Neurobiology Flashcards
Chromatin condensation and fragmentation, dilation and
blebbing of the nuclear membrane, and cellular shrinkage
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
Cellular injury, including
DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis
Apoptosis is a form of cell death that serves to eliminate unwanted host cells through preprogrammed mechanisms
that result in gene expression and controlled cell death. Apoptosis can be activated by both internal and external
stimuli and is characterized by a complex cascade of events that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products lmown as caspases. Two major pathways of caspase-dependent apoptosis have been identified.
One pathway is initiated by the formation of a death-inducing cell surface receptor
signaling complex (e.g., Fas), leading to aggrega tion and activation of caspase 8. A second pathway is triggered by
intracellular stress, such as DNA damage , and is primarily associated with the activation of caspase 9. During this latter
pathway, Signals received by the mitochondria (e.g., after DNA injury) stimulate the release of a variety of proapoptotic
molecules, including cytochrome c. Release of cytochrome c induces formation of the apoptosome, a muitiprotein
complex composed of APAF-I, caspase 9, cytochrome c , and ATP. This, in turn, leads to activa tion of caspase 9 via
allosteric regulation by APAF-I. Once activated, the initiator caspases, caspases 8 and 9, activate downstream caspases,
such as J and 7, by cleavage . These downstream effector caspases, in turn, cleave multiple cellular proteins, triggering a range of apopto tic events such as nuclear membrane blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response).
Mobilizes the immune system
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
Cellular injury, including
DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis.
Apoptosis is a form of cell death that serves to eliminate
unwanted host cells through preprogrammed mechanisms
that result in gene expression and controlled cell death.
Apoptosis can be activated by both internal and external
stimuli and is characterized by a complex cascade of events
that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products lmown
as caspases. Two major pathways of caspase-dependent
apoptosis have been identified. One pathway is initiated
by the formation of a death-inducing cell surface receptor
signaling complex (e.g., Fas), leading to aggrega tion and
activation of caspase 8. A second pathway is triggered by
intracellular stress, such as DNA damage , and is primarily
associated with the activation of caspase 9. During this latter
pathway, Signals received by the mitochondria (e.g., after
DNA injury) stimulate the release of a variety of proapoptotic
molecules, including cytochrome c. Release of cytochrome
c induces formation of the apoptosome, a muitiprotein
complex composed of APAF-I, caspase 9, cytochrome c , and
ATP. This, in turn, leads to activa tion of caspase 9 via
allosteric regulation by APAF-I. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as J and 7, by cleavage . These downstream effector
caspases, in turn, cleave multiple cellular proteins, triggering a range of apopto tic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response).
The mechanism of cell death after radiation therapy
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
A. Apoptosis
B. Necrosis
**C. Both **
D. None of the above
Cellular injury, including
DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis.
Apoptosis is a form of cell death that serves to eliminate
unwanted host cells through preprogrammed mechanisms
that result in gene expression and controlled cell death.
Apoptosis can be activated by both internal and external
stimuli and is characterized by a complex cascade of events
that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products lmown
as caspases. Two major pathways of caspase-dependent
apoptosis have been identified. One pathway is initiated
by the formation of a death-inducing cell surface receptor
signaling complex (e.g., Fas), leading to aggrega tion and
activation of caspase 8. A second pathway is triggered by
intracellular stress, such as DNA damage , and is primarily
associated with the activation of caspase 9. During this latter
pathway, Signals received by the mitochondria (e.g., after
DNA injury) stimulate the release of a variety of proapoptotic
molecules, including cytochrome c. Release of cytochrome
c induces formation of the apoptosome, a muitiprotein
complex composed of APAF-I, caspase 9, cytochrome c , and
ATP. This, in turn, leads to activa tion of caspase 9 via
allosteric regulation by APAF-I. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as J and 7, by cleavage . These downstream effector
caspases, in turn, cleave multiple cellular proteins, triggering a range of apopto tic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response).
Type of cell death detected by the annexin V/propidium
iodide assay
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
A. Apoptosis
B. Necrosis
**C. Both **
D. None of the above
Cellular injury, including
DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis.
Apoptosis is a form of cell death that serves to eliminate
unwanted host cells through preprogrammed mechanisms
that result in gene expression and controlled cell death.
Apoptosis can be activated by both internal and external
stimuli and is characterized by a complex cascade of events
that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products lmown
as caspases. Two major pathways of caspase-dependent
apoptosis have been identified. One pathway is initiated
by the formation of a death-inducing cell surface receptor
signaling complex (e.g., Fas), leading to aggrega tion and
activation of caspase 8. A second pathway is triggered by
intracellular stress, such as DNA damage , and is primarily
associated with the activation of caspase 9. During this latter
pathway, Signals received by the mitochondria (e.g., after
DNA injury) stimulate the release of a variety of proapoptotic
molecules, including cytochrome c. Release of cytochrome
c induces formation of the apoptosome, a muitiprotein
complex composed of APAF-I, caspase 9, cytochrome c , and
ATP. This, in turn, leads to activa tion of caspase 9 via
allosteric regulation by APAF-I. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as J and 7, by cleavage . These downstream effector
caspases, in turn, cleave multiple cellular proteins, triggering a range of apopto tic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response).
Pharmacologic strategies that inhibit caspase 8 may decrease this form of cell death
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
**A. Apoptosis **
B. Necrosis
C. Both
D. None of the above
Cellular injury, including
DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis.
Apoptosis is a form of cell death that serves to eliminate
unwanted host cells through preprogrammed mechanisms
that result in gene expression and controlled cell death.
Apoptosis can be activated by both internal and external
stimuli and is characterized by a complex cascade of events
that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products lmown
as caspases. Two major pathways of caspase-dependent
apoptosis have been identified. One pathway is initiated
by the formation of a death-inducing cell surface receptor
signaling complex (e.g., Fas), leading to aggrega tion and
activation of caspase 8. A second pathway is triggered by
intracellular stress, such as DNA damage , and is primarily
associated with the activation of caspase 9. During this latter
pathway, Signals received by the mitochondria (e.g., after
DNA injury) stimulate the release of a variety of proapoptotic
molecules, including cytochrome c. Release of cytochrome
c induces formation of the apoptosome, a muitiprotein
complex composed of APAF-I, caspase 9, cytochrome c , and
ATP. This, in turn, leads to activa tion of caspase 9 via
allosteric regulation by APAF-I. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as J and 7, by cleavage . These downstream effector
caspases, in turn, cleave multiple cellular proteins, triggering a range of apopto tic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response).
Rapid cell lysis
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
A. Apoptosis
**B. Necrosis **
C. Both
D. None of the above
Cellular injury, including
DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis.
Apoptosis is a form of cell death that serves to eliminate
unwanted host cells through preprogrammed mechanisms
that result in gene expression and controlled cell death.
Apoptosis can be activated by both internal and external
stimuli and is characterized by a complex cascade of events
that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products lmown
as caspases. Two major pathways of caspase-dependent
apoptosis have been identified. One pathway is initiated
by the formation of a death-inducing cell surface receptor
signaling complex (e.g., Fas), leading to aggrega tion and
activation of caspase 8. A second pathway is triggered by
intracellular stress, such as DNA damage , and is primarily
associated with the activation of caspase 9. During this latter
pathway, Signals received by the mitochondria (e.g., after
DNA injury) stimulate the release of a variety of proapoptotic
molecules, including cytochrome c. Release of cytochrome
c induces formation of the apoptosome, a muitiprotein
complex composed of APAF-I, caspase 9, cytochrome c , and
ATP. This, in turn, leads to activa tion of caspase 9 via
allosteric regulation by APAF-I. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as J and 7, by cleavage . These downstream effector
caspases, in turn, cleave multiple cellular proteins, triggering a range of apopto tic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response).
Translocation of phosphatidylserine to the outer plasma membrane is an early characteristic of this mode of cell death
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
**A. Apoptosis **
B. Necrosis
C. Both
D. None of the above
Cellular injury, including
DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis.
Apoptosis is a form of cell death that serves to eliminate
unwanted host cells through preprogrammed mechanisms
that result in gene expression and controlled cell death.
Apoptosis can be activated by both internal and external
stimuli and is characterized by a complex cascade of events
that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products lmown
as caspases. Two major pathways of caspase-dependent
apoptosis have been identified. One pathway is initiated
by the formation of a death-inducing cell surface receptor
signaling complex (e.g., Fas), leading to aggrega tion and
activation of caspase 8. A second pathway is triggered by
intracellular stress, such as DNA damage , and is primarily
associated with the activation of caspase 9. During this latter
pathway, Signals received by the mitochondria (e.g., after
DNA injury) stimulate the release of a variety of proapoptotic
molecules, including cytochrome c. Release of cytochrome
c induces formation of the apoptosome, a muitiprotein
complex composed of APAF-I, caspase 9, cytochrome c , and
ATP. This, in turn, leads to activa tion of caspase 9 via
allosteric regulation by APAF-I. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as J and 7, by cleavage . These downstream effector
caspases, in turn, cleave multiple cellular proteins, triggering a range of apopto tic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response).
DNA ladder formation on gel electrophoresis
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
**A. Apoptosis **
B. Necrosis
C. Both
D. None of the above
Cellular injury, including
DNA damage induced by radiation or certain chemotherapeutic drugs, can result in either necrosis or apoptosis.
Apoptosis is a form of cell death that serves to eliminate
unwanted host cells through preprogrammed mechanisms
that result in gene expression and controlled cell death.
Apoptosis can be activated by both internal and external
stimuli and is characterized by a complex cascade of events
that occur within a cell, involving the activation of both upstream (initiator) and downstream (effector) products lmown
as caspases. Two major pathways of caspase-dependent
apoptosis have been identified. One pathway is initiated
by the formation of a death-inducing cell surface receptor
signaling complex (e.g., Fas), leading to aggrega tion and
activation of caspase 8. A second pathway is triggered by
intracellular stress, such as DNA damage , and is primarily
associated with the activation of caspase 9. During this latter
pathway, Signals received by the mitochondria (e.g., after
DNA injury) stimulate the release of a variety of proapoptotic
molecules, including cytochrome c. Release of cytochrome
c induces formation of the apoptosome, a muitiprotein
complex composed of APAF-I, caspase 9, cytochrome c , and
ATP. This, in turn, leads to activa tion of caspase 9 via
allosteric regulation by APAF-I. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as J and 7, by cleavage . These downstream effector
caspases, in turn, cleave multiple cellular proteins, triggering a range of apopto tic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phagocytosis (avoiding an inflammatory response).
Which of the following ion channels is partly responsible for carrying current during the repolarization phase in cochlear hair cells?
A. Na+channel
B. Ca2+channel
C. Ca2+-sensitive K+channel
D. Cl- channel
E. Mg2+channel
A. Na+channel
B. Ca2+channel
**C. Ca2+-sensitive K+channel **
D. Cl- channel
E. Mg2+channel
The origin of electrical resonance during hearing
has been determined by recording isolated hair cells using
voltage-clamp techniques. A positive deflection of the hair
bundle or injection of current into the cell with a micro-
CHAPTER 1
Neurobiology Answers
electrode allows Ie influx into the cell and depolarization. 2
Depolarization opens voltage-sensitive Ca +channels, which 2
augments depolarization by allOWing Ca + entry into the 22
cell. As Ca +accumulates in the cytoplasm, it activates Ca +- sensitive K+ channels, which along with voltage-sensitive W channels allow for W efflux and repolarization of hair cells (Kandel, pp. 620- 622).
Which of the following causes an increase in decerebrate rigidity?
A. Sectioning the dorsal roots
B. Chemically inactivating the lateral vestibular nucleus
C. Sectioning the y motor neurons
D. Activating the medullary reticular formation
E. Destruction of the flocculonodular lobe of the cerebellum
A. Sectioning the dorsal roots
B. Chemically inactivating the lateral vestibular nucleus
C. Sectioning the y motor neurons
D. Activating the medullary reticular formation
E. Destruction of the flocculonodular lobe of the cerebellum
Decerebrate rigidity occurs following isolation of the
brainstem from more rostral regions of the brain. This was
demonstrated in animals that underwent surgical transection
between the superior and inferior colliculi, which
resulted in hyperreflexia and increased extensor tone due to
loss of descending inhibitory tracts. Transection results in
disruption of at least three key descending pathways. First,
the lateral vestibular nucleus and pontine reticular formation
are released from the inhibitory control of the cerebral
cortex, which facilitates extensor motor neurons of the arms
and legs. Second, projections from the red nucleus to the
spinal cord are disrupted; these normally inhibit extensor
motor neurons of the arms and legs. And last, the medullary
reticular formation, which also inhibits extensor tone, is
inoperative because of the loss of excitatory input from
the cerebral cortex. The net effect is profound facilitation
of extensor motor neurons of the arms and legs by the lateral
vestibular nuclei and pontine reticular formation.
Destruction of the vestibulocerebellum (flocculonodular
lobe) also increases contraction of tonic extensors by releasing
the lateral vestibular nucleus from tonic inhibition,
which facilitates extensor motor neurons of the arms and
legs. Sectioning the dorsal roots, chemically inactivating the
lateral vestibular nucleus, acute injury in the thoracic spine,
and sectioning of the ‘Y motor neurons all decrease decerebrate
rigidity.
Patients with significant brain injury above the level of the
red nucleus (or at its rostral margin) exhibit a postural state
called decorticate rigidity, characterized by contraction of
extensors in the legs and flexors of the arms. One reason for
this is that the rubrospinal tract in humans projects only
as far as the cervical spine, which may counteract vestibulospinal
facilitation of ann extensors but not leg extensors
Neurotransmitter release at the synaptic terminal is triggered mainly by which ion?
A. Na+
B. W
C. CJ
D. Ca 2+
E. Mg2+
A. Na+
B. W
C. CJ
**D. Ca 2+ **
E. Mg2+
The quantal release of neurotransmitter by synaptic
vesicles occurs by a specialized method of exocytosis at the
active zones of the presynaptic terminal requiring calcium.
Synaptic vesicles are bound to cytoskeletal elements near
the active zone by synapsins. With depolarization, calcium/
calmodulin-dependent protein kinase phosphorylates these
synapsin proteins, resulting in the release of the synaptic
vesicle (Kandel, pp. 262-274).
Which of the following would hyperpolarize a resting neuron?
A. Increase in Cl- conductance
B. Increase in Na+ conductance
C. Increase in Ca2 + conductance
D. Decrease in Ic+ conductance
E. Increase in Ic+ conductance
A. Increase in Cl- conductance
B. Increase in Na+ conductance
C. Increase in Ca2 + conductance
D. Decrease in Ic+ conductance
E. Increase in Ic+ conductance
A typical neuron has a resting membrane potential of
-65 mV. The equilibrium potential for W is -86 mV, and an
increase in conductance of this ion would result in movement of the neurons membrane potential toward -86 mV
and hyperpolarization. The Eel (-66 mV) is very similar to
the resting membrane potential of a neuron (-65 mV), and
an increase in conductance of this anion would not result
in any drastic change in the resting membrane potential of
a cell. Increasing Na+ and Ca2
+ conductance would lead to
depolarization of the neuron instead of hyperpolarization
(Kandel, pp. 150-170).
Which of the following would increase conduction velocity in an axon?
1. Increasing the diameter of an axon
2. Increasing the transmembrane resistance (Rm)
3. Decreasing the capacitance of the membrane (C”,)
4. Decreasing the membrane length constant (Ie)
A. 1, 2, and3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above
**A. 1, 2, and 3 are correct **
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above
How rapidly an action potential travels through an
axon depends on a number of factors, including the internal
resistance of an axon (R;), the transmembrane resistance of
the plasma membrane (Rm), (inversely related to the number
ofion channels), and membrane capacitance (CnJ To better
understand the relationship between these properties, we
can use the analogy of a leaky straw. There are two paths that
the water can take: one, down the inside of the straw, and the
other, through the leaky holes along the straw. How much
water flows along each of these paths depends on the relative
resistance of each of these pathways, as most of the water
will tend to go down the path of least resistance. The same principles apply to current flowing down an axon. The current can either continue to flow down the axon or exit the
axon through a leaky plasma membrane (ion channels).
Increasing the diameter of the axon will decrease the R; and
allow the action potential to be conducted down the a.xon
with increased conduction velocity. Increasing the Rm by
myelination facilitates flow down the axon as well, just as
wrapping tape around a leaky straw would also facilitate
water flow down the inside of the straw. The ratio of Rm to R;
is called the membrane length constant (A,) and represents
the distance between the point of peak depolarization produced by Na+ influx and the point where the depolarization
has declined to approximately 37% of peak value. A, indicates
that Na+ current is more likely to spread further along the
axon if the membrane resistance is higher than the cytoplasmic resistance (increasing A,).
In terms of C,m this property indicates how well the plasma
membrane can hold positive and negative charges. Thinner
membranes generally hold charges better than thicker ones
because the electrostatic attraction between ions on opposite sides of the plasma membrane increases with decreased
membrane thiclmess. Therefore thinner a.”Xons with increased
membrane capacitance have decreased conduction velocity
because it takes more time for current traveling down an
axon to change the electrical potential of the adjacent membrane (and continue current propagation down the axon).
The addition of myelin around an axon increases conduction
velocity because it decreases Cm (increases membrane thickness). Decreasing the relative refractory period does not
affect conduction velocity, but decreasing the diameter of
the axon does. In smaller-diameter axons, the resistance of
the axoplasm increases, resulting in decreased conduction
velocity (Kandel, pp. 147-148; Pritchard, pp. 20-22; Bear,
pp. 85- 86).**
Which of the following about the utricle and saccule is
correct?
A. With the head in an upright position, the utricle is oriented vertically on the medial wall of the vestibule
B. They respond to angular acceleration
C. In the utricular macula , the hair cells are arranged with the kinocilium oriented away from the striola
D. The surface of the macula extends into the membranous labyrinth and is bathed in perilymph
E. The tips of the hair cells are covered by the overlying otolithic membrane, which is embedded with calcium carbonate crystals (otoconia)
A. With the head in an upright position, the utricle is oriented vertically on the medial wall of the vestibule
B. They respond to angular acceleration
C. In the utricular macula , the hair cells are arranged with the kinocilium oriented away from the striola
D. The surface of the macula extends into the membranous labyrinth and is bathed in perilymph
E. The tips of the hair cells are covered by the overlying otolithic membrane, which is embedded with calcium carbonate crystals (otoconia)
Refer to Figure 1.14A. The utricle and saccule are
located in the vestibule , a large chamber that separates the
semicircular canals and the cochlea. The sensory epithelia of
the saccule and utricle are called the maculae. Each macula
consists of numerous hair cells surrounded by supporting
cells resting on a connective tissue base. The orderly
arrangement of hair cells within the macula gives the appearance of a curved equatorial line called the striola . In the
utricle, the hair cells are arranged with the kinocilium
oriented toward the striola, whereas in the saccule, the hair
cells are polarized away from the striola. This anatomic
polarity ensures that the two otolith organs can respond to
linear acceleration or head tilt in any direction. The surface
of the macula extends into the membranous labyrinth, which
is bathed in endolymph, not perilymph. The macular surface
is covered with a gelatinous structure, the otolithic membrane, which has calcium carbonate crystals (otoliths or
otoconia) embedded on its surface. Relative movement
between the otolithic membrane and the surface of hair
cells is the essential macular stimulus, since this produces movement (bending) of hair cells, which results in ionic
current flow at the base of hair cells and neurotransmitter
release. ‘With the head in a neutral position , the macula of
the utricle lies in the horizontal plane (011 the floor of the
vestibule) and the macula of the saccule lies in the vertical
plane (on the medial wall of the vestibule). Linear accelera tion
is detected by the maculae, whereas angular acceleration is
detected by the specialized hair cells of the semicircular
canals, called the cristae ampullaris (Kandel, pp. 802-814;
Pritchard, pp. 250-253).
A 52-year-old male underwent subtotal resection of a glioblastoma l11ultiforme originating in the right frontal lobe and extending into the deep nuclei of that hemisphere. Postoperatively, he underwent whole-brain radiation therapy
and received 1, 3-bis-2-chloroethyl-1 nitrosourea (BCNU). The patient succumbed to his disease process 8 months later.
Resistance of this tumor to BCNU may have resulted from
A. A high concentration of 06-alkylguanine-DNA alkyl transferase (06-AGAT) in tumor cells
B. The tumor was in the S phase of the cell cycle (resistant phase) during administration of BCNU
C. The tumor cells lacked topoisomerase II, which causes transient DNA strand breaks during chemotherapy induction
D. The tumor cells lacked cell surface proteins that recognize BCl’-nJ
E. An agent that disrupts the blood-brain barrier was not administered concurrently with BCNU
**A. A high concentration of 06-alkylguanine-DNA alkyl transferase (06-AGAT) in tumor cells **
B. The tumor was in the S phase of the cell cycle (resistant phase) during administration of BCNU
C. The tumor cells lacked topoisomerase II, which causes transient DNA strand breaks during chemotherapy induction
D. The tumor cells lacked cell surface proteins that recognize BCl’-nJ
E. An agent that disrupts the blood-brain barrier was not administered concurrently with BCNU
The nitrosoureas (BCNU, CCNU) are alkylating agents
and are the most widely used drugs for patients with malignant brain tumors. They alkylate DNA in multiple locations,
primarily on guanine but also on adenine and cytosine . The
resultant DNA cross links often produce single- or doublestranded DNA breaks and eventual tumor cell death. 0”-
AGAT is a repair enzyme that mediates repair of alkylation
products of nitrosoureas. It has been noted that approximately 70% of tumors have high levels of O”-AGAT and are
often resistant to nitrosourea chemotherapy (Bernstein,
pp.231- 232).
A 52-year-old male underwent subtotal resection of a glioblastoma l11ultiforme originating in the right frontal
lobe and extending into the deep nuclei of that hemisphere. Postoperatively, he underwent whole-brain radiation therapy and received 1, 3-bis-2-chloroethyl-1-nitrosourea (BCNU).
The patient succumbed to his disease process 8 months later
Which of the following agents could potentially increase response rates to BCl’-HJ chemotherapy?
A. Irinotecan (CPT-ll)
B. Tamoxifen
C. Suramin
D. 0 6-benzylguanine
E. 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCl’-,I1J)
A. Irinotecan (CPT-ll)
B. Tamoxifen
C. Suramin
**D. 0 6-benzylguanine **
E. 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea (CCl’-,I1J)
Attempts to modify resistance to nitrosoureas are
ongoing. As stated in the previous discussion (question 15),
0 6-AGAT mediates the repair of alkylating products of
nitrosoureas. Inhibition of this repair protein has been the
subject of a number of clinical trials using O”-benzylguanine,
a methylating agent. Tamoxifen inhibits protein kinase C,
CPT-II is a topoisomerase I inhibitor, and suramin works by
inhibiting growth factors (FGF, IGF-I, PDGF). These agents
do not modify resistance to alkylating agents. The addition
of CCNU can potentially increase the risk of nitrosoureainduced side effects (Bernstein, pp. 229-332).
Experimental studies using the IISV-tk/GCV suicide gene transfer approach in animal models have shown tUl110r regression and long-term survival in spite of transduction
efficiencies of less than 10%. Successful application of suicide gene cancer therapy in these studies despite incomplete delivery of genetic vector to all tumor cells was ill,ely the result of
A. The transfer of phosphorylated GCV (pGCV) into un transduced tumor cells via gap junctions
B. The ensuing inflammatory reaction produced by the viral vector, resulting in the activation of cell death signaling pathways (Fas/APO-1)
C. The upregulation of p53, which immediately causes release of apoptotic mediators (e.g., caspase 8) from the mitochondria
D. Upregulation of cAMP, a second messenger Imown to halt tumor proliferation in the G1 phase of the cell cycle
E. Transfer of viral vectors into untransduced tumor cells via clathrin-coated pits
**A. The transfer of phosphorylated GCV (pGCV) into un transduced tumor cells via gap junctions **
B. The ensuing inflammatory reaction produced by the viral vector, resulting in the activation of cell death signaling pathways (Fas/APO-1)
C. The upregulation of p53, which immediately causes release of apoptotic mediators (e.g., caspase 8) from the mitochondria
D. Upregulation of cAMP, a second messenger Imown to halt tumor proliferation in the G1 phase of the cell cycle
E. Transfer of viral vectors into untransduced tumor cells via clathrin-coated pits
The mechanism whereby un transduced tumor cells
die during gene therapy is called the “bystander effect. “ Until
recently, this mechanism was poorly understood; it requires
the presence of gap junctions that allow the transfer of
toxic metabolites into untransduced tumor cells. In the ITSVtk/GCV approach, the nucleoside analogue GCV becomes
cytotoxic after being converted to its triphosphorylated
form by I-ISV-tk and host cellular kinases. It acts as a chain
terminator and interrupts DNA synthesis in replicating cells.
Phosphorylated GCV can then be transported into surrounding untransduced cells via gap junctions and induce cell
death . The degree of bystander effect in individual tumors
depends on the cell type and its capability to express gap
junctions, the vector used, and the enzymatic activity of the
therapeutic gene. The other choices have not been shown to
propagate toxicity from transduced to un transduced cells
(Bernstein, pp. 280- 281).
What is the only neurotransmitter synthesized in the
synaptic vesicle ?
A. Dopamine
B. Norepinephrine
C. Acetylcholine
D. Serotonin
E. Substance P
A. Dopamine
**B. Norepinephrine **
C. Acetylcholine
D. Serotonin
E. Substance P
Acetylcholine (Ach) is synthesized from choline
and acetyl-CoA by the enzyme choline acetyltransferase.
ACh is utilized by spinal cord motor neurons at the neuromuscular junction, all preganglionic autonomic neurons,
postganglionic parasympathetic neurons, postganglionic sympathetic neurons to sweat glands, and within the nucleus
basalis of Meynert. ACh is metabolized in the synaptic cleft
by acetylcholinesterase into acetate and choline . Choline
is then recycled by reuptake into the terminal bouton via
receptor-mediated endocytosis. Dopamine (DA), norepinephrine (NE), and epinephrine are all synthesized from
the same precursor molecule, the amino acid L-tyrosine .
Tyrosine hydroxylase synthesizes L-DOPA from tyrosine
and is the rate-limiting enzyme for both DA and NE synthesis. Aromatic amino acid decarboxylase then synthesizes DA
from L-DOPA Dopamine is syntheSized by neurons in the
substantia nigra and arcuate nucleus of the hypothalamus
and is also active in some mesolimbic anc! mesocortical
tracts. Reserpine prevents the uptake of DA into synaptic
vesicles. Dopamine a.-hydroxylase is located on the membrane of synaptic veSicles, where it converts DA to NE in the
synaptic vesicle itself. !’om is the only neurotransmitter that is
synthesized within the synaptic vesicle. !’orE exerts negative
feedback on tyrosine hydroxylase. NE is the neurotransmitter of most postganglionic sympathetic neurons and is also found in the locus ceruleus. After NE is released into the
synaptic cleft, the termination of its bioactivity is primarily
accomplished by reuptake into the presynaptic neuron. NE
reuptake is blocked by cocaine. NE is also metabolized
by catechol O-methyltransferase (CO~ [T) and monoamine
oxidase (MAO) in the cytoplasm of numerous cells. The medications tropolone and selegiline inhibit the enzymes COMT
and MAOo, respectively. Serotonin (an indole) is synthesized
from the amino acid tryptophan. Tryptophan is initially converted into S-hydroxytryptophan by the enzyme tryptophan
hydroxylase, which represents the rate-limiting step. Then
S-hydroxytryptophan is converted into serotonin by the
enzyme 5-hydroxytryptophan decarboxylase. Serotonergic
neurons are primarily found in the raphe nuclei of the brainstem reticular formation. Serotonin reuptake is inhibited
by several antidepressants, including the selective serotonin
reuptake inhibitors (SSRIs; e .g., f1uoxetine) and the tricyclic
antidepressants (Kandel, pp. 280- 295; Pritchard, pp. 32- 45).
Most sensitive to skin stretch
A. Free nerve endings
B. lvleissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. l’l’lerkel’s discs
F. None of the above
A. Free nerve endings
B. lvleissner’s corpuscles
C. Pacinian corpuscles
**D. Ruffini’s corpuscles **
E. l’l’lerkel’s discs
F. None of the above
Sensory endings of the skin can be classified on a
structural basis into encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel’s discs, and hair follicle receptors. Encapsulated
endings include Meissner’s corpuscles, pacinian corpuscles,
and Ruffini’s corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract
and are found between epithelial cells of the skin, in the
cornea , and in a variety of connective tissues including the
dermis, fascia, ligaments, joint capsules, periosteum, and
muscle. They are either myelinated or unmyelinated, and most detect pain ; however, some detect crude touch, pressure, and tickling sensations. Merkel’s discs are found in
hairless regions of the body including the fingertips. They
terminate in the deeper aspects of the epidermis, are slowly
adapting, and transmit information about pressure and texture. Merkel’s disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the
skin. Meissner’s corpuscles also provide sharp resolution of
spatial patterns, but the image is generally not as sharp as the
one produced by Merkel’s endings because they have slightly
larger receptive fields. Merkel’s discs are normally found
in clusters at the center of the papillary ridge. Hair-follicle
receptors wind around hair follicles adjacent to a sebaceous
gland. Some surround the hair follicle and others run parallel
to it. These receptors are rapidly adapting and respond to the
bending of hair follicles.
Encapsulated receptors include Meissner’s corpuscles,
pacinian corpuscles, and Ruffini corpuscles. Meissner’s
corpuscles are located in the dermal papillae of the skin ,
especially in the palms and sales of the feet. They are oval
in shape and consist of a stack of flattened SchWalm cells
arranged transversely along their long axis. They are very
sensitive to touch (especially stroking, fluttering), are rapidly
adapting, and allow people to distinguish between two
pointed structures placed together on the skin. Pacinian
corpuscles are very similar physiologically to Meissner’s
corpuscles, are widely distributed , and are numerous in
the denniS, subcutaneous tissues, joint capsules, pleura,
pericardium, and nipples. Each pacinian corpuscle is ovoid
shape, measuring 2 mm long and about 100-500 ~1111 across
(largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve
enters the corpuscle, loses the myelin sheath, and then
passes through the central core before terminating in an
expanded fashion. Pacinian corpuscles are rapidly adapting
and sensitive mainly to vibration. Ruffini’s corpuscle is
located in the dermis of hairy areas, is a slowly adapting
mechanoreceptor, and responds mainly when the skin is
stretched. Muscle spindles and group Ia fibers innervate the
afferent limb of the stretch reflex (Kandel, pp. 430-450,
565).
Particularly sensitive to vibration (600 stimuli/second)
A. Free nerve endings
B. lvleissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. l’l’lerkel’s discs
F. None of the above
A. Free nerve endings
B. lvleissner’s corpuscles
**C. Pacinian corpuscles **
D. Ruffini’s corpuscles
E. l’l’lerkel’s discs
F. None of the above
Sensory endings of the skin can be classified on a
structural basis into encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel’s discs, and hair follicle receptors. Encapsulated
endings include Meissner’s corpuscles, pacinian corpuscles,
and Ruffini’s corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract
and are found between epithelial cells of the skin, in the
cornea , and in a variety of connective tissues including the
dermis, fascia, ligaments, joint capsules, periosteum, and
muscle. They are either myelinated or unmyelinated, and most detect pain ; however, some detect crude touch, pressure, and tickling sensations. Merkel’s discs are found in
hairless regions of the body including the fingertips. They
terminate in the deeper aspects of the epidermis, are slowly
adapting, and transmit information about pressure and texture. Merkel’s disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the
skin. Meissner’s corpuscles also provide sharp resolution of
spatial patterns, but the image is generally not as sharp as the
one produced by Merkel’s endings because they have slightly
larger receptive fields. Merkel’s discs are normally found
in clusters at the center of the papillary ridge. Hair-follicle
receptors wind around hair follicles adjacent to a sebaceous
gland. Some surround the hair follicle and others run parallel
to it. These receptors are rapidly adapting and respond to the
bending of hair follicles.
Encapsulated receptors include Meissner’s corpuscles,
pacinian corpuscles, and Ruffini corpuscles. Meissner’s
corpuscles are located in the dermal papillae of the skin ,
especially in the palms and sales of the feet. They are oval
in shape and consist of a stack of flattened SchWalm cells
arranged transversely along their long axis. They are very
sensitive to touch (especially stroking, fluttering), are rapidly
adapting, and allow people to distinguish between two
pointed structures placed together on the skin. Pacinian
corpuscles are very similar physiologically to Meissner’s
corpuscles, are widely distributed , and are numerous in
the denniS, subcutaneous tissues, joint capsules, pleura,
pericardium, and nipples. Each pacinian corpuscle is ovoid
shape, measuring 2 mm long and about 100-500 ~1111 across
(largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve
enters the corpuscle, loses the myelin sheath, and then
passes through the central core before terminating in an
expanded fashion. Pacinian corpuscles are rapidly adapting
and sensitive mainly to vibration. Ruffini’s corpuscle is
located in the dermis of hairy areas, is a slowly adapting
mechanoreceptor, and responds mainly when the skin is
stretched. Muscle spindles and group Ia fibers innervate the
afferent limb of the stretch reflex (Kandel, pp. 430-450,
565).
Mostly found in clusters at the center of the papillary ridge
A. Free nerve endings
B. lvleissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. l’l’lerkel’s discs
F. None of the above
A
B
C
D
E
F
Sensory endings of the skin can be classified on a
structural basis into encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel’s discs, and hair follicle receptors. Encapsulated
endings include Meissner’s corpuscles, pacinian corpuscles,
and Ruffini’s corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract
and are found between epithelial cells of the skin, in the
cornea , and in a variety of connective tissues including the
dermis, fascia, ligaments, joint capsules, periosteum, and
muscle. They are either myelinated or unmyelinated, and most detect pain ; however, some detect crude touch, pressure, and tickling sensations. Merkel’s discs are found in
hairless regions of the body including the fingertips. They
terminate in the deeper aspects of the epidermis, are slowly
adapting, and transmit information about pressure and texture. Merkel’s disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the
skin. Meissner’s corpuscles also provide sharp resolution of
spatial patterns, but the image is generally not as sharp as the
one produced by Merkel’s endings because they have slightly
larger receptive fields. Merkel’s discs are normally found
in clusters at the center of the papillary ridge. Hair-follicle
receptors wind around hair follicles adjacent to a sebaceous
gland. Some surround the hair follicle and others run parallel
to it. These receptors are rapidly adapting and respond to the
bending of hair follicles.
Encapsulated receptors include Meissner’s corpuscles,
pacinian corpuscles, and Ruffini corpuscles. Meissner’s
corpuscles are located in the dermal papillae of the skin ,
especially in the palms and sales of the feet. They are oval
in shape and consist of a stack of flattened SchWalm cells
arranged transversely along their long axis. They are very
sensitive to touch (especially stroking, fluttering), are rapidly
adapting, and allow people to distinguish between two
pointed structures placed together on the skin. Pacinian
corpuscles are very similar physiologically to Meissner’s
corpuscles, are widely distributed , and are numerous in
the denniS, subcutaneous tissues, joint capsules, pleura,
pericardium, and nipples. Each pacinian corpuscle is ovoid
shape, measuring 2 mm long and about 100-500 ~1111 across
(largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve
enters the corpuscle, loses the myelin sheath, and then
passes through the central core before terminating in an
expanded fashion. Pacinian corpuscles are rapidly adapting
and sensitive mainly to vibration. Ruffini’s corpuscle is
located in the dermis of hairy areas, is a slowly adapting
mechanoreceptor, and responds mainly when the skin is
stretched. Muscle spindles and group Ia fibers innervate the
afferent limb of the stretch reflex (Kandel, pp. 430-450,
565).
Provide shalvest resolution of spatial pattern
A. Free nerve endings
B. lvleissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. l’l’lerkel’s discs
F. None of the above
A
B
C
D
E
F
Sensory endings of the skin can be classified on a
structural basis into encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel’s discs, and hair follicle receptors. Encapsulated
endings include Meissner’s corpuscles, pacinian corpuscles,
and Ruffini’s corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract
and are found between epithelial cells of the skin, in the
cornea , and in a variety of connective tissues including the
dermis, fascia, ligaments, joint capsules, periosteum, and
muscle. They are either myelinated or unmyelinated, and most detect pain ; however, some detect crude touch, pressure, and tickling sensations. Merkel’s discs are found in
hairless regions of the body including the fingertips. They
terminate in the deeper aspects of the epidermis, are slowly
adapting, and transmit information about pressure and texture. Merkel’s disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the
skin. Meissner’s corpuscles also provide sharp resolution of
spatial patterns, but the image is generally not as sharp as the
one produced by Merkel’s endings because they have slightly
larger receptive fields. Merkel’s discs are normally found
in clusters at the center of the papillary ridge. Hair-follicle
receptors wind around hair follicles adjacent to a sebaceous
gland. Some surround the hair follicle and others run parallel
to it. These receptors are rapidly adapting and respond to the
bending of hair follicles.
Encapsulated receptors include Meissner’s corpuscles,
pacinian corpuscles, and Ruffini corpuscles. Meissner’s
corpuscles are located in the dermal papillae of the skin ,
especially in the palms and sales of the feet. They are oval
in shape and consist of a stack of flattened SchWalm cells
arranged transversely along their long axis. They are very
sensitive to touch (especially stroking, fluttering), are rapidly
adapting, and allow people to distinguish between two
pointed structures placed together on the skin. Pacinian
corpuscles are very similar physiologically to Meissner’s
corpuscles, are widely distributed , and are numerous in
the denniS, subcutaneous tissues, joint capsules, pleura,
pericardium, and nipples. Each pacinian corpuscle is ovoid
shape, measuring 2 mm long and about 100-500 ~1111 across
(largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve
enters the corpuscle, loses the myelin sheath, and then
passes through the central core before terminating in an
expanded fashion. Pacinian corpuscles are rapidly adapting
and sensitive mainly to vibration. Ruffini’s corpuscle is
located in the dermis of hairy areas, is a slowly adapting
mechanoreceptor, and responds mainly when the skin is
stretched. Muscle spindles and group Ia fibers innervate the
afferent limb of the stretch reflex (Kandel, pp. 430-450,
565).
Line the alimentary tract
A. Free nerve endings
B. lvleissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. l’l’lerkel’s discs
F. None of the above
A
B
C
D
E
F
Sensory endings of the skin can be classified on a
structural basis into encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel’s discs, and hair follicle receptors. Encapsulated
endings include Meissner’s corpuscles, pacinian corpuscles,
and Ruffini’s corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract
and are found between epithelial cells of the skin, in the
cornea , and in a variety of connective tissues including the
dermis, fascia, ligaments, joint capsules, periosteum, and
muscle. They are either myelinated or unmyelinated, and most detect pain ; however, some detect crude touch, pressure, and tickling sensations. Merkel’s discs are found in
hairless regions of the body including the fingertips. They
terminate in the deeper aspects of the epidermis, are slowly
adapting, and transmit information about pressure and texture. Merkel’s disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the
skin. Meissner’s corpuscles also provide sharp resolution of
spatial patterns, but the image is generally not as sharp as the
one produced by Merkel’s endings because they have slightly
larger receptive fields. Merkel’s discs are normally found
in clusters at the center of the papillary ridge. Hair-follicle
receptors wind around hair follicles adjacent to a sebaceous
gland. Some surround the hair follicle and others run parallel
to it. These receptors are rapidly adapting and respond to the
bending of hair follicles.
Encapsulated receptors include Meissner’s corpuscles,
pacinian corpuscles, and Ruffini corpuscles. Meissner’s
corpuscles are located in the dermal papillae of the skin ,
especially in the palms and sales of the feet. They are oval
in shape and consist of a stack of flattened SchWalm cells
arranged transversely along their long axis. They are very
sensitive to touch (especially stroking, fluttering), are rapidly
adapting, and allow people to distinguish between two
pointed structures placed together on the skin. Pacinian
corpuscles are very similar physiologically to Meissner’s
corpuscles, are widely distributed , and are numerous in
the denniS, subcutaneous tissues, joint capsules, pleura,
pericardium, and nipples. Each pacinian corpuscle is ovoid
shape, measuring 2 mm long and about 100-500 ~1111 across
(largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve
enters the corpuscle, loses the myelin sheath, and then
passes through the central core before terminating in an
expanded fashion. Pacinian corpuscles are rapidly adapting
and sensitive mainly to vibration. Ruffini’s corpuscle is
located in the dermis of hairy areas, is a slowly adapting
mechanoreceptor, and responds mainly when the skin is
stretched. Muscle spindles and group Ia fibers innervate the
afferent limb of the stretch reflex (Kandel, pp. 430-450,
565).
Afferent fibers to the stretch reflex
A. Free nerve endings
B. lvleissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. l’l’lerkel’s discs
F. None of the above
A
B
C
D
E
F
Sensory endings of the skin can be classified on a
structural basis into encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel’s discs, and hair follicle receptors. Encapsulated
endings include Meissner’s corpuscles, pacinian corpuscles,
and Ruffini’s corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract
and are found between epithelial cells of the skin, in the
cornea , and in a variety of connective tissues including the
dermis, fascia, ligaments, joint capsules, periosteum, and
muscle. They are either myelinated or unmyelinated, and most detect pain ; however, some detect crude touch, pressure, and tickling sensations. Merkel’s discs are found in
hairless regions of the body including the fingertips. They
terminate in the deeper aspects of the epidermis, are slowly
adapting, and transmit information about pressure and texture. Merkel’s disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the
skin. Meissner’s corpuscles also provide sharp resolution of
spatial patterns, but the image is generally not as sharp as the
one produced by Merkel’s endings because they have slightly
larger receptive fields. Merkel’s discs are normally found
in clusters at the center of the papillary ridge. Hair-follicle
receptors wind around hair follicles adjacent to a sebaceous
gland. Some surround the hair follicle and others run parallel
to it. These receptors are rapidly adapting and respond to the
bending of hair follicles.
Encapsulated receptors include Meissner’s corpuscles,
pacinian corpuscles, and Ruffini corpuscles. Meissner’s
corpuscles are located in the dermal papillae of the skin ,
especially in the palms and sales of the feet. They are oval
in shape and consist of a stack of flattened SchWalm cells
arranged transversely along their long axis. They are very
sensitive to touch (especially stroking, fluttering), are rapidly
adapting, and allow people to distinguish between two
pointed structures placed together on the skin. Pacinian
corpuscles are very similar physiologically to Meissner’s
corpuscles, are widely distributed , and are numerous in
the denniS, subcutaneous tissues, joint capsules, pleura,
pericardium, and nipples. Each pacinian corpuscle is ovoid
shape, measuring 2 mm long and about 100-500 ~1111 across
(largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve
enters the corpuscle, loses the myelin sheath, and then
passes through the central core before terminating in an
expanded fashion. Pacinian corpuscles are rapidly adapting
and sensitive mainly to vibration. Ruffini’s corpuscle is
located in the dermis of hairy areas, is a slowly adapting
mechanoreceptor, and responds mainly when the skin is
stretched. Muscle spindles and group Ia fibers innervate the
afferent limb of the stretch reflex (Kandel, pp. 430-450,
565).
Transmit information about pressure and texture
A. Free nerve endings
B. lvleissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. l’l’lerkel’s discs
F. None of the above
A
B
C
D
E
F
Sensory endings of the skin can be classified on a
structural basis into encapsulated and nonencapsulated receptors. Nonencapsulated receptors include free nerve endings, Merkel’s discs, and hair follicle receptors. Encapsulated
endings include Meissner’s corpuscles, pacinian corpuscles,
and Ruffini’s corpuscles. Free nerve endings are widely distributed throughout the body. They line the alimentary tract
and are found between epithelial cells of the skin, in the
cornea , and in a variety of connective tissues including the
dermis, fascia, ligaments, joint capsules, periosteum, and
muscle. They are either myelinated or unmyelinated, and most detect pain ; however, some detect crude touch, pressure, and tickling sensations. Merkel’s discs are found in
hairless regions of the body including the fingertips. They
terminate in the deeper aspects of the epidermis, are slowly
adapting, and transmit information about pressure and texture. Merkel’s disc receptors also provide the sharpest resolution of spatial patterns of all the sensory endings of the
skin. Meissner’s corpuscles also provide sharp resolution of
spatial patterns, but the image is generally not as sharp as the
one produced by Merkel’s endings because they have slightly
larger receptive fields. Merkel’s discs are normally found
in clusters at the center of the papillary ridge. Hair-follicle
receptors wind around hair follicles adjacent to a sebaceous
gland. Some surround the hair follicle and others run parallel
to it. These receptors are rapidly adapting and respond to the
bending of hair follicles.
Encapsulated receptors include Meissner’s corpuscles,
pacinian corpuscles, and Ruffini corpuscles. Meissner’s
corpuscles are located in the dermal papillae of the skin ,
especially in the palms and sales of the feet. They are oval
in shape and consist of a stack of flattened SchWalm cells
arranged transversely along their long axis. They are very
sensitive to touch (especially stroking, fluttering), are rapidly
adapting, and allow people to distinguish between two
pointed structures placed together on the skin. Pacinian
corpuscles are very similar physiologically to Meissner’s
corpuscles, are widely distributed , and are numerous in
the denniS, subcutaneous tissues, joint capsules, pleura,
pericardium, and nipples. Each pacinian corpuscle is ovoid
shape, measuring 2 mm long and about 100-500 ~1111 across
(largest sensory receptor). The capsule consists of concentric lamellae of flattened cells. A large myelinated nerve
enters the corpuscle, loses the myelin sheath, and then
passes through the central core before terminating in an
expanded fashion. Pacinian corpuscles are rapidly adapting
and sensitive mainly to vibration. Ruffini’s corpuscle is
located in the dermis of hairy areas, is a slowly adapting
mechanoreceptor, and responds mainly when the skin is
stretched. Muscle spindles and group Ia fibers innervate the
afferent limb of the stretch reflex (Kandel, pp. 430-450,
565).
Which of the following structures is assessed by the doll’s eye maneuver?
A. Lateral vestibulospinal tract
B. lvledial vestibulospinal tract
C. Vestibular nerve
D. Cerebellum
E. Cerebral cortex
A
B
C
D
E
The doll’s eye test assesses the integrity of the
vestibula-ocular reflexes, which include the vestibular
labyrinths, vestibular nerves bilaterally, vestibular nuclei,
and motor nuclei of the cranial nerves involved with eye
movements (nerves III, IV, and VI). The doll’s eye maneuver
does not test the integrity of the cerebral cortex, cerebellum,
or medial and lateral vestibulospinal tracts, as they are not
part of the vestibulo-ocular circuit. The vestibulo-ocular
reflex stabilizes the eyes during head movements in order to keep an image focused on the retina. Rotation of the head to the right initiates compensatory eye movements to the left as a result of endolymph in the right semicircular canal flowing
to the left (toward the utricle). As the endolymph flows through the ampulla, the cupula and underlying stereocilia
bend toward the utricle. The resultant depolarization of the
receptors causes an increase in the firing of the vestibular
nerve, which reaches the vestibular nuclei, which, in turn ,
project to the motor nuclei of the extraocular muscles. The
endolymph in the left (opposite) semicircular canal flows
away from the utricle , causing hyperpolarization of hair cells and a lower firing rate of cranial nerves and vestibular nuclei on that side (Kandel, pp. 802- 809).
Which of the following statements about phototransduction in the retina is correct?
A. Cones perform better than rods in most visual tasks except detection of dim light at night
B. The presence of light results in the opening of sodium channels in the photoreceptors of the retina
C. The flow of sodium into photoreceptor cells is mediated by cAMP channels
D. In the dark, the hyperpolarization of photoreceptor cells of the retina is the result of outward sodium flow
E. lvletarhodopsin II, a breakdown product of rhodopsin, deactivates phosphodiesterase molecules
A
B
C
D
E
The absorption of light by the photoreceptor cells of
the retina results in a cascade of events (three distinct
stages) that leads to a change in ionic fluxes across the
plasma membrane of these cells. In rod cells, the visual pigment rhodopsin has two parts. The protein portion, opsin, is
embedded in the disc membrane and does not absorb light,
whereas the light-absorbing portion, retina l (derivative of
vitamin A), can assume several different isomeric conformations, two of which absorb light. In the nonactivated form,
rhodopsin contains the ll-cis isomer of retinal, which fits
into the opsin binding site. In response to light, the II-cis
isomer changes to the all-trans configuration of rhodopsin,
which no longer fits inside the opsin binding site. The opsin
then undergoes a conformational change to semistable
metarhodopsin II, which triggers the second stage of phototransduction. In this stage, metarhodopsin II activates a large
number of phosphodiesterase molecules via an intermediate
molecule termed transducin. Transducin, in turn, catalyzes
the hydrolysis of cGMP molecules, which are required by
cGMP channels for sodium conductiol1 into the cell. This
results in less cGJ\,IP, and the closure of cGMP-dependent
sodium channels (stage 3 of the phototransduction cycle).
The light-evoked closing of these channels results in less
inward sodium current and, therefore, hyperpolarization of
the cell. In the absence of light, cGMP is 110 longer broken
down, sodium channels are reopened, and the cell becomes
depolarized again. Cones perform better than rods in all
visual tasks except the detection of dim light at night. Conernediated vision has higher acuity than rod-mediated vision,
provides better resolution of images, and mediates color
vision (Kandel, pp. 508- 514).
Gap junctions close in response to what stimuli?
A. Decreased concentration of intracellular Ca2+
B. Increased extracellular K+ concentration
C. Elevated intracellular proton concentration
D. Increased extracellular Ca 2+ concentration
E. Gap junctions, unlike ion channels, remain open continuously
A
B
C
D
E
Gap junctions are sensitive to different modulating
factors that control their opening and closing in different
tissues. For instance, most gap junctions close in response to
lowered cytoplasmic pH or elevated cytoplasmic Ca 2
+. These
two properties serve to decouple damaged cells from other
cells, since damaged cells have elevated levels of Ca2
+ and
protons (lower pH). Neurotransmitters released from other
cells can also modulate the opening and closing of gap junctions (Kandel, pp. 178- 180).
Unipolar neurons mainly innervate what structure(s) ?
A. Sympathetic nervous system
B. Exocrine gland secretions and smooth muscle contractility
C. Cardiac muscle cells (AV node)
D. Adrenal gland secretions and the renal glomerulus
E. Small and large bowel muscle contractility
A
B
C
D
E
Unipolar neurons are the simplest in morphology.
They have no dendrites and a single axon, which gives rise to
1111!ltiple processes at the terminal. In humans, they control exocrine gland secretions and smooth muscle contractility
(Martin, p. 2).
Which of the following statements about the cochlea is
correct?
A. High-frequency sounds cause the basilar membrane to vibrate maXimally at its apex
B. I-lair cells of the cochlea do not typically adapt to sustained stimuli unless provoked by low-frequency sounds
C. An endocochlear potential of + 40 mV exists between the perilymph and the endolymph
D. Deflection of stereocilia in either direction can cause depola riza tion
E. The hair cells form chemical synapses with bipolar cells of the spiral ganglion
A
B
C
D
E
The hair cells of the cochlea
form chemical synapses with bipolar cells of the spiral
ganglion. Although the precise neurotransmitter released
remains unclear, studies in animals show that transmitter
release by hair cells is evoked by presynaptic depolarization
and requires the presence of Ca2
+, as in most other synapses.
The neurotransmitter involved is believed to be glutamate.
The cochlea is a fluid-filled tube coiled 2112 times around
itself to resemble a snail shell. Reissner’s membrane and the
basilar membrane separate the cochlea into three chambers,
the scala vestibule (8V), scala tympani (8’1’), and scala media
(8M), which contains the organ of Corti. The 8V and 8T are
fi.lled with perilymph, which resembles C8F, and are continuous with one another at the helicotrema, a small opening
located at the apex of the cochlear coil. The 8M is filled with
endolymph , a clear liquid with high Ic+ concentration formed
by the stria vascularis. Pressure waves resulting from sound
cause the basilar membrane to move up and down, which
results in a shearing movement of hair cells against the tectorial membrane. It is the physical bending of the hair cells
toward the scala vestibuli that causes them to depolarize (I:
channels and voltage-sensitive Ca 2
+ channels). Movement in
the opposite direction causes hyperpolarization (Ca2
+-sensitive
W channels) (see discussion for question 9). The different
regions of the basilar membrane are sensitive to different frequencies of sound. High frequencies caLIse the membrane to vibrate maximally at its base, whereas low frequencies
cause maximal vibration near the apex. There is a marked
difference in ion concentrations between the perilymph of
the 8V and the endolymph of the 8M, which produces an
endocochlear potential of +80 mV. Hair cells do adjust to
sustained stimuli by a process of adaptation (to either highor low-frequency sounds), which manifests itself as a progressive decrement in receptor potential during protracted
hair-bundle deflection (Pritchard, pp. 229-248; Kandel,
pp.614- 624).
Which of the following statements about olfactory receptors is correct?
A. An olfactory receptor displays rapid adaptation initially
B. The life span of olfactory receptor cells is approximately 9 months
C. A Single olfactory receptor cell typically responds to only a single odorant
D. The receptor potential occurs when Na+ channels are closed in a manner similar to phototransduction They are cGMP-regulated
**A **
B
C
D
E
Olfactory receptors (ORs) display rapid adaptation
initially and little afterwards. Within the olfactory system, an
olfactory stimulus results in the opening of sodium channels,
which leads to depolarization and action potentials. These
action potentials can increase in frequency to about 20/s.
Adenylate cyclase activity catalyzes the formation of cAMP,
resulting in opening of many additional channels, which can
also increase the rate of discharge in olfactory neurons. Each
olfactory neuron is capable of responding to many different
odorants, as determined by electrophysiologic studies. The
life span of ORs varies from 30 to 120 days in mammalian
species. Replacement cells are delivered by mitosis of basal
cells. The relatively rapid turnover of ORs makes them partially susceptible to damage after radiation therapy and/or
chemotherapeutic agents, which target rapidly dividing cells
(Kandel, pp. 626- 636; Pritchard, pp. 266-267)
Which of the following sensory systems sends signals directly to both the thalamus and cerebral cortex?
A. Two-point discrimination
B. Taste
C. Olfaction
D. Pain
E. Balance
A
B
C
D
E
Taste and sensation from the head are carried to
the ventroposterior medial (VPM) nucleus of the thalamus.
Sensation and proprioception from the body reach the
ventroposterior lateral (VPL) nucleus of the thalamus. The
visua l system utilizes the lateral geniculate nucleus (LGN)
and the auditory system the medial geniculate nucleus
(]'IGN) prior to being relayed to the cortex. Some olfactory
information bypasses the thalamus to reach the orbitofrontal
cortex, but it should be noted that some projections
subserving smell can reach the orbitofrontal cortex via the
mediodorsal (MD) thalamic nucleus. The olfactory system,
therefore, relies on parallel processing to transmit olfactory
inputs to the cortex (Kandel, p. 633).
Cells most sensitive to radiation therapy
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.E
Cells are most sensitive to radiation during the G2 and M phases of the
cell cycle and most resistant in the late 8 phase. Gl cells
have intermediate sensitivity. The precise mechanism(s)
accounting for these variations remains unclear, but studies
have shown that differences in a cell’s ability to repair DNA
damage in different phases after radiation may play an
important part. In the Gl phase of the cycle, the nucleus has
a diploid amount of DNA (2C), which increases to 4C by the
end of the 8 phase. Only cells in the 8 phase (DNA synthetic
phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion
and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle;
such cells can eventually re-enter the cell cycle at a later
point in time. Mitosis is the most easily identifiable stage of
the cell cycle by light microscopy. The genes encoding p16
(CDIm2A) and pIS (CDIv’i2B) map onto chromosome 9p21,
a site that is associated with homozygous deletions in highgrade astrocytomas in about two-thirds of gliomas. These
proteins act as inhibitors of cyclin-dependent kinases and
other pathways during the Gl phase of the cell cycle and help
control proliferation at the G1I8 phase of the cell cycle. The
TPs.1 protein assists in several cellular processes, including
cell cycle regulation, response of cells to DNA damage (Ps."
dependent growth arrest following DNA damage occurs in Gl
phase of the cell cycle), cell death , cell differentiation, and
neovascularization (WHO, pp. 11- 14; Berger, pp. 204- 209).
Nutrient depletion or pbysical crowding are conditions that encourage cells to move into this phase of the cell cycle
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.E
Cells are most sensitive to radiation during the G2 and M phases of the
cell cycle and most resistant in the late 8 phase. Gl cells
have intermediate sensitivity. The precise mechanism(s)
accounting for these variations remains unclear, but studies
have shown that differences in a cell’s ability to repair DNA
damage in different phases after radiation may play an
important part. In the Gl phase of the cycle, the nucleus has
a diploid amount of DNA (2C), which increases to 4C by the
end of the 8 phase. Only cells in the 8 phase (DNA synthetic
phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion
and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle;
such cells can eventually re-enter the cell cycle at a later
point in time. Mitosis is the most easily identifiable stage of
the cell cycle by light microscopy. The genes encoding p16
(CDIm2A) and pIS (CDIv’i2B) map onto chromosome 9p21,
a site that is associated with homozygous deletions in highgrade astrocytomas in about two-thirds of gliomas. These
proteins act as inhibitors of cyclin-dependent kinases and
other pathways during the Gl phase of the cell cycle and help
control proliferation at the G1I8 phase of the cell cycle. The
TPs.1 protein assists in several cellular processes, including
cell cycle regulation, response of cells to DNA damage (Ps."
dependent growth arrest following DNA damage occurs in Gl
phase of the cell cycle), cell death , cell differentiation, and
neovascularization (WHO, pp. 11- 14; Berger, pp. 204- 209).
Cells can incorporate thymidine analogues into their
nuclear DNA
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.E
Cells are most sensitive to radiation during the G2 and M phases of the
cell cycle and most resistant in the late 8 phase. Gl cells
have intermediate sensitivity. The precise mechanism(s)
accounting for these variations remains unclear, but studies
have shown that differences in a cell’s ability to repair DNA
damage in different phases after radiation may play an
important part. In the Gl phase of the cycle, the nucleus has
a diploid amount of DNA (2C), which increases to 4C by the
end of the 8 phase. Only cells in the 8 phase (DNA synthetic
phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion
and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle;
such cells can eventually re-enter the cell cycle at a later
point in time. Mitosis is the most easily identifiable stage of
the cell cycle by light microscopy. The genes encoding p16
(CDIm2A) and pIS (CDIv’i2B) map onto chromosome 9p21,
a site that is associated with homozygous deletions in highgrade astrocytomas in about two-thirds of gliomas. These
proteins act as inhibitors of cyclin-dependent kinases and
other pathways during the Gl phase of the cell cycle and help
control proliferation at the G1I8 phase of the cell cycle. The
TPs.1 protein assists in several cellular processes, including
cell cycle regulation, response of cells to DNA damage (Ps."
dependent growth arrest following DNA damage occurs in Gl
phase of the cell cycle), cell death , cell differentiation, and
neovascularization (WHO, pp. 11- 14; Berger, pp. 204- 209).
Cells most resistant to radiation therapy
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.E
Cells are most sensitive to radiation during the G2 and M phases of the
cell cycle and most resistant in the late 8 phase. Gl cells
have intermediate sensitivity. The precise mechanism(s)
accounting for these variations remains unclear, but studies
have shown that differences in a cell’s ability to repair DNA
damage in different phases after radiation may play an
important part. In the Gl phase of the cycle, the nucleus has
a diploid amount of DNA (2C), which increases to 4C by the
end of the 8 phase. Only cells in the 8 phase (DNA synthetic
phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion
and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle;
such cells can eventually re-enter the cell cycle at a later
point in time. Mitosis is the most easily identifiable stage of
the cell cycle by light microscopy. The genes encoding p16
(CDIm2A) and pIS (CDIv’i2B) map onto chromosome 9p21,
a site that is associated with homozygous deletions in highgrade astrocytomas in about two-thirds of gliomas. These
proteins act as inhibitors of cyclin-dependent kinases and
other pathways during the Gl phase of the cell cycle and help
control proliferation at the G1I8 phase of the cell cycle. The
TPs.1 protein assists in several cellular processes, including
cell cycle regulation, response of cells to DNA damage (Ps."
dependent growth arrest following DNA damage occurs in Gl
phase of the cell cycle), cell death , cell differentiation, and
neovascularization (WHO, pp. 11- 14; Berger, pp. 204- 209).
PIS and p16 cause growth arrest in this cell-cycle phase
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.E
Cells are most sensitive to radiation during the G2 and M phases of the
cell cycle and most resistant in the late 8 phase. Gl cells
have intermediate sensitivity. The precise mechanism(s)
accounting for these variations remains unclear, but studies
have shown that differences in a cell’s ability to repair DNA
damage in different phases after radiation may play an
important part. In the Gl phase of the cycle, the nucleus has
a diploid amount of DNA (2C), which increases to 4C by the
end of the 8 phase. Only cells in the 8 phase (DNA synthetic
phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion
and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle;
such cells can eventually re-enter the cell cycle at a later
point in time. Mitosis is the most easily identifiable stage of
the cell cycle by light microscopy. The genes encoding p16
(CDIm2A) and pIS (CDIv’i2B) map onto chromosome 9p21,
a site that is associated with homozygous deletions in highgrade astrocytomas in about two-thirds of gliomas. These
proteins act as inhibitors of cyclin-dependent kinases and
other pathways during the Gl phase of the cell cycle and help
control proliferation at the G1I8 phase of the cell cycle. The
TPs.1 protein assists in several cellular processes, including
cell cycle regulation, response of cells to DNA damage (Ps."
dependent growth arrest following DNA damage occurs in Gl
phase of the cell cycle), cell death , cell differentiation, and
neovascularization (WHO, pp. 11- 14; Berger, pp. 204- 209).
TP53-dependent growth arrest following DNA damage occurs in this phase
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.E
Cells are most sensitive to radiation during the G2 and M phases of the
cell cycle and most resistant in the late 8 phase. Gl cells
have intermediate sensitivity. The precise mechanism(s)
accounting for these variations remains unclear, but studies
have shown that differences in a cell’s ability to repair DNA
damage in different phases after radiation may play an
important part. In the Gl phase of the cycle, the nucleus has
a diploid amount of DNA (2C), which increases to 4C by the
end of the 8 phase. Only cells in the 8 phase (DNA synthetic
phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion
and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle;
such cells can eventually re-enter the cell cycle at a later
point in time. Mitosis is the most easily identifiable stage of
the cell cycle by light microscopy. The genes encoding p16
(CDIm2A) and pIS (CDIv’i2B) map onto chromosome 9p21,
a site that is associated with homozygous deletions in highgrade astrocytomas in about two-thirds of gliomas. These
proteins act as inhibitors of cyclin-dependent kinases and
other pathways during the Gl phase of the cell cycle and help
control proliferation at the G1I8 phase of the cell cycle. The
TPs.1 protein assists in several cellular processes, including
cell cycle regulation, response of cells to DNA damage (Ps."
dependent growth arrest following DNA damage occurs in Gl
phase of the cell cycle), cell death , cell differentiation, and
neovascularization (WHO, pp. 11- 14; Berger, pp. 204- 209).
Most variable phase of the cell cycle in terms of duration
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.E
Cells are most sensitive to radiation during the G2 and M phases of the
cell cycle and most resistant in the late 8 phase. Gl cells
have intermediate sensitivity. The precise mechanism(s)
accounting for these variations remains unclear, but studies
have shown that differences in a cell’s ability to repair DNA
damage in different phases after radiation may play an
important part. In the Gl phase of the cycle, the nucleus has
a diploid amount of DNA (2C), which increases to 4C by the
end of the 8 phase. Only cells in the 8 phase (DNA synthetic
phase) are able to incorporate thymidine analogues (bromodeoxyuridine) into their nuclear DNA. Nutrient depletion
and crowding can result in the movement of cells into the quiescent or nonproliferating phase (GO) of the cell cycle;
such cells can eventually re-enter the cell cycle at a later
point in time. Mitosis is the most easily identifiable stage of
the cell cycle by light microscopy. The genes encoding p16
(CDIm2A) and pIS (CDIv’i2B) map onto chromosome 9p21,
a site that is associated with homozygous deletions in highgrade astrocytomas in about two-thirds of gliomas. These
proteins act as inhibitors of cyclin-dependent kinases and
other pathways during the Gl phase of the cell cycle and help
control proliferation at the G1I8 phase of the cell cycle. The
TPs.1 protein assists in several cellular processes, including
cell cycle regulation, response of cells to DNA damage (Ps."
dependent growth arrest following DNA damage occurs in Gl
phase of the cell cycle), cell death , cell differentiation, and
neovascularization (WHO, pp. 11- 14; Berger, pp. 204- 209).
What is the resting membrane potential for nerve cells?
A. -100 mV
B. - 90 mV
C. - 80 mV
D. - 65 mV
E. -40 mV
A
B
C
D
E
In resting nerve cells the resting membrane potential
is -65 mV. This negative polarity is largely the result of two
factors: the selective permeability of the cell membrane to W
through voltage-gated channels and the Na+, W pump, which
pumps three Na+ ions out of the cell for every two K+ ions that
are pumped inside.
In terms of K permeability, as 1<.+ leaks out of the cell
down its concentration gradient, the cell membrane begins
to develop a potential difference due to the accumulation of
negative charges inside the cell. This eventuall y slows the
continued efflux of K+ ions out of the cell as a result of the
electrostatic attraction between the inside of the cell and positively charged 1<.+ ions outside the cell. Eventually the rate of
J<+ flow inside and outside the cell reaches a state of equilibrium (equilibrium potential for Ie) due to the balanCing of
the electrical and chemical forces. This produces a net flow
of 1<.+ ions that is zero and a net negative potential difference
across the cell membrane. This is called the equilibrium
potential for Ic+ and can be calculated by the Nernst equation.
E = RT/F log(ion).,,,/(ion)in = 61 log (150/5.5) = -86 111V
Using standard values of concentration gradients (see discussion question 41, RT/F = 61), the equilibrium potential for
K+ is -86 111V, which would also be the resting membrane
potential across the cell membrane if K+ were the only ion
contributing to the membrane potential. However, rarely
does one ion contribute solely to the membrane potential,
which is often a combination of multiple ions diffuSing
through the membrane. For this reason, the Goldman equation was developed to account for the relationship between
membrane potential (V) and relative permeability (P) of
each population of ion channels. Given this, the resting
membrane potential in neurons (-65 111V) is not identical
to EI
(+ (-86 mV), since the membrane is slightly permeable to
other ions as well.
V = 6110 P~ (W)”u,+ PNa+ (Na+)”u,+ PCI (Cn”
g P,,+ (IC+)i” + PNa+ (Na+)in + PCI (CnOl”
The inequality of charge on either side of the cell membrane is also the result of the Na+, Ic+ pump, which is a large
membrane-spanning protein with Na+, Ic+, and ATP binding
sites. If this pump were not present, the gradient across
the cell membrane would eventually dissipate. This pump
utilizes one ATP molecule to pump 3 Na+ ions out of and 2 K+
ions into the cell. An increase in permeability of Cl- channels
usually has little effect on membrane potential, since the
resting potential of a typical neuron (-65 mV) and equilibrium potential for Cl- (-66 m V) are very similar (Kandel,
pp. 125- 139).
What is the extracellular concentration of Ca 2+ ions in
the brain?
A. 0.7 mM/L
B. 2 mM/L
C. 125 mM/L
D. 150 mM/L
E. None of the above
A
B
C
D
E
Neurons maintain a high concentration of Ic+ ions and organic anions inside the cell, and
ions such as Na+, ct, and Ca 2
+ are more highly concentrated
outside of the cell (Kandel, pp. 125- 139).
Columns of neurons in area 3a of the somatic sensory
cortex receive input primarily from what type of receptor(s)?
1. Rapidly adapting skin receptors
2. Slowly and rapidly adapting skin receptors
3. Pressure and joint position receptors
4. Muscle stretch receptors
A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above
A
B
C
D
E
All of the following statements about the semicircular canals are correct EXCEPT?
A. The movement of endolymph within each canal is opposite to the direction of head rotation
B. Primary afferent fibers do not discharge after head rotation ceases
C. Linear acceleration of the head is sufficient to activate the posterior semicircular canal
D. The floor of the ampulla contains a ridge of speCialized hair cells that is covered by a layer of gelatin called the cupula
E. I-lair cells in the horizontal canal are polarized toward the utricle, and those in the anterior and posterior semicircular canals are polarized away from the utricle
A
B
C
D
E
Refer to Figure 1.48A. One end of each semicircular
canal contains an enlarged region Imown as the ampulla,
where the flow of endolymph serves as a mechanical stimulus for sensory transduction . The floor of the ampulla contains speCialized hair cells, the crista ampullaris, and is
covered by a gelatinous layer known as the cupula. The stereocilia of the hair cells insert into the cupula. These hair cells
are stimulated by changes in endolymph circulation induced
by head rotation. The movement of endolymph within each
canal is opposite to the direction of head rotation. The
response in each pair of semicircular canals (one on each
side of the head) is opposite as well. Rotation of the head
or angular acceleration is sufficient to stimulate a response
in the semicircular canals but insufficient to stimulate the
macula of the utricle, which requires linear acceleration.
Firing typically ceases once head movement stops. I-lair
cells in the horizontal canal are polarized toward the utricle ,
and those in the anterior and posterior semicircular canals
are polarized away from the utricle (Kandel, pp. 802- 806;
Pritchard, pp. 250-253).
Striking the ligamentum patellae with a reflex hammer
results in the activation of which of the following structure(s)?
1. Annulospiral endings
2. Flower spray endings
3. (J. motor neurons
4. Quadriceps muscle
A. 1,2, and 3 are correct
B. 1 and 3 are correct
C. 2 and 4 are correct
D. Only 4 is correct
E. All of the above are correct
A
B
C
D
**E **
Striking the ligamentum patellae results in stretching of the intrafusal muscle spindles of
the quadriceps muscle. In turn, this causes activation of both
annulospiral and flower-spray sensory endings (responsive
to stretching around the central region of intrafusal muscle
fibers), which are carried to the dorsal horn of the spinal cord
within the femoral nerve (L 2, 3, 4). These afferent fibers
synapse with large a motor neurons in the anterior gray
horns of the spinal cord. Nerve impulses then travel via efferent a motor neurons of the femoral nerve and stimulate
the extrafusal fibers of the quadriceps muscle , which contracts. The motor neurons of the antagonist muscles are
inhibited. After the muscle contracts, there comes a point at
which the intrafusalmuscle fibers slacken and are unable to
signal any further changes in muscle length, which results in
a decreased amount of firing of the afferent sensory fibers
(annulospiral and flower spray). At this point, one role of y
motor fibers is to maintain tension on muscle spindle poles
during muscle contraction to ensure their firing during
movement. The y motor neurons accomplish this task by
terminating as small branches on motor end plates located
on both ends of the intrafusalmuscle fibers. Stimulation of
these motor nerves causes the ends of the intrafusal fibers to
contract, which in turn activates sensory endings. Thus, the
y motor neurons provide a mechanism for adjusting the sensitivity of the muscle spindles to keep them under constant
tension during muscle movement. In many voluntary movements, the y motor neurons are activated at the same time as
a motor neurons to automatically maintain a level of spindle
loading. This is called alpha-gamma coactivation. Under resting conditions, the muscle spindles give rise to afferent nerve
impulses at a constant rate , which is not conSCiously perceived. Although the details remain unclear, it is believed that this constant baseline firing of muscle spindles helps
maintain tone (Kandel, pp. 713- 736).
Composed solely of actin filaments
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.E
Shortens during muscle
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.E
H zone
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.E
A band
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.E
Z disc
A.A
B.B
C.C
D.D
E.E
A.A
B.B
C.C
D.D
E.EA
Match the gestational age with the embryologic
milestone using each answer once, more than once, or not at
all. Each question has only one correct answer.
A. Day 12
B. Day 14
C. Day 16
D. Day 18
E. Day 21
F. Day 24
G. Day 26
H. None of the above
Caudal neuropore closure
A
B
C
D
E
F
G
H
Match the gestational age with the embryologic
milestone using each answer once, more than once, or not at
all. Each question has only one correct answer.
A. Day 12
B. Day 14
C. Day 16
D. Day 18
E. Day 21
F. Day 24
G. Day 26
H. None of the above
Notochord begins to develop
A
B
C
D
E
F
G
H
Match the gestational age with the embryologic
milestone using each answer once, more than once, or not at
all. Each question has only one correct answer.
A. Day 12
B. Day 14
C. Day 16
D. Day 18
E. Day 21
F. Day 24
G. Day 26
H. None of the above
Neural folds almost fused
A
B
C
D
E
F
G
H
Match the gestational age with the embryologic
milestone using each answer once, more than once, or not at
all. Each question has only one correct answer.
A. Day 12
B. Day 14
C. Day 16
D. Day 18
E. Day 21
F. Day 24
G. Day 26
H. None of the above
Rostral neuropore closure
A
B
C
D
E
F
G
H
Match the gestational age with the embryologic
milestone using each answer once, more than once, or not at
all. Each question has only one correct answer.
A. Day 12
B. Day 14
C. Day 16
D. Day 18
E. Day 21
F. Day 24
G. Day 26
H. None of the above
Neural groove development
A
B
C
D
E
F
G
H
Match the gestational age with the embryologic
milestone using each answer once, more than once, or not at
all. Each question has only one correct answer.
A. Day 12
B. Day 14
C. Day 16
D. Day 18
E. Day 21
F. Day 24
G. Day 26
H. None of the above
Bilaminar disc formed
A
B
C
D
E
F
G
H
Match the gestational age with the embryologic
milestone using each answer once, more than once, or not at
all. Each question has only one correct answer.
A. Day 12
B. Day 14
C. Day 16
D. Day 18
E. Day 21
F. Day 24
G. Day 26
H. None of the above
Prosencephalon divides into telencephalon and diencephalon
A
B
C
D
E
F
G
H
An 81-year-old female presents with complaints of gradual, painless bilateral vision loss and a visual glare. On physical examination, there is a marked decrease in visual acuity and upon ophthalmoscopy, there is an increased opacity in the pathological structure. The structure causing the symptoms refracts light. Which structure of the eye refracts light?
- Lens
- Iris
- Retina
- Conjunctiva
1
2
3
4
The patient is presenting with symptoms of cataracts. Senile- cataracts present with gradual vision loss and increases in the opacity of the lens.
The light travels through the iris which controls the amount of light entering the eye. It does this by changing the diameter of the pupil.
The lens lies behind the iris and in front of the vitreous body. It is a biconvex structure allowing it to refract light onto the retina. Increasing the thickness of the lens can decrease the focus of the light onto the retina, decreasing the visual acuity.
After the light is refracted by the lens, it is focused onto the retina. The retina then stimulates the optic nerve which sends information to the brain.
