Neuroscience Fundamentals Rehabilitation 4th Edition Lundy Ekman – Test Bank
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Lundy-Ekman: Neuroscience: Fundamentals for Rehabilitation, 4th
Edition
Chapter 3: Synapses and Synaptic Transmission
Test Bank
1. The
second messenger in a second messenger system is a(n):
2. G-protein
3. α
chain of the G-protein
4. Enzyme
inside the neuron that can trigger responses within the neuron
5. Neurotransmitter
6. Gene
ANS: C
Rationale: The G-protein–mediated second-messenger system involves:
(1) binding of a neurotransmitter (first messenger) to a G-protein–associated
membrane receptor; (2) activation of an effector enzyme (second messenger); (3)
increased levels of the second messenger that elicits responses within the
neuron.
2. Second
messengers may initiate the:
3. Opening
of membrane ion channels
4. Activation
of genes, causing increased synthesis of specific cellular products
5. Modulation
of Ca+2 levels inside the cell
6. A, B,
and C
7. None
of the above
ANS: D
Rationale: Second messengers activate responses inside the cell.
In these cases, a single neurotransmitter might turn on a molecular pathway
that ends with a change in gene expression, the opening of ion channels, and/or
phosphorylation of a structural protein.
3. Which
one of the following can serve as the postsynaptic cell of a synapse?
4. Smooth
muscle cell in an artery
5. Hepatocyte
in the liver
6. Neuron
in the thalamus
7. Muscle
cell in the triceps
8. All
of the above
ANS: E
Rationale: A postsynaptic cell is any cell of an organ, gland,
blood vessel, neuron, or muscle cell that synapses with a neuron.
4. ACh
receptor subtypes include:
5. Adrenergic
and noradrenergic
6. Nicotinic
and muscarinic
7. Alpha
and beta
8. Alpha
and gamma
9. None
of the above
ANS: B
Rationale: Receptors that bind ACh fall into two categories:
nicotinic and muscarinic. These receptors are distinguished by their ability to
bind certain drugs. Nicotine, derived from tobacco, selectively activates the
nicotinic receptors. Muscarine, a poison derived from mushrooms, activates only
the muscarinic receptors.
5. How
does onabotulinumtoxinA (BOTOX) therapeutically produce paresis in overactive
muscles?
6. Acts
as an antagonist by binding to the ACh receptor on the postsynaptic membrane.
7. Rapidly
degrades ACh in the synaptic cleft.
8. Facilitates
the reuptake and sequestration of ACh into the presynaptic cell.
9. Disrupts
the protein structure of the muscle cell receptor, thus preventing ACh from
binding.
10. Inhibits
the release of ACh from the presynaptic terminal at the neuromuscular junction.
ANS: E
Rationale: Botulinum toxin is naturally produced by a family of
bacteria and, when ingested, causes widespread paralysis by inhibiting the
release of ACh at the neuromuscular junction. When small doses of BOTOX are
therapeutically injected directly into an overactive muscle, the inhibition of
ACh release reduces or prevents contraction of the injected muscle.
6. N-methyl-D-aspartate
(NMDA) receptors:
7. Are
involved in long-term potentiation.
8. Bind
glutamate.
9. Have
been implicated in pathologic changes in the nervous system.
10. A, B,
and C
11. None
of the above
ANS: D
Rationale: The ligand-gated ion channels that bind glutamate are
alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate, and
NMDA receptors. The NMDA receptor is unique because glutamate must be bound to
the receptor and, simultaneously, the membrane must depolarize to open the ion
channel. Thus the NMDA receptor is both voltage- and ligand-gated. Activation
of an NMDA receptor causes the associated channel to open and close very
slowly, resulting in prolonged ionic changes inside the postsynaptic neuron.
This produces long-term potentiation (LTP), a prolonged increase in the size of
the postsynaptic response to a given stimulus. Abnormal NMDA receptor activity
has been implicated in epilepsy, chronic pain, Parkinson’s disease, stroke, and
schizophrenia
7. Myasthenia
gravis:
8. Is
caused by the destruction of gamma-aminobutyric acid (GABA) receptors on the
postsynaptic membrane of muscles.
9. Results
in the decreased release of ACh at the neuromuscular junction.
10. Is an
autoimmune disease that destroys ACh receptors on the postsynaptic membrane of
muscles, thus interferes with ACh binding for repetitive muscle contractions.
11. Is
successfully treated with removal of the pituitary gland.
12. All
of the above
ANS: C
Rationale: Myasthenia gravis is an autoimmune disease during
which antibodies attack and destroy nicotinic receptors on muscle cells. Normal
amounts of ACh are released into the cleft, but few receptors are available for
binding, resulting in increasing weakness with repetitive muscle contractions.
8. Which
of the following is a type of synaptic connection between neurons?
9. Axosomatic
10. Axoaxonic
11. Axodendritic
12. All
of the above
ANS: D
Rationale: Synapses can exist between (1) the axon of a
presynaptic neuron and the cell body of a postsynaptic neuron (axosomatic); (2)
the axon of a presynaptic neuron and the dendrites of a postsynaptic neuron
(axodendritic); and (3) the axon of a presynaptic neuron and the axon of a
postsynaptic neuron (axoaxonic).
9. Which
one of the following is the first step in the sequence of actions in the
G-protein receptor activity cycle?
10. α
chain activates a target protein.
11. Neurotransmitter
binds with receptor.
12. Membrane
channels open, or intracellular target proteins are activated.
13. Receptor
protein changes shape.
ANS: B
Rationale: The G-protein receptor activation cycle consists of
the following steps: (1) neurotransmitter binds to the G-protein; (2) receptor
protein changes shape; (3) G-protein subunits break free as cytoplasmic
shuttling units; (4) subunits bind to the membrane ion channel; (5) ion channel
changes shape; and 6) subunits deactivate and reassociate with the G-protein
receptor.
10. When
an action potential arrives at the presynaptic terminal:
11. Voltage-gated
calcium channels are activated.
12. Intracellular
calcium stores are released.
13. Synaptic
vesicles fuse to the membrane of the soma.
14. Calcium
is actively transported out of the neuron terminal.
15. A, B,
and D
ANS: B
Rationale: Arrival of an action potential at the presynaptic
terminal triggers the opening of voltage-gated calcium channels. This results
in an influx of calcium into the neuron terminal and triggers the movement of
synaptic vesicles toward release sites. The synaptic vesicles fuse with the
presynaptic membrane and release neurotransmitters into the synaptic cleft.
11. The
binding of ACh at the neuromuscular junction results in:
12. An
inhibitory postsynaptic potential.
13. Presynaptic
facilitation.
14. Presynaptic
inhibition.
15. An
excitatory postsynaptic potential.
ANS: D
Rationale: The binding of ACh at the neuromuscular junction
results in the opening of Na+ channels
and depolarization of the postsynaptic cell membrane. This is an example of an
excitatory postsynaptic potential. In contrast, an inhibitory postsynaptic
potential results in the opening of potassium and chloride ion channels and
hyperpolarization of the postsynaptic cell membrane. Presynaptic facilitation
and inhibition refer to the amount of neurotransmitter released into the
synapse.
12. Neurotransmitters
that act ________ are classified as ________, whereas neurotransmitters that
act ________are classified as ________.
13. Directly;
slow-acting; indirectly; fast-acting
14. Directly;
inhibitory; indirectly; excitatory
15. Directly;
fast-acting; indirectly; slow-acting
16. Directly;
excitatory; indirectly; inhibitory
ANS: C
Rationale: Neurotransmitters act either directly, by activating
ion channels (ionotropic); or indirectly, by activating postsynaptic neuron
proteins (metabotropic). Direct-acting neurotransmitters are classified as
fast-acting, because their effects last less than 1/1000 of a second. Indirect
acting neurotransmitters are classified as slow-acting, because their effects
require 1/10 of a second to several minutes.
13. Which
of the following neurotransmitters is paired with its correct description?
14. Glutamate;
excitatory transmitter, is important in learning and development.
15. Dopamine;
inhibitory transmitter, increases attention to sensory information.
16. GABA;
excitatory transmitter, modulates neural activity in the CNS.
17. Acetylcholine;
excitatory transmitter, affects mood, arousal, and pain perception.
18. Both
A and C
ANS: A
Rationale: Glutamate is the principle excitatory transmitter of
the CNS and is important in eliciting the neural changes associated with
learning and development. Dopamine is an excitatory neurotransmitter that
affects motor activity, cognition, pleasure, and reward behavior. GABA is the
principle inhibitory transmitter in the CNS, preventing neural overactivity,
particularly in the spinal cord. Acetylcholine is the major neurotransmitter in
the peripheral nervous system (PNS), regulating the control of movement and
autonomic function. In the CNS, ACh is involved in the selection of objects for
attention.
14. Substance
P is an example of a(n):
15. Amino
acid transmitter.
16. Amine
transmitter.
17. Peptide
transmitter.
18. Histamine
transmitter.
ANS: C
Rationale: Substance P, calcitonin gene–related peptide,
galanin, and opioids, are examples of neuroactive peptide transmitters.
Examples of amino acid transmitters include glutamate, glycine, and GABA.
Dopamine, norepinephrine, serotonin, and histamine are examples of amine
transmitters.
15. Which
of the following is associated with post-traumatic stress disorder?
16. Elevated
serotonin levels
17. Reduced
dopamine reuptake
18. Hyperactivity
of the norepinephrine system
19. All
of the above
ANS: C
Rationale: Norepinephrine is a critical mediator of attention
and arousal. Overactivity of the norepinephrine system contributes to panic and
post-traumatic stress disorder.
16. Which
of the following neurotransmitters and modulators are implicated in pain
perception?
17. Opioid
peptides
18. Substance
P
19. Dopamine
20. Both
A and B
21. All
of the above
ANS: D
Rationale: Opioid peptides and substance P are linked to pain
perception and modulation.
17. Receptor
tyrosine kinases:
18. Act
through second messenger systems.
19. Are
usually activated by neuropeptides or hormones.
20. Function
through phosphorylation of tyrosine.
21. Both
A and C
22. All
of the above
ANS: E
Rationale: Tyrosine kinsase receptors act through second
messenger systems and are typically activated by neuropeptides or hormones.
These receptors are named for an intracellular site that alters its properties
by adding phosphate groups to tyrosine when extracellular ligand binding
occurs. This phosphorylation activates downstream molecules, initiating a
signalling cascade.
18. Receptor
activity is regulated by:
19. Decreasing
the number of receptors through internalization.
20. Decreasing
the number of available receptors through inactivation.
21. Increasing
the number of active receptors.
22. Both
A and B
23. All
of the above
ANS: E
Rationale: Cells can regulate receptor activity by decreasing
the number of receptors through internalization, decreasing the number of
functional receptors through inactivation, or increasing the number of active
receptors in response to low neurotransmitter levels or infrequent receptor
activation.
19. Which
one of the following is used to treat myasthenia gravis?
20. Medications
that inhibit the breakdown of acetylcholine
21. Medications
that activate the immune system
22. Removal
of the pancreas, which contributes to receptor damage
23. Frequent
blood transfusions to prevent anemia
24. All
of the above
ANS: A
Rationale: Treatment of myasthenia gravis commonly involves
medications that inhibit the breakdown of acetylcholine, immunosuppressant
medications, removal of the thymus gland, and/or plasmapheresis to filter and
replace plasma.
20. An
antagonist drug acts by:
21. Preventing
the release of a neurotransmitter.
22. Binding
to a receptor to facilitate the effect of a neurotransmitter.
23. Elevating
neurotransmitter levels in the synaptic cleft.
24. Increasing
the number of active receptors on a cell membrane.
ANS: A
Rationale: Antagonist drugs act by preventing neurotransmitter
release or by binding to a receptor and impeding the effects of a naturally
occurring transmitter.
Lundy-Ekman: Neuroscience: Fundamentals for Rehabilitation, 4th
Edition
Chapter 4: Neuroplasticity
Test Bank
1. Neurons
that are deprived of oxygen for a prolonged period:
2. Release
glycine, which inhibits the postsynaptic neurons and prevents neural function
even in neurons not directly affected by the oxygen deprivation.
3. Become
inactive and slowly regenerate.
4. Release
glutamate, which causes overexcitation of the surrounding neurons.
5. A, B,
and C
6. None
of the above
ANS: C
Rationale: When a person suffers a stroke or traumatic injury,
neurons in the brain that are deprived of oxygen for a prolonged period die and
do not regenerate. Oxygen-deprived neurons release large quantities of
glutamate, an excitatory neurotransmitter, from their axon terminals.
2. Excitotoxicity
begins with:
3. Excessive
production of lactic acid.
4. Destruction
of cellular proteins.
5. Cellular
edema.
6. Persistent
binding of glutamate to N-methyl-D-aspartate (NMDA)–type receptors in the
postsynaptic cell membrane.
7. Interference
of mitochondria functions.
ANS: D
Rationale: First, glutamate binds persistently to the NMDA-type
glutamate receptor in the cell membrane. Stimulation of this receptor results
in an influx of calcium ions (Ca+2)
into the cell, and indirectly facilitates the release of internal Ca+2 stores.
An influx of sodium ions (Na+)
into the cell results in further stimulation of NMDA receptors and an additional
influx of Ca+2 into the cell. Channels that are permeable to Ca+2 open
because of the injury. With the increase in Ca+2 inside
the cell, more potassium ions (K+)
diffuse out of the cell, requiring increased glycolysis that provides energy
for the Na+/K+ pump to actively transport K+ into
the cell. Together, the increased glycolysis and the increased Ca+2 lead
to several destructive consequences for neurons.
3. Cellular
effects of excitotoxicity include:
4. Excessive
production of lactic acid.
5. Destruction
of cellular proteins.
6. Cellular
edema.
7. Interference
of mitochondria functions.
8. All
of the above
ANS: E
Rationale: Excitotoxicity causes excessive production of lactic
acid, destroys cellular proteins, causes cellular edema, and interferes with
the function of mitochondria.
4. Which
one of the following types of memory is affected by an injury to the
hippocampus?
5. Memory
of how to ride a bicycle
6. Memory
of names and events
7. Memory
of how to tie shoe laces
8. Both
A and B
9. A, B,
and C
ANS: B
Rationale: The hippocampus, located in the temporal lobe, is
essential for processing memories that are easily verbalized. For example, the
hippocampus is important in remembering names and events (declarative memory)
but not in remembering how to perform motor acts (procedural memory; riding a
bicycle and tying shoe laces are examples of procedural memory).
5. In
the mature central nervous system (CNS), axonal regeneration is impeded by
which of the following?
6. Glial
scar formation
7. Absence
of neural growth factor
8. Release
of growth inhibiting factors
9. Both
A and B
10. A, B,
and C
ANS: E
Rationale: Development of glial scars, limited expression or
complete absence of nerve growth factor (NGF), and growth inhibiting factors
prevent functional axonal regeneration in the brain and spinal cord.
6. Constraint-induced
movement after a stroke requires which one of the following?
7. Immobilization
of the affected upper extremity (UE) to control spasticity
8. Repetitive
closed-chain resistance training
9. Aggressive
range of motion and exercise within 12 hours after a stroke
10. Repetitive,
task-specific functional movements of only the affected UE
11. Weight
bearing and prolonged stretching of the affected UE
ANS: D
Rationale: Constraint-induced movement is one type of
task-specific training used in individuals with chronic dysfunction resulting
from a stroke. In this technique, use of the unaffected UE is constrained by a
sling. The patient then undergoes intense practice of functional movements with
the affected UE.
7. Learning
an individual’s name requires:
8. Sprouting
9. LTP
10. Habituation
11. Central
chromatolysis
ANS: B
Rationale: Experience-dependent plasticity requires the
synthesis of new proteins, the growth of new synapses, and the modification of
existing synapses. With repetition of a specific stimulus or the paring of
presynaptic and postsynaptic firing, the synthesis and activation of proteins
alter the neuron’s excitability and promote or inhibit the growth of new
synapses, especially at dendritic spines. Several mechanisms of experience-dependent
plasticity occur, depending on the type of synapse and location involved; LTP
is one of these mechanisms.
8. Experience-dependent
plasticity is also referred to as which of the following?
9. Use-dependent
plasticity
10. Activity-dependent
plasticity
11. Habituation
12. Both
A and B
ANS: D
Rationale: Experience-dependent plasticity is also referred to
as use-dependent or activity-dependent plasticity.
9. After
learning how to play the violin:
10. Large,
diffuse regions of the brain show increased activity.
11. Small,
distinct regions of the brain show increased activity.
12. Small,
distinct regions of the brain show increased activity while playing the flute.
13. None
of the above
ANS: B
Rationale: With repetition of a task, a reduction in the number
of active regions occurs in the brain. Eventually, when a motor task is
learned, only small, distinct regions of the brain show increased activity when
performing the task. For example, learning to play a musical instrument
requires numerous brain regions. As skill increases, fewer areas are activated
because less attention is required, motor control is optimized, and only the
brain areas required to perform the task efficiently are active. Eventually,
playing the instrument requires only a few small, specific regions.
10. Which
one of the following processes contributes to experience-dependent plasticity?
11. Synthesis
of new proteins
12. Growth
of new synapses
13. Modification
of existing synapses
14. A, B,
and C
ANS: D
Rationale: Experience-dependent plasticity requires the synthesis
of new proteins, the growth of new synapses, and the modification of existing
synapses.
11. Long-term
depression (LTD) is due to which of the following?
12. Conversion
of silent synapses to active synapses
13. Removal
of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors
from the postsynaptic membrane
14. Addition
of dopamine receptors to the presynaptic membrane
15. Pairing
of presynaptic and postsynaptic firing
ANS: B
Rationale: LTD is the conversion of an active synapse to a
silent synapse by the removal of AMPA receptors from the membrane into the
cytoplasm.
12. Which
one of the following externally applied devices is capable of enhancing or
inhibiting motor learning and memory formation?
13. Transcranial
magnetic stimulation (TMS)
14. Magnetic
resonance imaging (MRI)
15. Functional
magnetic resonance imaging (fMRI)
16. Computed
tomography (CT)
ANS: A
Rationale: TMS to the motor cortex and other brain areas
involved in motor learning can either enhance or inhibit motor learning and
memory formation, depending on the frequency and experimental protocol used.
For example, TMS of the primary motor cortex enhances the duration of motor
memory, and stimulation of the dorsal premotor cortex enhances motor memory
consolidation. TMS is also used to induce a transient “virtual lesion” to
assess the impact different brain areas have on motor learning. For example,
inhibitory TMS applied to the primary somatosensory cortex impairs motor
learning. Magnetic stimulation of the brain is thought to induce synaptic
plasticity via LTP- or LTD-type mechanisms.
13. Astrocytes
may impact synaptic plasticity by:
14. Modulating
neurotransmitter release
15. Modulating
postsynaptic receptor expression
16. Modulating
new synapse formation
17. All
of the above
ANS: D
Rationale: Astrocytes influence synaptic plasticity through
modulating neurotransmitter release and receptor expression at the postsynaptic
membrane. Astrocytes may also be important for new synapse formation after a
stroke.
14. Functional
regeneration of axons occurs more frequently in the peripheral nervous system
(PNS) than in the CNS because of the:
15. Production
of nerve growth factor (NGF).
16. Effective
clearing of debris.
17. Formation
of bands of Büngner.
18. All
of the above
ANS: D
Rationale: Functional regeneration of axons occurs more
frequently in the PNS than in the CNS, because Schwann cells produce nerve
growth factor, debris is effectively cleared away from the site of injury, and
the bands of Büngner form to guide axonal regrowth to the target.
15. Which
of the following rehabilitation mechanisms promotes beneficial neural
plasticity?
16. Task-specific
practice
17. Early
initiation of rehabilitation
18. Bed
rest
19. Both
A and B
ANS: D
Rationale: Conclusive evidence indicates that early
rehabilitation is key to improved recovery, whereas delayed rehabilitation
reduces the impact of therapy. Task-specific practice is essential for motor
learning because task-specific practice produces long-lasting cortical
reorganization in the brain areas activated. Bed rest promotes harmful neural
plasticity.
16. Neurogenesis
is defined as the:
17. Release
of NGF to stimulate axonal regeneration.
18. Addition
of AMPA receptors to the postsynaptic membrane.
19. Ability
of stem cells to create new neurons in the brain.
20. None
of the above
ANS: C
Rationale: Stem cells in the adult human brain are capable of
creating new neurons. Stem cells are suspected to be involved in brain
remodelling after a neurologic injury, including stroke and traumatic brain
injury, and neurodegenerative disease.
17. Which
one of the following rehabilitation mechanisms promotes neural plasticity?
18. Task-specific
practice
19. Early
initiation of rehabilitation
20. Bed
rest
21. Both
A and B
ANS: D
Rationale: Conclusive evidence indicates that early
rehabilitation is key to improved recovery, whereas delayed rehabilitation
reduces the impact of therapy. Task-specific practice is essential for motor
learning, as opposed to traditional stroke rehabilitation, which produces
long-lasting cortical reorganization in the brain areas activated.
18. Which
one of the following statements about constraint-induced movement therapy
(CIMT) is true?
19. CIMT
results in functional reorganization of the cortex.
20. CIMT
should be initiated within 5 days after the onset of stroke.
21. CIMT
involves the constraint of the unaffected UE and intense task-related practice
of the affected UE.
22. Both
A and C
ANS: D
Rationale: Constraint-induced movement is one type of
task-specific training used in individuals with chronic dysfunction resulting
from a stroke. In this technique, the use of the unaffected UE is constrained
by a sling. The patient then undergoes intense practice of functional movements
with the affected UE. CIMT appears to induce functional reorganization of the
cortex in individuals with stroke.
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