to which division of the nervous system?

Calcium ions (Ca+2) are released from the sarcoplasmic reticulum (SR). They bind to troponin. Binding of Ca+2 ions to troponin causes the troponin to change its shape, which pulls on tropomyosin. This pull reveals the myosin binding sites on actin. In order to bind to actin, the myosin head must have bound to ATP and split ATP into ADP and P using an ATPase. This change allows the myosin to bind to the actin, and the high energy phosphate provides the energy for the head of myosin to change shape and pull the actin toward the M line. Release of the ADP leads to another change in the myosin, which allows it to again bind ATP. This binding leads to a final shape change in the myosin, which causes it to let go of actin, and the process begins again.

Please list and briefly describe the steps of muscle contraction, starting with calcium release from the sarcoplasmic reticulum. Include the roles of the calcium ions, troponin, tropomyosin, ATP, actin, and myosin.

M line

Region where adjacent myosin filaments attach to each other

I band

Region where the myosin filaments don't overlap the actin filaments

H zone

Region within the A band in which the actin filaments don't overlap the myosin filaments.

Nicotinic Acetylcholine Receptor (nAChR)

Responsible for opening a ligand-gated Na+/K+ channel in the muscle membrane when the proper ligand binds to it.

No ATP is available to released attached actin and myosin molecules.

Rigor mortis occurs because ________.

Muscle cell > Myofibril > Myofilament

Select the letter below that lists the components of muscle in order from largest to smallest.

synaptic vesicles

Store neurotransmitters, and following a Ca2+ driven signal, dump neurotransmitters into the synapse.

The runners' use of stored oxygen, glucose, and creatine phosphate is being replenished

The 100-meter dash is a quick and short run requiring explosive speed. On completion of the dash, the runners will continue to breathe hard for several seconds to minutes even though they are no longer running. Which of the following is the best explanation for why this is so?

sodium

The ion responsible for depolarizing the muscle membrane by traveling through the nACh receptor, down its electrochemical gradient.

uni: smooth and cardiac multi: skeletal

Which types of muscle are uninucleate? Which types of muscle are multinucleate?

Allows for the efflux (diffusion out) of potassium ions.

The depolarization phase of an action potential is punctuated by the closing of inactivation gates in the voltage gated sodium ion channels. All of the following are consequences of this inactivation except one. Choose the statement below that is not a consequence of the closing of inactivating gates.

True

The effect of a neurotransmitter on the muscle cell membrane is to modify its ion permeability properties temporarily.

Acetylcholinesterase (AChE)

The enzyme responsible for stopping the ACh signal. Functions by metabolizing ACh into choline, which is recycled, and acetate.

sarcomere

The functional unit of the muscle fiber that includes the A-band, I-band, H-zone and the M-line.

Sarcolemma

The plasma membrane of a muscle fiber

synaptic terminal

The structure at the end of the axon that contains neurotransmitters and vesicles.

T-tubule

These invaginations allow depolarization of the muscle membrane to quickly penetrate from the sarcolemma to the myofibril

myosin

Thick filamentous contractile protein involved in cross-bridge formation, has a club-like appearance with a "head."

The use of the high energy phosphate which changes the shape of the head of myosin. This shape change allows the head of myosin to pull the actin toward the M line.

Think back to the beginning of the case study where you wrote out the steps of the sliding filament model for muscle contraction. What portion of the sliding filament model actually causes the muscle to contract?

Type I fibers tend to be smaller than type II fibers, because they require oxygen to produce ATP. The oxygen needs to diffuse from the capillaries, at the edges of the muscle fiber, through the layers of connective tissue, the plasma membrane of the muscle cell, and the contractile machinery in order to reach the mitochondria. The larger a muscle fiber, the longer the distance the oxygen needs to diffuse. Thus, fibers that rely on aerobic respiration to produce ATP are usually smaller than those that use anaerobic respiration.

Thinking about the ways in which these fibers produce the ATP necessary for contraction and what the fibers need in order to produce ATP, why might type I fibers be smaller than type II fibers?

Actin

Titin contractile protein involved in cross-bridge formation, comes in filamentous or globular forms.

He is referring to potassium leakage channels. These channels are involved in setting up the resting membrane potential. They allow K+ to leave the cell. Note: although most leakage channels are always open, there are some that are not. These additional leakage channels can open or close as needed based on the sensitivity of the cell. In addition, some of these channel proteins can migrate in and out of the cell membrane.

To what other type of potassium channel is Oligodendrog referring?

Calcium binds with troponin, which causes the protein to undergo a conformational change. This change in shape of troponin moves tropomyosin to expose the myosin binding site on the actin molecule. Then the myosin head is able to attach to the actin binding sites, forming the cross bridge. ATP binds to the myosin head and myosin hydrolyzes ATP into ADP + Pi. The energy released is used to "cock" the myosin head. The cocked myosin can now bind to the exposed site on actin. The myosin head then ratchets forward, pulling the actin filaments closer together, thus shortening the sarcomere and contracting the muscle cell. Since actin filaments are attached to Z-bands, we will see that the opposing Z bands are also brought closer together. This results in a shortened H zone, or the distance between opposing actin filaments and a shortened I band while the A band remains the same size.

Using the sliding filament theory, explain (or draw) the process of sarcomere shortening. Start from the point where calcium would interact with troponin. Make sure to discuss the roles of actin, myosin, and ATP.

This change in the extracellular potassium concentration would likely cause seizures, because of the increased likelihood that the neurons would produce action potentials.

What "terror" will this method produce if injected into your brain tissue?

The sarcomere is split into the H-zone, A-band, I-band, M line and Z line. The H-zone consists of myosin only, the I-band consists of actin only and the A-band contains both actin and myosin. The M-line holds together the thick myosin filaments. The Z-line differentiates between each sarcomere

What are the I band, H zone, and M line?

Tropomyosin blocks myosin binding sites on actin molecules, preventing cross-bridge formation, which prevents contraction in a muscle without nervous input. The protein complex troponin binds to tropomyosin, helping to position it on the actin molecule.

What are the roles of troponin and tropomyosin in muscle contraction?

The opening of more K+ leakage channels will allow more K+ out of the cell. The movement of K+ ions out of the cell will cause the cell to hyperpolarize - become more negative on the inside. This change in membrane potential will make it more difficult to fire an action potential. The stimulus will need to be larger in order to bring the potential to threshold.

What effect will opening more of these channels have on the excitability of a neuron?

This toxin affects some of the voltage-gated potassium channels in the nodes of Ranvier. These channels are required in order for the membrane to repolarize. K+ leaves the cell and reestablishes the resting membrane potential. If these channels do not open, the action potential will be prolonged. Thus, the neuron will continue to release neurotransmitter and produce a burst of signals.

What effect will the dendrotoxin have on the signaling capability of the neuron?

The presence of myelin allows the action potential to jump from node of Ranvier to node of Ranvier. If the myelin is destroyed, the action potential will move more slowly down the axon, because the entire axon now needs to depolarize, rather than just the nodes. In addition, because regions of the axon without voltage-gated channels are now not insulated by myelin, the ions can leak out. This leakage may prevent the formation of an action potential, so the propagation of the signal may stop completely.

What effect will the destruction of myelin have on the signaling capability of a neuron?

movement/mobility, posture, stabilization, and thermoregulation

What functions do muscles perform for the body?

contains intercalated discs and is involuntary

What is a unique feature of cardiac muscle, and what is the function of this feature?

A tendon is a projection of connective tissue beyond the ends of the muscle that attaches to bone. An aponeurosis is a broad fibrous sheet of connective tissue that connects muscles to adjacent muscles.

What is the difference between a tendon and an aponeurosis?

Produce smooth, continuous muscle contraction

What is the primary function of wave summation?

Dystrophin protein has four main functional domains; an actin-binding amino-terminal domain (ABD1), a central rod domain, a cysteine-rich domain and a carboxyl-terminus (Figure 2A). ABD1 contains 2 calponin homology domains (CH1 and CH2) it links actin to the sarcolemma and has helper proteins to do so

What is the role of calcium in the contraction of muscle?

A sarcomere is the basic contractile unit of muscle fiber. Each sarcomere is composed of two main protein filaments—actin and myosin—which are the active structures responsible for muscular contraction. A sarcomere is defined as the region of a myofibril contained between two cytoskeletal structures called Z-discs (also called Z-lines), and the striated appearance of skeletal muscle fibers is due to the arrangement of the thick and thin myofilaments within each sarcomere

What is the term for the main contractile unit of muscle and how would you describe its anatomy?

These alterations will initially produce muscle spasms, which will paralyze the subject. However, a neuron only has so much acetylcholine, so once the reserves of the neuron are released into the synapse, it will not be able to continue to stimulate skeletal muscles. Similar problems are experienced by the neurons that innervate the heart.

What nasty effects will this toxin have on motor pathways?

There needs to be less Ach reaching the muscle's sarcolemma. Thus, we need to restore the level of AChE in the synaptic cleft to normal. Solution - Administer oxime. This chemical can reactivate the AChE that was inactivated by the binding of sarin.

What needs to happen to Jeff's post-synaptic membrane to remedy his paralysis? Physiologically what do we need more of, and where?

These neurons carry information about pain.

What type of information do nociceptive neurons carry?

Motor neurons would continue to release acetylcholine into the synaptic cleft. The release of this neurotransmitter would lead to increased muscle contraction, which may cause spasms and tremors. These spasms or tremors, if experienced by the diaphragm, the main muscle of inspiration in mammals, a victim could die of respiratory failure.

What will happen if your motor neurons are exposed to this toxin?

If the action potentials in your nervous system start traveling more slowly down axons, you will not be able to respond to stimuli as quickly. If the "juice" affects your motor neurons, you may experience muscle weakness or if it affects your optic nerve, you may experience visual disturbances. If the action potentials stop moving down your axons, you could experience paralysis or loss of vision.

What will happen to you if you drink the alien "orange juice"?

Reducing the activity of these neurons will reduce your level of consciousness and respiratory rate. If the level of the anesthetic is high enough, it will produce anesthesia.

What will happen to you when sevoflurane reaches the reticular formation neurons that control sleep and consciousness.

The I bands to appear smaller

When a sarcomere contracts and thin filaments move over thick filaments you would expect to see ________.

striated

Which feature do skeletal and cardiac muscle share?

Jeff's AChE activity is low.

Which of Jeff's levels are abnormal?

Motor units with larger, less excitable neurons

Which of the following would be recruited later in muscle stimulation when contractile strength increases?

myosin

Which protein makes up a thick filament?

actin

Which protein makes up a thin filament?

Muscle fibers are composed of myofibrils which are composed of sarcomeres linked in series

Which structures make up a muscle fiber?

connective tissue

Which tissues make up a skeletal muscle?

· The intensity of the activity; where very intense activities require large amounts of ATP in a short period of time and use lots of O2 quickly- faster than the body can deliver O2 to the muscles. · The amount of blood flow to the muscles involved; muscles have different amounts of veins and arteries, depending on the way the muscle is typically used. Muscles that are best adapted to short duration, intense activity have less blood flow to them while muscles that are adapted for long duration, endurance activities have many blood vessels. · The amount of mitochondria availabe in the muscle; it is possible for some muscles to receive plenty of O2 for their activities without being able to use that O2 effectively because of a lack of mitochondria. Remember, the mitochondria is where the products of the citric acid cycle are converted in large amounts of ATP when O2 is available.

While answering question #3, you may have discussed a number of factors that influence whether aerobic or anaerobic respiration is used. Here are some of the factors that have an effect on this:

The mutant version of this gene would cause us not to be able to sense pain. Unfortunately, although the lack of the ability to feel pain might sound appealing, pain is a mechanism that our body uses to keep us safe. For example, when we touch a hot stove, we pull our hand away from it. Individuals that have this mutation can suffer broken bones or scalding burns, because their protective mechanism is not functioning. Children with this mutation have a hard time learning which actions could potentially hurt or kill them.

Why would having this mutant gene be so terrible?

The breast meat of chickens is light in color. Thus, it does not have a lot of myoglobin. The lack of myoglobin in the flight muscles of chickens reveals that these muscles rely on anaerobic metabolism to produce ATP. Thus, the muscles of these animals are not built for endurance. They are built for short flights. Note: The leg muscles of chickens are "dark meat." Thus, these muscles contain more myoglobin and are built for long distance running.

With that in mind, predict whether a domestic chicken is adapted for long flights requiring lots of endurance, or short flights. The breast meat is the muscle that is responsible for powering flight in birds, so what color is chicken breast and what does that mean for the endurance of the animal?

Usain Bolt - more type II muscle fibers - more power over a short period of time; contract quickly to drive a sprint Eliud Kipchoge - more type I muscle fibers - less power over a longer period of time; contract slowly to conserve oxygen and glycogen

With this in mind, predict whether Usain Bolt, the most accomplished sprinter in human history, has a greater amount of type I or type II muscle fibers. Similarly, predict whether Eliud Kipchoge, who recently broke the world record for the fastest marathon time (1 h 59 min 40 sec), has a greater amount of type I or type II muscle fibers. Why do you think this?

Calcium remains in the sarcoplasmic reticulum until released by a stimulus. Calcium then binds to troponin, causing the troponin to change shape and remove the tropomyosin from the binding sites

With which muscle protein does calcium interact?