🏷️ LIMITED TIME OFFER: GET 20% OFF GRADE+ YEARLY SUBSCRIPTION →
Log in
HomeStudy Guides420,000CA160,000

BIOA02H3 Study Guide - Midterm Guide: Phosphate, Cytosol, Conformational Change

69 views4 pages
School
UTSC
Department
Biological Sciences
Course
BIOA02H3
Professor
Stephen Reid

For unlimited access to Study Guides, a Grade+ subscription is required.

hans15149 and 39222 others unlocked
BIOA02H3 Full Course Notes
43
BIOA02H3 Full Course Notes
Verified Note
43 documents

Document Summary

Neuromuscular junction is the synaptic connection between a motor nerve and a skeletal muscle. Motor nerves = nerves that regulate skeletal muscle function. Action potential arrives at axon terminal it released acetylcholine (ach) which is stored in membrane- bound secretory vesicles. Ach is released between the pre-synaptic cell and the post-synaptic cell then it binds to an acetylcholine receptor on the post-synaptic membrane. Skeletal muscles cells are called muscle bres, they are packaged with connective tissue in bundles called fascicles. Muscle bres consists of myo brils which are bundles of actin and myosin laments. Sarcolemma = plasma membrane of the skeletal muscle cell. Action potential travels along the sacrilege and spread into the muscle cell via t-tubules. This causes release of ca2+ form the sarcoplasmic reticulum and this calcium triggers the muscle contraction. Sarcomere is a unit of arranged thick and thin laments.

Get access

Grade+20% off
$8 USD/m$10 USD/m
Billed $96 USD annually
Grade+
Homework Help
Study Guides
Textbook Solutions
Class Notes
Textbook Notes
Booster Class
40 Verified Answers

Related Documents

BIOA02H3 Lecture Notes - Lecture 4: Atp Hydrolysis, Conformational Change, Rigor Mortis
magentaguinea-pig824
BIOA02H3 Lecture Notes - Lecture 15: Neuromuscular Junction, Hydrolysis, Troponin
cerisegiraffe538
BIOA02H3 Lecture Notes - Lecture 4: Nicotinic Acetylcholine Receptor, Neuromuscular Junction, Skeletal Muscle
hassanalibhai

Related Questions

1. Which of the following structures is NOT a part of the musclefiber?

A. transverse tubule
B. motor end plate
C. sarcolemma
D. synaptic knob
E. sarcoplasmic reticulum

2. You briefly apply a high concentration of acetylcholine (ACh)directly to the motor end plate and observe no contraction of thefiber. Since muscular dysgenesis only affects one type of cell inthe body you would suspect that the motor neurons of dysgenic micework normally. True or False?

A. True
B. False

3. Arrange the events at the neuromuscular junction in the propersequence from first to last

1. arrival of the action potential at the synaptic knob
2. generation of action potential in sarcolemma
3. binding of ACh to ACh receptors in the motor end plate
4. release of ACh into the synaptic cleft
5. removal of ACh from the cleft by acetylcholinesterase

A. 1, 2, 3, 5, 4
B. 2, 3, 1, 4, 5
C. 1, 4, 3, 2, 5
D. 2, 5, 1, 4, 3

4. After you apply acetylcholine to the muscle fiber you find thatan action potential is generated in the sarcolemma. This resultproves that certain events or conditions occur normally within theneuromuscular junction. Which event or condition is NOT PROVED bythe above result?

A. ACh receptors are present in the membrane of the motor endplate
B. ACh receptors bind to ACh
C. Sodium permeability of the end plate membrane is increased
D. Acetylcholinesterase breaks down ACh

5. Arrange the events of excitation contraction coupling in theproper sequence from first to last

1. cross-bridge cycling
2. action potential in the sarcolemma reaches the triads
3. release of calcium from the sarcoplasmic reticulum
4. exposure of active site on the thin filaments
5. binding of calcium to troponin

A. 2, 3, 5, 4, 1
B. 5, 3, 4, 2, 1
C. 5, 1, 3, 2, 4
D. 3, 5, 2, 4, 1

6. You artificially raise the calcium concentration within thesarcoplasm of the muscle fiber and observe that the cell contractsnormally. From this observation you conclude that the defect inmuscular dysgeny occurs at which step in control of the musclefiber?

A. Exposure of the active site on thin (actin) filaments
B. Binding of calcium to troponin
C. Release of calcium ions from the sarcoplasmic reticulum into thesarcoplasm
D. Repeated cycles of crossbridge binding, pivoting, anddetachment

7. Where in the muscle fiber do you suspect that the normal proteinmade by the mdg gene functions in normal mice?

A. motor end plate
B. triad
C. myofibrils
D. thin filaments

8. All of the following conditions would have same effect onmuscles (flaccid paralysis) as muscular dysgeny with a singleexception. What is the EXCEPTION?

A. botulism
B. poisoning with atropine
C. poisoning with military nerve gas
D. myasthenia gravis

9. You would expect the muscles from an animal afflicted withmuscular dysgenesis to exhibit:

A. hypertrophy
B. atrophy

10. You would expect that a dysgenic mouse dies shortly after birthbecause:

A. the heart fails to beat
B. vasoconstriction of the carotid artery prevents blood flow tothe brain
C. vasodilation of the systemic blood vessels causes the bloodpressure to drop to lethal levels
D. the respiratory muscles are unable to contract

1. Which of the following structures is NOT a part of the musclefiber?

A. transverse tubule
B. motor end plate
C. sarcolemma
D. synaptic knob
E. sarcoplasmic reticulum

2. You briefly apply a high concentration of acetylcholine (ACh)directly to the motor end plate and observe no contraction of thefiber. Since muscular dysgenesis only affects one type of cell inthe body you would suspect that the motor neurons of dysgenic micework normally. True or False?

A. True
B. False

3. Arrange the events at the neuromuscular junction in the propersequence from first to last

1. arrival of the action potential at the synaptic knob
2. generation of action potential in sarcolemma
3. binding of ACh to ACh receptors in the motor end plate
4. release of ACh into the synaptic cleft
5. removal of ACh from the cleft by acetylcholinesterase

A. 1, 2, 3, 5, 4
B. 2, 3, 1, 4, 5
C. 1, 4, 3, 2, 5
D. 2, 5, 1, 4, 3

4. After you apply acetylcholine to the muscle fiber you find thatan action potential is generated in the sarcolemma. This resultproves that certain events or conditions occur normally within theneuromuscular junction. Which event or condition is NOT PROVED bythe above result?

A. ACh receptors are present in the membrane of the motor endplate
B. ACh receptors bind to ACh
C. Sodium permeability of the end plate membrane is increased
D. Acetylcholinesterase breaks down ACh

5. Arrange the events of excitation contraction coupling in theproper sequence from first to last

1. cross-bridge cycling
2. action potential in the sarcolemma reaches the triads
3. release of calcium from the sarcoplasmic reticulum
4. exposure of active site on the thin filaments
5. binding of calcium to troponin

A. 2, 3, 5, 4, 1
B. 5, 3, 4, 2, 1
C. 5, 1, 3, 2, 4
D. 3, 5, 2, 4, 1

6. You artificially raise the calcium concentration within thesarcoplasm of the muscle fiber and observe that the cell contractsnormally. From this observation you conclude that the defect inmuscular dysgeny occurs at which step in control of the musclefiber?

A. Exposure of the active site on thin (actin) filaments
B. Binding of calcium to troponin
C. Release of calcium ions from the sarcoplasmic reticulum into thesarcoplasm
D. Repeated cycles of crossbridge binding, pivoting, anddetachment

7. Where in the muscle fiber do you suspect that the normal proteinmade by the mdg gene functions in normal mice?

A. motor end plate
B. triad
C. myofibrils
D. thin filaments

8. All of the following conditions would have same effect onmuscles (flaccid paralysis) as muscular dysgeny with a singleexception. What is the EXCEPTION?

A. botulism
B. poisoning with atropine
C. poisoning with military nerve gas
D. myasthenia gravis

9. You would expect the muscles from an animal afflicted withmuscular dysgenesis to exhibit:

A. hypertrophy
B. atrophy

10. You would expect that a dysgenic mouse dies shortly after birthbecause:

A. the heart fails to beat
B. vasoconstriction of the carotid artery prevents blood flow tothe brain
C. vasodilation of the systemic blood vessels causes the bloodpressure to drop to lethal levels
D. the respiratory muscles are unable to contract

The junction specialized for the transmission between a neuron and another cell is called a (1) _____ ______. Usually, the signal being sent to the receiving cell is carried by chemical messengers called (2) _____. (3) _____ is an example of this type of chemical messenger, which diffuses across the synaptic cleft, combines with protein receptor molecules on the muscle cell membrane, and soon thereafter is rapidly broken down by enzymes. At an (4) ____ synapse, the membrane potential is driven toward the threshold value and increases the likelihood that depolarization and an action potential will occur. At an (5) ____ synapse, the membrane potential is driven away form the threshold value, and the receiving neuron becomes hyperpolarized and is less likely to achieve an action potential. A specific transmitter substance can have either excitatory or inhibitory effects depending on which type of protein channel it opens up in the (6) ____ membrane. (7) ____ are neuromodulators that inhibit perceptions of pain and may have roles in memory and learning, emotional states, temperature regulation, and sexual behavior. (8) ____ ________ at the cellular level is the moment-by-moment tallying of all excitatory and inhibitory signals acting on a neuron. Incoming information is (9) ____ by the cell bodies, and the charge differences across the membranes are either enhanced or inhibited. Some narrow-diameter neurons are wrapped in lipid-rich (10) _______ produced by specialized neuroglial called Schwann cells; each of these is separated from the next by a(n) (11) ________ ________ - a small gap where the axon is exposed to extracellular fluid. A (12) ____ is an involuntary sequence of events elicited by a stimulus. During a (13) _______ ________, a muscle contracts involuntary whenever conditions cause a stretch in length; many of these help you maintain an upright posture despite small shifts in balance. Imbalances can occur at chemical synapses; a neurotoxin produced by Clostridium tetani blocks the release of GABA and glycine, thus freeing the motor neurons from (14) _____ control, which may cause tetanus – a prolonged, spastic paralysis that can lead to death. A. Excitatory H. Stretch reflex B. Inhibitory I. Summed C. Myelin J. Neurotransmitters D. Chemical synapse K. Postsynaptic E. Synaptic integration L. Endorphins F. Exposed node M. Acetylcholine (ACh)