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Question 6

Part I: A series of questions

a. At the muscle what type of potential is measured?

b. Is it excitatory or inhibitory?

c. What neurotransmitter is released from the agonist motor neuron?

d. What neurotransmitter is released from the antagonist motor neuron?

e. What is the action at the muscle of each?

f. Is it always excitatory?

g. In the knee jerk reflex we can’t have antagonist muscles all firing together, is the opposing muscle inhibited or is excitation decreased instead?

Part II: What type of potential is measured at the neuromuscular junction (NMJ)?

a. EPSP (Excitatory Post-Synaptic Potential)

b. IPSP (Inhibitory Post-Synaptic Potential

c. Receptor Potential (RP)

d. End Plate Potential (EPP)

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Related questions

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)

Tetraethylammonium (TEA) is a drug that blocks voltage-gated potassium channels. What effect would this have on an action potential?

(a)Prevent the rising phase

(b)Prevent the cell from reaching the threshold to trigger an action potential

(c)Prevent or prolong the falling phase

(d)None of the above

The hyperpolarization phase of the action potential is due to:

(a)The opening of voltage-gated Cl- channels

(b)Prolonged opening of voltage gated K+ channels

(c)The closure of resting Na+ channels

(d)Rapid inactivation of voltage-gated K+ channels

The period when it is difficult to initiate another action potential for several milliseconds due to voltage-gated sodium channel inactivation is referred to as the:

(a)Relative refractory period

(b)Absolute refractory period

(c)Resting period

(d)Hyperpolarization period

In the human central nervous system, Gap junctions are found:

(a)Only between neurons

(b)Only between astrocytes

(c)In both neurons and astrocytes

(d)In all cells

Small molecule transmitters such as acetylcholine are synthesized in:

(a)The nerve terminal

B) The cell body and transported to the nerve terminal

C) Synaptic vesicles

D) Endoplasmic reticulum

Prior to Otto Loewi’s classical experiment, which of the following was not known:

(a)stimulation of the vagus nerve slows the heart

(b)extracts of frog heart, made following vagal nerve stimulation, slow the heart

(c)some acetylcholine effects are similar to those produced by muscarine

(d)vagal nerve stimulation releases a substance which slows the heart

Which of the following is most important in determining if neurotransmission is excitatory or inhibitory?

(a)The structure of the synapse

(b)The neurotransmitter released by the presynaptic neuron

(c)The neurotransmitter receptor

(d)The strength of the stimulus

Benzodiazepines such as Valium allosterically regulate GABA receptors by:

(a)Binding at receptor sites other than the transmitter binding site

(b)Binding at the transmitter (GABA) binding site on the receptor

(c)Blocking the action of the endogenous transmitter

(d)Mimicking the action of the endogenous transmitter

GABA-A receptors are ligand-gated Cl- channels. The equilibrium potential of Cl- is -65 mV. At the neuronal resting membrane potential of -65 mV, GABA binding to the GABA-A receptor would result in the opening the Cl- channel, resulting in:

(a)no net flow of Cl- ions

(b)Cl- inflow and hyperpolarization

(c)Cl- outflow and depolarization

(d)Cl- outflow and hyperpolarization

At the mammalian neuromuscular junction, the released neurotransmitter acts on:

(a)muscarinic receptors

(b)nicotinic receptors

(c)adrenergic receptors

(d)Beta receptors

Neurotransmitters are packaged into synaptic vesicles by:

(a)endocytosis following transmitter release

(b)presynaptic membrane transporters

(c)vesicular transporters

(d)all of the above

. Which of the following are NOT types of ion channels?

Voltage-gated

(a)Ligand-gated

(b)G protein coupled receptor (GPCR)-gated

(c)Leak channels

(d)NONE of the above

NMDA receptors are unique in that their ion channel is:

(a)Ligand-gated

(b)Voltage-gated

(c)Ligand- and voltage-gated ion channels

(d)GPCR-gated

. Which of the following is INCORRECT regarding Catecholamine neurotransmitters

(a)Includes Dopamine, Norepinerphrine, and Epinephrine

(b)Contain a Catechol Ring

(c)Synthesized from Tryptophan

(d)Are produced by neurons whose cell bodies are located in the upper brainstem

The largest and most diverse group of receptors in eukaryotes is:

(a)Ligand gated receptors

(b)Glutamate receptors

(c)G-Protein coupled receptors

(d)Allosteric receptors

The most abundant G-protein coupled receptor in the brain is:

(a)Glutamate receptors

(b)Acetylcholine receptors

(c)Cannabinoid receptors

(d)Dopamine receptors

Which of the following drugs DOES NOT block voltage-gated Na+ channels

(a)Lidocaine

(b)Riluzole

(c)Reserpine

(d)Tetrodotoxin

Sarin, a nerve gas, exerts its toxicity by:

(a)blocking nicotinic receptors

(b)inhibiting choline acetyltransferase

(c)inhibiting acetylcholinesterase

(d)inhibiting voltage-gated Na+ channels

Botulinum Toxin (BoTox) interferes with transmitter release by:

(a)cleaving protein(s) involved in transmitter release

(b)blocking voltage-gated Ca2+ channels

(c)blocking voltage-gated Na+ channels

(d)blocking voltage-gated K+ channels

Atropine is:

(a)An agonist of the acetylcholine ionotropic receptor

(b)An antagonist of the acetylcholine ionotropic receptor

(c)An agonist of the acetylcholine metabotropic receptor

(d)An antagonist of the acetylcholine metabotropic receptor

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

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