NeuroBiology 1-30 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
Cellular injury, including
DNA damage induced by radiation or certain chemothera-peutic 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 up-stream (initiator) and downstream (effector) products known
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 aggregation 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 multiprotein
complex composed of APAF-1, caspase 9, cytochrome c, and
ATP. This, in turn, leads to activation of caspase 9 via
allosteric regulation by APAF-1. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as 3 and 7, by cleavage. These downstream effector
caspases, in turn, cleave multiple cellular proteins, trigger-ing a range of apoptotic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phago-cytosis (avoiding an inflammatory response).
Necrosis, on the other hand, results in rapid cell lysis and
a widespread inflammatory reaction without the activation
of internal cell death pathways. Sometimes it is referred to as
“extrinsic cell death,” as opposed to apoptosis, which is the
result of endogenous cell death pathways. A characteristic
biochemical feature of apoptosis is DNA fragmentation into
multiple smaller fragments, which are readily detected by
agarose gel electrophoresis as a characteristic “DNA ladder”
formation. In contrast, necrosis causes random cleavage of
DNA, resulting in a diffuse smear on DNA electrophoresis.
The annexin V (AV)/propidium iodide (PI) assay appears
to be the most sensitive, specific, and user-friendly method
for measuring apoptosis but also concurrently provides
quantitative data about the number of vital and necrotic
cells. In the early stages of apoptosis, phosphatidyl serine
(PS) is externalized to the outer plasma membrane.
Fluorescein isothiocyanate (FITC)-labeled AV, in the
presence of calcium ions, immediately adheres to PS, which
results in green fluorescence of the cells. This binding serves
as a specific indicator of early-stage apoptosis in cells whose
cell membrane is still intact, as demonstrated by the exclu-sion of the nuclear stain propidium iodide (PI). In cells that
have lost their membrane integrity (necrotic cells), PI read-ily traverses the leaky membrane and binds to the DNA,
inducing red fluorescence of the nucleus. The AV/PI assay
can, therefore, not only measure the extent of early apopto-sis (AV7PF) but also concurrently provides information
about the number of vital cells (AVTPr) and necrotic cells
(AV7PI
+
). Of note, differentiating between necrotic (AVTPF)
and late apopfotic (AV7PI
+
) cells may be difficult with this
assay. The terminal deoxynucleotidyl transferase nick-end
labeling (TUNEL) method also measures cellular apoptosis
(the method traditionally used), but it has proven to be less
specific and sensitive and more time-consuming and expen-sive than the AV/PI assay, as described in the literature
(Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross,
pp. 41-44; Schwartz, pp. 1268-1279).
- Mobilizes the immune system
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
B. Necrosis
Cellular injury, including
DNA damage induced by radiation or certain chemothera-peutic 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 up-stream (initiator) and downstream (effector) products known
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 aggregation 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 multiprotein
complex composed of APAF-1, caspase 9, cytochrome c, and
ATP. This, in turn, leads to activation of caspase 9 via
allosteric regulation by APAF-1. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as 3 and 7, by cleavage. These downstream effector
caspases, in turn, cleave multiple cellular proteins, trigger-ing a range of apoptotic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phago-cytosis (avoiding an inflammatory response).
Necrosis, on the other hand, results in rapid cell lysis and
a widespread inflammatory reaction without the activation
of internal cell death pathways. Sometimes it is referred to as
“extrinsic cell death,” as opposed to apoptosis, which is the
result of endogenous cell death pathways. A characteristic
biochemical feature of apoptosis is DNA fragmentation into
multiple smaller fragments, which are readily detected by
agarose gel electrophoresis as a characteristic “DNA ladder”
formation. In contrast, necrosis causes random cleavage of
DNA, resulting in a diffuse smear on DNA electrophoresis.
The annexin V (AV)/propidium iodide (PI) assay appears
to be the most sensitive, specific, and user-friendly method
for measuring apoptosis but also concurrently provides
quantitative data about the number of vital and necrotic
cells. In the early stages of apoptosis, phosphatidyl serine
(PS) is externalized to the outer plasma membrane.
Fluorescein isothiocyanate (FITC)-labeled AV, in the
presence of calcium ions, immediately adheres to PS, which
results in green fluorescence of the cells. This binding serves
as a specific indicator of early-stage apoptosis in cells whose
cell membrane is still intact, as demonstrated by the exclu-sion of the nuclear stain propidium iodide (PI). In cells that
have lost their membrane integrity (necrotic cells), PI read-ily traverses the leaky membrane and binds to the DNA,
inducing red fluorescence of the nucleus. The AV/PI assay
can, therefore, not only measure the extent of early apopto-sis (AV7PF) but also concurrently provides information
about the number of vital cells (AVTPr) and necrotic cells
(AV7PI+). Of note, differentiating between necrotic (AVTPF)
and late apopfotic (AV7PI+) cells may be difficult with this
assay. The terminal deoxynucleotidyl transferase nick-end
labeling (TUNEL) method also measures cellular apoptosis
(the method traditionally used), but it has proven to be less
specific and sensitive and more time-consuming and expen-sive than the AV/PI assay, as described in the literature
(Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross,
pp. 41-44; Schwartz, pp. 1268-1279).
- The mechanism of cell death after radiation therapy
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
C. Both
Cellular injury, including
DNA damage induced by radiation or certain chemothera-peutic 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 up-stream (initiator) and downstream (effector) products known
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 aggregation 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 multiprotein
complex composed of APAF-1, caspase 9, cytochrome c, and
ATP. This, in turn, leads to activation of caspase 9 via
allosteric regulation by APAF-1. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as 3 and 7, by cleavage. These downstream effector
caspases, in turn, cleave multiple cellular proteins, trigger-ing a range of apoptotic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phago-cytosis (avoiding an inflammatory response).
Necrosis, on the other hand, results in rapid cell lysis and
a widespread inflammatory reaction without the activation
of internal cell death pathways. Sometimes it is referred to as
“extrinsic cell death,” as opposed to apoptosis, which is the
result of endogenous cell death pathways. A characteristic
biochemical feature of apoptosis is DNA fragmentation into
multiple smaller fragments, which are readily detected by
agarose gel electrophoresis as a characteristic “DNA ladder”
formation. In contrast, necrosis causes random cleavage of
DNA, resulting in a diffuse smear on DNA electrophoresis.
The annexin V (AV)/propidium iodide (PI) assay appears
to be the most sensitive, specific, and user-friendly method
for measuring apoptosis but also concurrently provides
quantitative data about the number of vital and necrotic
cells. In the early stages of apoptosis, phosphatidyl serine
(PS) is externalized to the outer plasma membrane.
Fluorescein isothiocyanate (FITC)-labeled AV, in the
presence of calcium ions, immediately adheres to PS, which
results in green fluorescence of the cells. This binding serves
as a specific indicator of early-stage apoptosis in cells whose
cell membrane is still intact, as demonstrated by the exclu-sion of the nuclear stain propidium iodide (PI). In cells that
have lost their membrane integrity (necrotic cells), PI read-ily traverses the leaky membrane and binds to the DNA,
inducing red fluorescence of the nucleus. The AV/PI assay
can, therefore, not only measure the extent of early apopto-sis (AV7PF) but also concurrently provides information
about the number of vital cells (AVTPr) and necrotic cells
(AV7PI+). Of note, differentiating between necrotic (AVTPF)
and late apopfotic (AV7PI+) cells may be difficult with this
assay. The terminal deoxynucleotidyl transferase nick-end
labeling (TUNEL) method also measures cellular apoptosis
(the method traditionally used), but it has proven to be less
specific and sensitive and more time-consuming and expen-sive than the AV/PI assay, as described in the literature
(Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross,
pp. 41-44; Schwartz, pp. 1268-1279).
- Type of cell death detected by the annexin V/propidium
iodide assay
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
C. Both
Cellular injury, including
DNA damage induced by radiation or certain chemothera-peutic 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 up-stream (initiator) and downstream (effector) products known
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 aggregation 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 multiprotein
complex composed of APAF-1, caspase 9, cytochrome c, and
ATP. This, in turn, leads to activation of caspase 9 via
allosteric regulation by APAF-1. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as 3 and 7, by cleavage. These downstream effector
caspases, in turn, cleave multiple cellular proteins, trigger-ing a range of apoptotic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phago-cytosis (avoiding an inflammatory response).
Necrosis, on the other hand, results in rapid cell lysis and
a widespread inflammatory reaction without the activation
of internal cell death pathways. Sometimes it is referred to as
“extrinsic cell death,” as opposed to apoptosis, which is the
result of endogenous cell death pathways. A characteristic
biochemical feature of apoptosis is DNA fragmentation into
multiple smaller fragments, which are readily detected by
agarose gel electrophoresis as a characteristic “DNA ladder”
formation. In contrast, necrosis causes random cleavage of
DNA, resulting in a diffuse smear on DNA electrophoresis.
The annexin V (AV)/propidium iodide (PI) assay appears
to be the most sensitive, specific, and user-friendly method
for measuring apoptosis but also concurrently provides
quantitative data about the number of vital and necrotic
cells. In the early stages of apoptosis, phosphatidyl serine
(PS) is externalized to the outer plasma membrane.
Fluorescein isothiocyanate (FITC)-labeled AV, in the
presence of calcium ions, immediately adheres to PS, which
results in green fluorescence of the cells. This binding serves
as a specific indicator of early-stage apoptosis in cells whose
cell membrane is still intact, as demonstrated by the exclu-sion of the nuclear stain propidium iodide (PI). In cells that
have lost their membrane integrity (necrotic cells), PI read-ily traverses the leaky membrane and binds to the DNA,
inducing red fluorescence of the nucleus. The AV/PI assay
can, therefore, not only measure the extent of early apopto-sis (AV7PF) but also concurrently provides information
about the number of vital cells (AVTPr) and necrotic cells
(AV7PI+). Of note, differentiating between necrotic (AVTPF)
and late apopfotic (AV7PI+) cells may be difficult with this
assay. The terminal deoxynucleotidyl transferase nick-end
labeling (TUNEL) method also measures cellular apoptosis
(the method traditionally used), but it has proven to be less
specific and sensitive and more time-consuming and expen-sive than the AV/PI assay, as described in the literature
(Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross,
pp. 41-44; Schwartz, pp. 1268-1279).
- 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
Cellular injury, including
DNA damage induced by radiation or certain chemothera-peutic 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 up-stream (initiator) and downstream (effector) products known
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 aggregation 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 multiprotein
complex composed of APAF-1, caspase 9, cytochrome c, and
ATP. This, in turn, leads to activation of caspase 9 via
allosteric regulation by APAF-1. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as 3 and 7, by cleavage. These downstream effector
caspases, in turn, cleave multiple cellular proteins, trigger-ing a range of apoptotic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phago-cytosis (avoiding an inflammatory response).
Necrosis, on the other hand, results in rapid cell lysis and
a widespread inflammatory reaction without the activation
of internal cell death pathways. Sometimes it is referred to as
“extrinsic cell death,” as opposed to apoptosis, which is the
result of endogenous cell death pathways. A characteristic
biochemical feature of apoptosis is DNA fragmentation into
multiple smaller fragments, which are readily detected by
agarose gel electrophoresis as a characteristic “DNA ladder”
formation. In contrast, necrosis causes random cleavage of
DNA, resulting in a diffuse smear on DNA electrophoresis.
The annexin V (AV)/propidium iodide (PI) assay appears
to be the most sensitive, specific, and user-friendly method
for measuring apoptosis but also concurrently provides
quantitative data about the number of vital and necrotic
cells. In the early stages of apoptosis, phosphatidyl serine
(PS) is externalized to the outer plasma membrane.
Fluorescein isothiocyanate (FITC)-labeled AV, in the
presence of calcium ions, immediately adheres to PS, which
results in green fluorescence of the cells. This binding serves
as a specific indicator of early-stage apoptosis in cells whose
cell membrane is still intact, as demonstrated by the exclu-sion of the nuclear stain propidium iodide (PI). In cells that
have lost their membrane integrity (necrotic cells), PI read-ily traverses the leaky membrane and binds to the DNA,
inducing red fluorescence of the nucleus. The AV/PI assay
can, therefore, not only measure the extent of early apopto-sis (AV7PF) but also concurrently provides information
about the number of vital cells (AVTPr) and necrotic cells
(AV7PI+). Of note, differentiating between necrotic (AVTPF)
and late apopfotic (AV7PI+) cells may be difficult with this
assay. The terminal deoxynucleotidyl transferase nick-end
labeling (TUNEL) method also measures cellular apoptosis
(the method traditionally used), but it has proven to be less
specific and sensitive and more time-consuming and expen-sive than the AV/PI assay, as described in the literature
(Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross,
pp. 41-44; Schwartz, pp. 1268-1279).
- Rapid cell lysis
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
B. Necrosis
Cellular injury, including
DNA damage induced by radiation or certain chemothera-peutic 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 up-stream (initiator) and downstream (effector) products known
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 aggregation 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 multiprotein
complex composed of APAF-1, caspase 9, cytochrome c, and
ATP. This, in turn, leads to activation of caspase 9 via
allosteric regulation by APAF-1. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as 3 and 7, by cleavage. These downstream effector
caspases, in turn, cleave multiple cellular proteins, trigger-ing a range of apoptotic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phago-cytosis (avoiding an inflammatory response).
Necrosis, on the other hand, results in rapid cell lysis and
a widespread inflammatory reaction without the activation
of internal cell death pathways. Sometimes it is referred to as
“extrinsic cell death,” as opposed to apoptosis, which is the
result of endogenous cell death pathways. A characteristic
biochemical feature of apoptosis is DNA fragmentation into
multiple smaller fragments, which are readily detected by
agarose gel electrophoresis as a characteristic “DNA ladder”
formation. In contrast, necrosis causes random cleavage of
DNA, resulting in a diffuse smear on DNA electrophoresis.
The annexin V (AV)/propidium iodide (PI) assay appears
to be the most sensitive, specific, and user-friendly method
for measuring apoptosis but also concurrently provides
quantitative data about the number of vital and necrotic
cells. In the early stages of apoptosis, phosphatidyl serine
(PS) is externalized to the outer plasma membrane.
Fluorescein isothiocyanate (FITC)-labeled AV, in the
presence of calcium ions, immediately adheres to PS, which
results in green fluorescence of the cells. This binding serves
as a specific indicator of early-stage apoptosis in cells whose
cell membrane is still intact, as demonstrated by the exclu-sion of the nuclear stain propidium iodide (PI). In cells that
have lost their membrane integrity (necrotic cells), PI read-ily traverses the leaky membrane and binds to the DNA,
inducing red fluorescence of the nucleus. The AV/PI assay
can, therefore, not only measure the extent of early apopto-sis (AV7PF) but also concurrently provides information
about the number of vital cells (AVTPr) and necrotic cells
(AV7PI+). Of note, differentiating between necrotic (AVTPF)
and late apopfotic (AV7PI+) cells may be difficult with this
assay. The terminal deoxynucleotidyl transferase nick-end
labeling (TUNEL) method also measures cellular apoptosis
(the method traditionally used), but it has proven to be less
specific and sensitive and more time-consuming and expen-sive than the AV/PI assay, as described in the literature
(Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross,
pp. 41-44; Schwartz, pp. 1268-1279).
- 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
Cellular injury, including
DNA damage induced by radiation or certain chemothera-peutic 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 up-stream (initiator) and downstream (effector) products known
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 aggregation 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 multiprotein
complex composed of APAF-1, caspase 9, cytochrome c, and
ATP. This, in turn, leads to activation of caspase 9 via
allosteric regulation by APAF-1. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as 3 and 7, by cleavage. These downstream effector
caspases, in turn, cleave multiple cellular proteins, trigger-ing a range of apoptotic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phago-cytosis (avoiding an inflammatory response).
Necrosis, on the other hand, results in rapid cell lysis and
a widespread inflammatory reaction without the activation
of internal cell death pathways. Sometimes it is referred to as
“extrinsic cell death,” as opposed to apoptosis, which is the
result of endogenous cell death pathways. A characteristic
biochemical feature of apoptosis is DNA fragmentation into
multiple smaller fragments, which are readily detected by
agarose gel electrophoresis as a characteristic “DNA ladder”
formation. In contrast, necrosis causes random cleavage of
DNA, resulting in a diffuse smear on DNA electrophoresis.
The annexin V (AV)/propidium iodide (PI) assay appears
to be the most sensitive, specific, and user-friendly method
for measuring apoptosis but also concurrently provides
quantitative data about the number of vital and necrotic
cells. In the early stages of apoptosis, phosphatidyl serine
(PS) is externalized to the outer plasma membrane.
Fluorescein isothiocyanate (FITC)-labeled AV, in the
presence of calcium ions, immediately adheres to PS, which
results in green fluorescence of the cells. This binding serves
as a specific indicator of early-stage apoptosis in cells whose
cell membrane is still intact, as demonstrated by the exclu-sion of the nuclear stain propidium iodide (PI). In cells that
have lost their membrane integrity (necrotic cells), PI read-ily traverses the leaky membrane and binds to the DNA,
inducing red fluorescence of the nucleus. The AV/PI assay
can, therefore, not only measure the extent of early apopto-sis (AV7PF) but also concurrently provides information
about the number of vital cells (AVTPr) and necrotic cells
(AV7PI+). Of note, differentiating between necrotic (AVTPF)
and late apopfotic (AV7PI+) cells may be difficult with this
assay. The terminal deoxynucleotidyl transferase nick-end
labeling (TUNEL) method also measures cellular apoptosis
(the method traditionally used), but it has proven to be less
specific and sensitive and more time-consuming and expen-sive than the AV/PI assay, as described in the literature
(Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross,
pp. 41-44; Schwartz, pp. 1268-1279).
- DNA ladder formation on gel electrophoresis
A. Apoptosis
B. Necrosis
C. Both
D. None of the above
A. Apoptosis
Cellular injury, including
DNA damage induced by radiation or certain chemothera-peutic 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 up-stream (initiator) and downstream (effector) products known
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 aggregation 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 multiprotein
complex composed of APAF-1, caspase 9, cytochrome c, and
ATP. This, in turn, leads to activation of caspase 9 via
allosteric regulation by APAF-1. Once activated, the initiator
caspases, caspases 8 and 9, activate downstream caspases,
such as 3 and 7, by cleavage. These downstream effector
caspases, in turn, cleave multiple cellular proteins, trigger-ing a range of apoptotic events such as nuclear membrane
blebbing, DNA condensation and fragmentation, and phago-cytosis (avoiding an inflammatory response).
Necrosis, on the other hand, results in rapid cell lysis and
a widespread inflammatory reaction without the activation
of internal cell death pathways. Sometimes it is referred to as
“extrinsic cell death,” as opposed to apoptosis, which is the
result of endogenous cell death pathways. A characteristic
biochemical feature of apoptosis is DNA fragmentation into
multiple smaller fragments, which are readily detected by
agarose gel electrophoresis as a characteristic “DNA ladder”
formation. In contrast, necrosis causes random cleavage of
DNA, resulting in a diffuse smear on DNA electrophoresis.
The annexin V (AV)/propidium iodide (PI) assay appears
to be the most sensitive, specific, and user-friendly method
for measuring apoptosis but also concurrently provides
quantitative data about the number of vital and necrotic
cells. In the early stages of apoptosis, phosphatidyl serine
(PS) is externalized to the outer plasma membrane.
Fluorescein isothiocyanate (FITC)-labeled AV, in the
presence of calcium ions, immediately adheres to PS, which
results in green fluorescence of the cells. This binding serves
as a specific indicator of early-stage apoptosis in cells whose
cell membrane is still intact, as demonstrated by the exclu-sion of the nuclear stain propidium iodide (PI). In cells that
have lost their membrane integrity (necrotic cells), PI read-ily traverses the leaky membrane and binds to the DNA,
inducing red fluorescence of the nucleus. The AV/PI assay
can, therefore, not only measure the extent of early apopto-sis (AV7PF) but also concurrently provides information
about the number of vital cells (AVTPr) and necrotic cells
(AV7PI+). Of note, differentiating between necrotic (AVTPF)
and late apopfotic (AV7PI+) cells may be difficult with this
assay. The terminal deoxynucleotidyl transferase nick-end
labeling (TUNEL) method also measures cellular apoptosis
(the method traditionally used), but it has proven to be less
specific and sensitive and more time-consuming and expen-sive than the AV/PI assay, as described in the literature
(Kandel, pp. 1058-1061; Overbeeke, pp. 115-121; Ross,
pp. 41-44; Schwartz, pp. 1268-1279).
- 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. Gl” channel
E. Mg2+channel
C. Ca2+-sensitive K+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-electrode allows K+
influx into the cell and depolarization.
Depolarization opens voltage-sensitive Ca2+
channels, which augments depolarization by allowing Ca2+ entry into the cell. As Ca2+
accumulates in the cytoplasm, it activates Ca2+
-sensitive K+ channels, which along with voltage-sensitive K+ channels allow for K+ 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
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 transec-tion 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 forma-tion 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 releas-ing 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 decere-brate 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 vestibu-lospinal facilitation of arm extensors but not leg extensors
(Kandel, pp. 654-656, 717, 841; Greenberg, pp. 118-119; Pritchard, pp. 254-259; Merritt, p. 18).
- Neurotransmitter release at the synaptic terminal is trig-gered mainly by which ion?
A. Na+
B. K+
C. Cl”
D. Ca2+
E. Mg2+
D. Ca2+
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 CI” conductance
B. Increase in Na+conductance
C. Increase in Ca2+conductance
D. Decrease in K+conductance
E. Increase in K+conductance
E. Increase in K+conductance
.A typical neuron has a resting membrane potential of
-65 mV. The equilibrium potential for K+ is -86 mV, and an increase in conductance of this ion would result in move-ment of the neurons membrane potential toward -86 mV and hyperpolarization. The EQ (-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 Ga2+conductance would lead to
depolarization of the neuron instead of hyperpolarization
(Kandel, pp. 150-170).
- Which of the following would increase conduction vel-
ocity in an axon? - Increasing the diameter of an axon
- Increasing the transmembrane resistance (P^)
- Decreasing the capacitance of the membrane (Cm)
- Decreasing the membrane length constant (A,)
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. 1, 2, and 3 are correct
How rapidly an action potential travels through an
axon depends on a number of factors, including the internal resistance of an axon (Rj), the transmembrane resistance of the plasma membrane (PO , (inversely related to the number of ion channels), and membrane capacitance (Gm). 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 cur-rent 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 Rj and allow the action potential to be conducted down the axon with increased conduction velocity. Increasing the R^ 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 R^, to Rj
is called the membrane length constant (A.) and represents the distance between the point of peak depolarization pro-duced 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 cytoplas-mic resistance (increasing X). In terms of Cm, 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 oppo-site sides of the plasma membrane increases with decreased membrane thickness. Therefore thinner axons 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 mem-brane (and continue current propagation down the axon). The addition of myelin around an axon increases conduction velocity because it decreases Gm (increases membrane thick-ness). 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 membra-
nous 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)
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 appear-ance 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 mem-brane, 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 (on the floor of the vestibule) and the macula of the saccule lies in the vertical plane (on the medial wall of the vestibule). Linear acceleration 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).
Scenario: A 52-year-old male underwent subtotal resection of a glioblastoma multiforme 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, 3-6is-2-chloroethyl-l-nitrosourea (BGNU). The patient succumbed to his disease process 8 months later.
- Resistance of this tumor to BGNU may have resulted from
A. A high concentration of C-alkylguanine-DNA alkyl-
transferase (06-AGAT) in tumor cells
B. The tumor was in the S phase of the cell cycle (resis-tant phase) during administration of BGNU
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 recog-nize BGNU
E. An agent that disrupts the blood-brain barrier was not administered concurrently with BGNU
A. A high concentration of C-alkylguanine-DNA alkyl-
transferase (06-AGAT) in tumor cells
The nitrosoureas (BGNU, CGNU) are alkylating agents and are the most widely used drugs for patients with malig-nant 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 double-stranded DNA breaks and eventual tumor cell death. 06-AGAT is a repair enzyme that mediates repair of alkylation products of nitrosoureas. It has been noted that approxi-mately 70% of tumors have high levels of 06-AGAT and are often resistant to nitrosourea chemotherapy (Bernstein, pp. 231-232).
- Most sensitive to skin stretch
A. Free nerve endings
B. Meissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. Merkel’s discs
F. None of the above
D. Ruffini’s corpuscles
Refer to Figure 1.19-1.25A. Sensory endings of the skin can be classified on a structural basis into encapsulated and nonencapsulated re-ceptors. Nonencapsulated receptors include free nerve end-ings, MerkePs discs, and hair follicle receptors. Encapsulated endings include Meissner’s corpuscles, pacinian corpuscles, and Ruffini’s corpuscles. Free nerve endings are widely dis-tributed 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, pres-sure, and tickling sensations. MerkePs 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 tex-ture. MerkePs disc receptors also provide the sharpest res-olution 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 MerkePs endings because they have slightly
larger receptive fields. MerkePs 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 soles of the feet. They are oval in shape and consist of a stack of flattened Schwann 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 dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 100-500 Jim across (largest sensory receptor). The capsule consists of concen-tric 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 la 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. Meissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. Merkel’s discs
F. None of the above
C. Pacinian corpuscles
Refer to Figure 1.19-1.25A. Sensory endings of the skin can be classified on a structural basis into encapsulated and nonencapsulated re-ceptors. Nonencapsulated receptors include free nerve end-ings, MerkePs discs, and hair follicle receptors. Encapsulated endings include Meissner’s corpuscles, pacinian corpuscles, and Ruffini’s corpuscles. Free nerve endings are widely dis-tributed 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, pres-sure, and tickling sensations. MerkePs 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 tex-ture. MerkePs disc receptors also provide the sharpest res-olution 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 MerkePs endings because they have slightly
larger receptive fields. MerkePs 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 soles of the feet. They are oval in shape and consist of a stack of flattened Schwann 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 dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 100-500 Jim across (largest sensory receptor). The capsule consists of concen-tric 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 la fibers innervate the afferent limb of the stretch reflex (Kandel, pp. 430-450,565).
- Mostly found in clusters at the center of the papillary rjdge
A. Free nerve endings
B. Meissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. Merkel’s discs
F. None of the above
F. None of the above
Refer to Figure 1.19-1.25A. Sensory endings of the skin can be classified on a structural basis into encapsulated and nonencapsulated re-ceptors. Nonencapsulated receptors include free nerve end-ings, MerkePs discs, and hair follicle receptors. Encapsulated endings include Meissner’s corpuscles, pacinian corpuscles, and Ruffini’s corpuscles. Free nerve endings are widely dis-tributed 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, pres-sure, and tickling sensations. MerkePs 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 tex-ture. MerkePs disc receptors also provide the sharpest res-olution 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 MerkePs endings because they have slightly
larger receptive fields. MerkePs 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 soles of the feet. They are oval in shape and consist of a stack of flattened Schwann 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 dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 100-500 Jim across (largest sensory receptor). The capsule consists of concen-tric 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 la fibers innervate the afferent limb of the stretch reflex (Kandel, pp. 430-450,565).
- Provide sharpest resolution of spatial pattern
A. Free nerve endings
B. Meissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. Merkel’s discs
F. None of the above
F. None of the above
Refer to Figure 1.19-1.25A. Sensory endings of the skin can be classified on a structural basis into encapsulated and nonencapsulated re-ceptors. Nonencapsulated receptors include free nerve end-ings, MerkePs discs, and hair follicle receptors. Encapsulated endings include Meissner’s corpuscles, pacinian corpuscles, and Ruffini’s corpuscles. Free nerve endings are widely dis-tributed 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, pres-sure, and tickling sensations. MerkePs 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 tex-ture. MerkePs disc receptors also provide the sharpest res-olution 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 MerkePs endings because they have slightly
larger receptive fields. MerkePs 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 soles of the feet. They are oval in shape and consist of a stack of flattened Schwann 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 dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 100-500 Jim across (largest sensory receptor). The capsule consists of concen-tric 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 la fibers innervate the afferent limb of the stretch reflex (Kandel, pp. 430-450,565).
- Line the alimentary tract
A. Free nerve endings
B. Meissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. Merkel’s discs
F. None of the above
A. Free nerve endings
Refer to Figure 1.19-1.25A. Sensory endings of the skin can be classified on a structural basis into encapsulated and nonencapsulated re-ceptors. Nonencapsulated receptors include free nerve end-ings, MerkePs discs, and hair follicle receptors. Encapsulated endings include Meissner’s corpuscles, pacinian corpuscles, and Ruffini’s corpuscles. Free nerve endings are widely dis-tributed 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, pres-sure, and tickling sensations. MerkePs 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 tex-ture. MerkePs disc receptors also provide the sharpest res-olution 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 MerkePs endings because they have slightly
larger receptive fields. MerkePs 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 soles of the feet. They are oval in shape and consist of a stack of flattened Schwann 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 dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 100-500 Jim across (largest sensory receptor). The capsule consists of concen-tric 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 la 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. Meissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. Merkel’s discs
F. None of the above
F. None of the above
Refer to Figure 1.19-1.25A. Sensory endings of the skin can be classified on a structural basis into encapsulated and nonencapsulated re-ceptors. Nonencapsulated receptors include free nerve end-ings, MerkePs discs, and hair follicle receptors. Encapsulated endings include Meissner’s corpuscles, pacinian corpuscles, and Ruffini’s corpuscles. Free nerve endings are widely dis-tributed 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, pres-sure, and tickling sensations. MerkePs 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 tex-ture. MerkePs disc receptors also provide the sharpest res-olution 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 MerkePs endings because they have slightly
larger receptive fields. MerkePs 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 soles of the feet. They are oval in shape and consist of a stack of flattened Schwann 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 dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 100-500 Jim across (largest sensory receptor). The capsule consists of concen-tric 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 la 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. Meissner’s corpuscles
C. Pacinian corpuscles
D. Ruffini’s corpuscles
E. Merkel’s discs
F. None of the above
E. Merkel’s discs
Refer to Figure 1.19-1.25A. Sensory endings of the skin can be classified on a structural basis into encapsulated and nonencapsulated re-ceptors. Nonencapsulated receptors include free nerve end-ings, MerkePs discs, and hair follicle receptors. Encapsulated endings include Meissner’s corpuscles, pacinian corpuscles, and Ruffini’s corpuscles. Free nerve endings are widely dis-tributed 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, pres-sure, and tickling sensations. MerkePs 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 tex-ture. MerkePs disc receptors also provide the sharpest res-olution 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 MerkePs endings because they have slightly
larger receptive fields. MerkePs 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 soles of the feet. They are oval in shape and consist of a stack of flattened Schwann 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 dermis, subcutaneous tissues, joint capsules, pleura, pericardium, and nipples. Each pacinian corpuscle is ovoid shape, measuring 2 mm long and about 100-500 Jim across (largest sensory receptor). The capsule consists of concen-tric 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 la fibers innervate the afferent limb of the stretch reflex (Kandel, pp. 430-450,565).
