(Download PDF) Development of The Nervous System 3rd Edition Sanes Test Bank Full Chapter

Development of the Nervous System
3rd Edition Sanes Test Bank

Go to download the full and correct content document:
https://testbankfan.com/product/development-of-the-nervous-system-3rd-edition-sane
s-test-bank/
More products digital (pdf, epub, mobi) instant
download maybe you interests ...
Muscular System Manual The Skeletal Muscles of the

Human Body 3rd Edition Muscolino Test Bank
https://testbankfan.com/product/muscular-system-manual-the-
skeletal-muscles-of-the-human-body-3rd-edition-muscolino-test-
bank/
Money Banking and the Financial System 3rd Edition

Hubbard Test Bank
https://testbankfan.com/product/money-banking-and-the-financial-
system-3rd-edition-hubbard-test-bank/
Understanding the Australian Health Care System 3rd

Edition Willis Test Bank
https://testbankfan.com/product/understanding-the-australian-
health-care-system-3rd-edition-willis-test-bank/
Basics of the U.S. Health Care System 2nd Edition Niles

Test Bank
https://testbankfan.com/product/basics-of-the-u-s-health-care-
system-2nd-edition-niles-test-bank/
Money Banking and the Financial System 3rd Edition
Hubbard Solutions Manual
https://testbankfan.com/product/money-banking-and-the-financial-
system-3rd-edition-hubbard-solutions-manual/
American Political System 3rd Edition Kollman Test Bank
https://testbankfan.com/product/american-political-system-3rd-
edition-kollman-test-bank/
Essentials of Life Span Development 3rd Edition

Santrock Test Bank
https://testbankfan.com/product/essentials-of-life-span-
development-3rd-edition-santrock-test-bank/
Essentials of Life-Span Development 3rd Edition

Santrock Test Bank
https://testbankfan.com/product/essentials-of-life-span-
development-3rd-edition-santrock-test-bank-2/
Basic Immunology Functions And Disorders Of The Immune

System 5th Edition Abbas Test Bank
https://testbankfan.com/product/basic-immunology-functions-and-
disorders-of-the-immune-system-5th-edition-abbas-test-bank/
Sanes Chapter 7 questions
[1] Does the weight of the human brain change after neurogenesis is complete?
a. Yes, it doubles in weight

b. Yes, it adds over 3 times its weight*
c. Yes, it adds over 5 times its weight
d. Yes, it adds weight then loses weight by adulthood
[2] During development of the nervous system, programmed cell death is best
defined as
a. Post-mitotic nerve cells that fail to reach their post-synaptic targets die
b. Post-mitotic nerve cells actively die through protein synthesis and gene
transcription*
c. Depending upon the region of the brain 20% to 80% of differentiated post-
mitotic neurons degenerate during maturation
d. None of these is a good definition
[3] To escape programmed cell death neurons receive survival signals from
several sources; which one of these is NOT a source of these trophic factors?
a. Synaptic inputs from other neurons

b. Glial cells in the cellular matrix
c. Blood-borne factors from distant sources
d. Microtubules within the neuron itself*
[4] The general process by which programmed cell death usually occurs is called
a. Pyknosis
b. Phagocytosis
c. Apoptosis*
d. Enzyme cleavage of DNA
[5] The purpose of TUNEL labeling is
a. To label DNA in dying neurons before fragmentation

b. To detect the nuclei of dying neurons before the cells are phagocytosed*
c. To detect phagocytosis of the cells of dying neurons
1
d. To detect pyknosis in dying neurons
[6] A second form of programmed cell death, though to possibly be a late stage, is
a. An autophagic process
b. An autolysosomic process
c. An autophagosomic process
d. All of these are correct*
[7] In necrosis as opposed to apoptosis neurons ________ as they degenerate.
a. Swell*
b. Shrink
c. Remain approximately the same size
d. None of these are correct
[8] The earliest stage of PCD eliminates some progenitor neural cells from the
proliferative zone.
a. True*
b. False
[9] In addition to the PCD of neurons, about ______ percent of oligodendrocytes

in the rat optic nerve undergo PCD
a. 50*
b. 20
c. 37
d. 67
[10] Difficulty in obtaining an accurate count of the number of neurons during

development is exacerbated by
a. PCD and neurogenesis overlapping in time

b. Changes in the size of neurons during development
c. Changes in the packing density of cells in neural tissue
2
[11] Experiments that manipulate the afferent target of developing neurons such
as removing muscle or transplanting an extra limb bud have shown that
a. The number of neurons that die off due to PCD is relatively constant
b. The number of neurons that survive PCD varies according to the size of the
afferent target*
c. The number of neurons that survive PCD is relatively constant
d. There is little relationship between the size of the afferent target and the
number of neurons that survive PCD
[12] A disparity in the rate of PCD in pre- and post-synaptic nuclei in the
embryonic chick auditory system strongly suggests that
a. Change in target size is the sole determinant of neuron survival

b. Change in target size is unrelated to neuron survival
c. Change in target size is one factor influencing neuron survival*
[13] Transient interactions of growing axons with nearby tissue, before the axons
reach their targets, have virtually no effect on neuron survival.
a. True
b. False*
[14] The Levi-Montalcini and Hamburger experiments in the early 1950’s, in which
mouse tumor cells were transplanted into chick hind limb, demonstrated for the
first time that
a. There was a diffusible chemical that influenced sensory neuron survival*

b. Sensory neuron survival critically depended on afferent targets
c. Any target tissue could substitute for the hind limb muscle target for
regulating sensory neuron survival
d. The only sensory neurons whose survival was affected by target tissue were
those making direct physical connections to the target
[15] The accidental discovery that snake venom had a growth-promoting effect on
sympathetic ganglia suggested that
3
a. NGF was not a protein because venom breaks down proteins

b. NGF was a nucleic acid because venom breaks down proteins
c. NGF could be found in mammalian salivary glands*
d. NGF was found in many vertebrates but not mammals
[16] Placing cells from a sarcoma tumor line into a chick embryo on the
chorioallantoic membrane, causes
a. All sympathetic and DRG to increase in size*

b. Only ipsilateral sympathetic and DRG to increase in size
c. No changes in sympathetic and DRG growth
[17] Injecting an antibody directed against NGF in neonatal rodents demonstrated

that
a. NGF is necessary for sympathetic neuron survival

b. NGF is not necessary for DRG cell survival
c. DRG cells can only be destroyed by prenatal exposure to NGF antibody
[18] NGF antibody treatment at an early embryonic stage of development will

adversely affect the survival of all DRG cells and all sensory neurons.
a. True
b. False*
[19] Some neurons may be NGF dependent and independent, at different stages
of development.
a. True*
b. False
[20] When brain derived growth factor (BDNF), was first purified and its amino
acid sequence determined, its structure displayed a striking similarity to
a. NGF*
b. NT-3
c. NT-4/5
4
d. NT-6
[21] The region of each neurotrophin that is responsible for its binding to a
specific receptor are
a. The unique amino acid sequences*
b. One or more of the six hydrophobic regions
c. The hodimers formed from the pro-peptides
d. All of these are true
[22] Different members of the neurotrophin family play a role in the survival of
a. Species-specific classes of neurons
b. General central neuron populations
c. Specific peripheral neuron populations*
d. Neurons in most vertebrates except fish
[23] Neurotrophin ligands bind selectively to the tyrosine kinase family of

receptors; NT-3 in particular binds
a. Selectively to the same receptor, TrkA, as NGF
b. Selectively to the same receptor, TrkB, as BDNF
c. Selectively to receptors that also bind NGF, BDNF and NT-4/5*
d. Selectively to the same receptor, p75NTR, as proNGF
[24] Eliminating one of the Trk tyrosine kinase receptors and thus preventing one
of the neurotrophins from binding to it, typically results in
a. Extensive cell death of a particular class of neurons such as the trigeminal
b. Moderate to extensive cell death of several neuron classes*
c. Few changes in PCD because of the redundant function of other receptors
d. General, unspecific changes in PCD
[25] The loss of NT-3 expression in single-gene knockout mice is likely to affect
DRG neurons when they first extend their axons, well before reaching their target.
a. True*
b. False
[26] Each TrK receptor gene is differentially spliced; trkC genes may encode for up
to eight different TrkC receptor proteins.
a. True*
5
b. False
[27] If a Trk receptor is activated in the absence of a neurotrophin, the process is

called
a. Autophosphorylation
b. Transactivation*
c. Coactivation
d. Non-neurotrophin activatio
[28] Each TrK receptor has a high specific affinity for

a. A single neurotrophin
b. One or two neurotrophins*
c. All neurotrophins
[29] Which tropomyosin related kinase proteins are high-affinity binding sites for
neurotrophins?
a. TrkB which binds BDNF or NT-4
b. TrkC which binds NT-3
c. Both TrkB and TrkC are high-affinity binding sites*
d. Neither TrkB and TrkC are high-affinity binding sites
[30] Any Trk receptor may be activated in the absence of any neurotrophin.
a. True*
b. False
[31] What is transactivation?

a. TrkB receptor being activated by NGF
b. TrkC receptor being activated by NGF
c. A Trk receptor being activated from within the neuron*
d. All of these are correct
[32] The observed pattern of NT-3 expression is that it is typically found

surrounding
a. The end of the limb that is not yet innervated
b. Around DRG but not sensory motor projection
c. Around sensory motor projection, DRG but not the end of the limb*
6
[33] What is the best evidence that Trk receptors mediate survival signals to
neurons?
a. Pc12 cells that lack TrkA protein do not respond to NGF
b. Transgenic mice lacking Trk receptors display extensive neuron death in
specific neuron populations
c. TrkC receptor deletion leads to loss of half of cochlear ganglion neurons
even though nodose and trigeminal neurons are spared
d. All of these are supporting evidence for Trk receptor mediated survival
signals*
[34] If the axons of cholinergic cells in the basal forebrain are cut, exogenous NGF
is able to keep them alive.
a. True*
b. False
[35] If the axons of cholinergic cells in the basal forebrain are cut, exogenous NT-3
or NT-4 is able to keep them alive.
a. True
b. False*
[36] In an experiment to determine how the neurotrophin NGF signal reaches the
soma of the developing neuron, sympathetic neuron cell bodies were cultured in
isolation from their neuritic processes. If the antibody against NGF is added to the
cultured cell bodies and NGF is added to the growing neurites, 95% of the
neurons survive; If the antibody against NGF is added to the cultured cell bodies
and NGF covalently bound to beads is added to the growing neurites, 81% of the
neurons survive. This demonstrates that
a. All of the NGF signal is acquired at the axon tip
b. Most of the NGF signal is acquired at the axon tip*
c. None of the NGF signal is acquired at the axon tip
d. All of the NGF signal is acquired directly by the cell body
[37] The neurotrophin signal that enters the axon tip during neurite growth gets
transported
a. Anterogradely to the cell nucleus along microtubules
7
b. Retrogradely to the cell nucleus along microtubules*

c. By diffusion through the extracellular medium
d. All of these are correct
[38] Neurotrophins released as uncleaved pro-peptides, which bind with high-

affinity to the P75NTR, are also known as
a. Proneurotrophins*
b. NGF
c. NT-3 or NT-4
d. BDNF
[39] The tumor necrosis factor receptor P75 differs from Trk receptors in that it
a. Does not have an intracellular signaling pathway*
b. Cannot activate intracellular signaling pathways
c. Is not homologous with other members of the TNFR family
d. Has no ‘death domain’ analogous to the reaper gene in Drosophila
[40] Among the processes by which P75NTR influences neuron death or survival is
a. Release of transcription activator NF-kB which enters the nucleus
b. Release of neurotrophin receptor interacting factor which activates c-Jun N-
terminal kinase (JNK)
c. c-Jun enters the nucleus to promote the transcription of pro-apoptotic
genes
d. all of these are among those processes*
[41] The beta amyloid peptide binds to the P75NTR which may contribute to the
degeneration of cholinergic brainstem neurons in Alzheimer’s
a. True*
b. False
[42] The convention for naming a cytokine is

a. derived from it’s most important biological function
b. derived from it’s first-discovered biological function*
c. derived from the cells on which its receptor is located
d. an arbitrary choice by the person who discovered it
8
[43] Cytokines have been shown to act as pro-apoptotic signals but not to support
neuron survival.
a. True
b. False*
[44] Elimination of one growth factor alone will typically have a major effect on
the survival of central neurons, unlike peripheral ganglion cells.
a. True
b. False*
[45] Glial cell line-derived neurotrophic factor (GDNF)

a. Prevents naturally-occurring motor neuron death
b. Ligand-receptor complexes become associated with a transmembrane
tyrosine kinase (RET)
c. Over-expression in mouse musculature led to increased survival of most
motor neuron populations
d. All of these are true*
[46] When neonatal male rats are castrated and reared with the androgen
agonist, flutamide
a. There is an increased number of SNB motor neurons
b. There is a decreased number of SNB motor neurons*
c. There is no change in the number of SNB motor neurons
d. Changes in the number of SNB motor neurons is independent of both
target muscle size and the type of treatment
[47] The differentiation of the sexually dimorphic nucleus of the preoptic area
evidently arises because estradiol protects against apoptosis in these neurons.
a. True*
b. False
[48] The earlier view was that endocrine signaling leading to sexual dimorphisms
in songbird telencephalic nuclei arises because of
a. Selective loss of cells in males
b. Hormonal influences on cell survival in females
c. Hormonal influences on cell survival in males*
9
[49] The current view is that endocrine signaling leading to sexual dimorphisms in
songbird telencephalic nuclei arises because of circulating steroid hormones
secreted by testicular tissue
a. True
b. False*
[50] A factor suggesting that steroid hormones widely influence naturally-

occurring cell death in areas beyond the sexually dimorphic pre-optic area is that
a. Cell death in male rat primary visual cortex ends almost two weeks before
that of females
b. Cell death in female sympathetic ganglia that innervate the face area is
greater than in males
c. Both of these are true*
d. Neither of these are true
[51] Circulating growth hormone (GH) released from the pituitary, acts directly on
organs such as the liver to stimulate Insulin-like growth factor 1 (IGF-1); IGF-1 may
also be synthesized in local regions of brain. If the expression of IGF-1 is
genetically increased in mice, what happens to the cerebral cortex?
a. Natural PCD was inhibited and the surviving cells persisted to adulthood*
b. Natural PCD was increased resulting in selective neuronal loss in certain
brain regions
c. The increased IGF-1 binds to TRs, creating a TH deficiency
d. Increased IGF-1 had no effect on PCD but dramatically increased the
number of TUNEL-positive cells in the ganglion cell layer
[52] Endocrine signals are responsible for remodeling the insect nervous system
during metamorphosis
a. A large decrease in 20-hydroxecdysone triggers pupa formation in moths
b. A small increase in 20-hydroxecdysone triggers the death of specific
abdominal motor neurons in the moth*
c. A large decrease in 20-hydroxecdysone triggers the molt in which the larva
sheds its cuticle and grows
d. In fruit flies, when levels of 20-hydroxecdysone rise, neurons in the ventral
cord die
10
[53] In vitro, sympathetic neurons die within two days if NGF is removed from the
culture medium; these neurons can be rescued if
a. A translation blocker is added to the medium
b. A transcription blocker is added to the medium
c. Either of these is added to the medium*
d. Neither of these is added to the medium
[54] If chick embryos are treated with either cycloheximide or actinomycin-D at

the stage when the PCD of DRG and motor neurons is at a peak, what happens?
a. The number of pyknotic neurons decreases
b. Fewer DRG cells die
c. Fewer motor neurons die
[55] Protein synthesis must occur in order for cells to die.

a. True*
b. False
[56] Gene transcription must occur in order for cells to die.

a. True*
b. False
[57] Which set is the correct sequence of neurotrophin signal transduction:

a. NT dimer binds to Trk , Trk dimerizes, adaptor proteins bind to
phosphorylation sites, ligand-receptor complex transphosphorylates
tyrosine residues, adaptor proteins are phosphorylated
b. NT dimer binds to Trk, adaptor proteins bind to phosphorylation sites, Trk
dimerizes, ligand-receptor complex transphosphorylates tyrosine residues,
adaptor proteins are phosphorylated
c. NT dimer binds to Trk, ligand-receptor complex transphosphorylates
tyrosine residues, adaptor proteins bind to phosphorylation sites, Trk
dimerizes, adaptor proteins are phosphorylated
d. NT dimer binds to Trk, Trk dimerizes, ligand-receptor complex
transphosphorylates tyrosine residues, adaptor proteins bind to
phosphorylation sites, adaptor proteins are phosphorylated*
11
[58] Following the first phosphorylation of an adaptor protein (Shc), two

intracellular pathways lead to the phosphorylation of cytoplasmic components
that participate in cell survival; these are
a. P13K-Akt and MAPK pathways*
b. JNK and Cdk pathways
c. P13K-Akt and JNK pathways
d. MAPK and Cdk pathways
[59] How do the two major NGF kinase pathways prevent cell death?
a. Inactivating pro-apoptotic proteins in cytoplasm and increasing
transcription of anti-apoptotic proteins*
b. Activating pro-apoptotic proteins in cytoplasm and increasing transcription
of anti-apoptotic proteins
c. Inactivating pro-apoptotic proteins in cytoplasm and decreasing
transcription of anti-apoptotic proteins
d. Activating pro-apoptotic proteins in cytoplasm and decreasing transcription
of anti-apoptotic proteins
[60] When neurotrophin-dependent neurons are deprived of NGF, what happens?

a. The JNK pathway becomes activated, leading to cell death*
b. The MAPK pathway becomes activated, leading to cell death
c. The JNK pathway becomes activated, leading to cell survival
d. The MAPK pathway becomes activated, leading to cell survival
[61] Which is an example of a pro-apoptotic protein?

a. CREB
b. Ras
c. Bcl-2
d. Bim*
[62] Regarding the Cdk intracellular signaling pathway, the consequence, in vitro,
of blockading cyclin-dependent kinases with Cdk inhibitors is to promote motor,
sensory, sympathetic, retinal and cerebellar neuron death.
a. True
b. False*
12
[63] Apoptosis in C. elegans requires the expression of genes, ced-3 and ced-4,
either within the cell or in a neighboring cell.
a. True
b. False*
[64] In worms, mammals and fruit flies, the pathways that regulate the effector
proteases that lead to naturally occurring apoptosis, share many of the same
components, including
a. pro- and anti-apoptotic regulators*
b. initiator proteases
c. regulatory IAP components
d. identical gene-expressed activating factors
[65] Cell death may occur without DNA fragmentation, but it would still be
identified with TUNEL labeling.
a. True
b. False*
[66] Free radicals such as O2.- and mitochondrial flavoproteins (AIF)may be

caspase-independent pathways for cell death.
a. True*
b. False
[67] A neuron’s mitochondrion outer membrane becomes permeable and

releases cytochrome c, AIF or Smac, causing the neuron to die. This is an example
of
a. A caspase pathway
b. A caspase-independent pathway*
c. An extra-cellular pathway
d. None of these
[68] In mammals, the Bcl-2 family of membrane-associated proteins

a. Are pro-apoptotic
b. Are anti-apoptotic
c. Are mostly pro-apoptotic (12 to 5)*
d. Are mostly anti-apoptotic (12 to 5)
13
[69] Transgenic mice that overexpress the Bcl-2 protein,

a. Have much bigger brains than controls*
b. Have much smaller brains than controls
c. Have brains the same size as controls except that the facial nucleus and
retina display a 40% increase in neuron number
d. Have brains the same size as controls except that the facial nucleus and
retina display a 40% decrease in neuron number
[70] The two major points in the nerve cell where regulation of apoptosis occurs
are:
a. Mitochondrial membrane and at the caspases*
b. At the caspases and the nerve cell’s outer membrane
c. At the nerve cell’s outer membrane and at the mitochondrial membrane
d. At the caspases and at the neurotrophins
[71] The inhibitors of apoptosis proteins (IAPs) serve as one of the so-called
‘safety latches’ on caspase activation; in Drosophila if three gene products (grim,
reaper, hid) that inhibit IAP function are lost, what happens?
a. Unrestrained activation of caspases and cell death
b. Almost no detectable PCD
c. Caspase activation is unaffected because of alternate pathway regulation
d. Extensive release of cytochrome c from the mitochondrial membrane
[72] Experiments with C. elegans double mutants (both decreased killer gene
function (weak ced-3) and a null engulfment gene) showed that
a. The double mutants displayed more surviving cells than single mutants with
weak ced-3
b. Dying neurons may be able to recover unless they are engulfed and
phagocytized
c. Single mutants with weak ced-3 displayed more surviving cells than non-
mutants
[73] The movement of phosphatidylserine (PS) from the inner to the outer leaflet
of the plasma membrane
a. Exposes PS so that microglia can recognize a dying cell*
14
b. Is the normal movement of this transporter in a healthy cell

c. Masks PS so that dying neurons do not become engulfed
[74] Contrary to the prediction that the formation of functional synapses

influences the survival of the growing neuron by regulating trophic support,
blocking synaptic transmission with an acetylcholine receptor antagonist in the
chick embryo during the period of motor neuron death resulted in a dramatic
decrease in motor neuron death.
a. True*
b. False
[75] Studies of the effects of cochlear ablation on the number of cells in the
nucleus magnocellularis in the chick central auditory system
a. Supported the hypothesis of afferent-regulated survival
b. Showed massive cell loss early in development and almost no cell loss later
c. Showed that the transition from massive cell loss to no cell loss may occur
in as little as two days
[76] In vitro studies of nucleus magnocellularis cells together with auditory nerve
afferents, examined protein synthesis as a marker of potential cell death.
a. When auditory nerve was stimulated, protein synthesis was maintained in
NM cells*
b. When NM axons were stimulated to produce antidromic action potentials
in their cell body, protein synthesis was maintained in NM cells
c. When auditory nerve was stimulated, protein synthesis was not maintained
in NM cells
[77] The N-methyl D-aspartate (NMDA) receptor, is activated by the

neurotransmitter, glutamate, and is permeable to calcium. In mice whose NMDA
receptors are deleted transgenically,
a. Displayed dramatically increased Naturally occurring neuron death
b. Provided evidence for the role of calcium in neuron survival and death
c. Both of these are true*
d. Neither of these are true
15
[78] It is believed that calcium-dependent neuron survival happens because the

entry of calcium into neurons causes an increase in BDNF expression.
a. True*
b. False
[79] When cultures of embryonic cortex neurons are depolarized by adding KCl to
the culture dish, calcium enters the neurons and
a. The level of BDNF expression increases and more neurons survive*
b. The level of BDNF expression decreases and more neurons survive
c. The level of BDNF expression increases and fewer neurons survive
d. The level of BDNF expression decreases and fewer neurons survive
16
Another random document with
no related content on Scribd:
THE FULL PROJECT GUTENBERG LICENSE
PLEASE READ THIS BEFORE YOU DISTRIBUTE OR USE THIS WORK
To protect the Project Gutenberg™ mission of promoting the free

distribution of electronic works, by using or distributing this work (or
any other work associated in any way with the phrase “Project
Gutenberg”), you agree to comply with all the terms of the Full
Project Gutenberg™ License available with this file or online at
www.gutenberg.org/license.
Section 1. General Terms of Use and

Redistributing Project Gutenberg™
electronic works
1.A. By reading or using any part of this Project Gutenberg™
electronic work, you indicate that you have read, understand, agree
to and accept all the terms of this license and intellectual property
(trademark/copyright) agreement. If you do not agree to abide by all
the terms of this agreement, you must cease using and return or
destroy all copies of Project Gutenberg™ electronic works in your
possession. If you paid a fee for obtaining a copy of or access to a
Project Gutenberg™ electronic work and you do not agree to be
bound by the terms of this agreement, you may obtain a refund from
the person or entity to whom you paid the fee as set forth in
paragraph 1.E.8.
1.B. “Project Gutenberg” is a registered trademark. It may only be

used on or associated in any way with an electronic work by people
who agree to be bound by the terms of this agreement. There are a
few things that you can do with most Project Gutenberg™ electronic
works even without complying with the full terms of this agreement.
See paragraph 1.C below. There are a lot of things you can do with
Project Gutenberg™ electronic works if you follow the terms of this
agreement and help preserve free future access to Project
Gutenberg™ electronic works. See paragraph 1.E below.
1.C. The Project Gutenberg Literary Archive Foundation (“the
Foundation” or PGLAF), owns a compilation copyright in the
collection of Project Gutenberg™ electronic works. Nearly all the
individual works in the collection are in the public domain in the
United States. If an individual work is unprotected by copyright law in
the United States and you are located in the United States, we do
not claim a right to prevent you from copying, distributing,
performing, displaying or creating derivative works based on the
work as long as all references to Project Gutenberg are removed. Of
course, we hope that you will support the Project Gutenberg™
mission of promoting free access to electronic works by freely
sharing Project Gutenberg™ works in compliance with the terms of
this agreement for keeping the Project Gutenberg™ name
associated with the work. You can easily comply with the terms of
this agreement by keeping this work in the same format with its
attached full Project Gutenberg™ License when you share it without
charge with others.
1.D. The copyright laws of the place where you are located also
govern what you can do with this work. Copyright laws in most
countries are in a constant state of change. If you are outside the
United States, check the laws of your country in addition to the terms
of this agreement before downloading, copying, displaying,
performing, distributing or creating derivative works based on this
work or any other Project Gutenberg™ work. The Foundation makes
no representations concerning the copyright status of any work in
any country other than the United States.
1.E. Unless you have removed all references to Project Gutenberg:
1.E.1. The following sentence, with active links to, or other

immediate access to, the full Project Gutenberg™ License must
appear prominently whenever any copy of a Project Gutenberg™
work (any work on which the phrase “Project Gutenberg” appears, or
with which the phrase “Project Gutenberg” is associated) is
accessed, displayed, performed, viewed, copied or distributed:
This eBook is for the use of anyone anywhere in the United
States and most other parts of the world at no cost and with
almost no restrictions whatsoever. You may copy it, give it away
or re-use it under the terms of the Project Gutenberg License
included with this eBook or online at www.gutenberg.org. If you
are not located in the United States, you will have to check the
laws of the country where you are located before using this
eBook.
1.E.2. If an individual Project Gutenberg™ electronic work is derived

from texts not protected by U.S. copyright law (does not contain a
notice indicating that it is posted with permission of the copyright
holder), the work can be copied and distributed to anyone in the
United States without paying any fees or charges. If you are
redistributing or providing access to a work with the phrase “Project
Gutenberg” associated with or appearing on the work, you must
comply either with the requirements of paragraphs 1.E.1 through
1.E.7 or obtain permission for the use of the work and the Project
Gutenberg™ trademark as set forth in paragraphs 1.E.8 or 1.E.9.
1.E.3. If an individual Project Gutenberg™ electronic work is posted

with the permission of the copyright holder, your use and distribution
must comply with both paragraphs 1.E.1 through 1.E.7 and any
additional terms imposed by the copyright holder. Additional terms
will be linked to the Project Gutenberg™ License for all works posted
with the permission of the copyright holder found at the beginning of
this work.
1.E.4. Do not unlink or detach or remove the full Project

Gutenberg™ License terms from this work, or any files containing a
part of this work or any other work associated with Project
Gutenberg™.
1.E.5. Do not copy, display, perform, distribute or redistribute this

electronic work, or any part of this electronic work, without
prominently displaying the sentence set forth in paragraph 1.E.1 with
active links or immediate access to the full terms of the Project
Gutenberg™ License.
1.E.6. You may convert to and distribute this work in any binary,
compressed, marked up, nonproprietary or proprietary form,
including any word processing or hypertext form. However, if you
provide access to or distribute copies of a Project Gutenberg™ work
in a format other than “Plain Vanilla ASCII” or other format used in
the official version posted on the official Project Gutenberg™ website
(www.gutenberg.org), you must, at no additional cost, fee or expense
to the user, provide a copy, a means of exporting a copy, or a means
of obtaining a copy upon request, of the work in its original “Plain
Vanilla ASCII” or other form. Any alternate format must include the
full Project Gutenberg™ License as specified in paragraph 1.E.1.
1.E.7. Do not charge a fee for access to, viewing, displaying,

performing, copying or distributing any Project Gutenberg™ works
unless you comply with paragraph 1.E.8 or 1.E.9.
1.E.8. You may charge a reasonable fee for copies of or providing

access to or distributing Project Gutenberg™ electronic works
provided that:
• You pay a royalty fee of 20% of the gross profits you derive from
the use of Project Gutenberg™ works calculated using the
method you already use to calculate your applicable taxes. The
fee is owed to the owner of the Project Gutenberg™ trademark,
but he has agreed to donate royalties under this paragraph to
the Project Gutenberg Literary Archive Foundation. Royalty
payments must be paid within 60 days following each date on
which you prepare (or are legally required to prepare) your
periodic tax returns. Royalty payments should be clearly marked
as such and sent to the Project Gutenberg Literary Archive
Foundation at the address specified in Section 4, “Information
about donations to the Project Gutenberg Literary Archive
Foundation.”
• You provide a full refund of any money paid by a user who

notifies you in writing (or by e-mail) within 30 days of receipt that
s/he does not agree to the terms of the full Project Gutenberg™
License. You must require such a user to return or destroy all
copies of the works possessed in a physical medium and
discontinue all use of and all access to other copies of Project
Gutenberg™ works.
• You provide, in accordance with paragraph 1.F.3, a full refund of

any money paid for a work or a replacement copy, if a defect in
the electronic work is discovered and reported to you within 90
days of receipt of the work.
• You comply with all other terms of this agreement for free
distribution of Project Gutenberg™ works.
1.E.9. If you wish to charge a fee or distribute a Project Gutenberg™

electronic work or group of works on different terms than are set
forth in this agreement, you must obtain permission in writing from
the Project Gutenberg Literary Archive Foundation, the manager of
the Project Gutenberg™ trademark. Contact the Foundation as set
forth in Section 3 below.
1.F.
1.F.1. Project Gutenberg volunteers and employees expend

considerable effort to identify, do copyright research on, transcribe
and proofread works not protected by U.S. copyright law in creating
the Project Gutenberg™ collection. Despite these efforts, Project
Gutenberg™ electronic works, and the medium on which they may
be stored, may contain “Defects,” such as, but not limited to,
incomplete, inaccurate or corrupt data, transcription errors, a
copyright or other intellectual property infringement, a defective or
damaged disk or other medium, a computer virus, or computer
codes that damage or cannot be read by your equipment.
1.F.2. LIMITED WARRANTY, DISCLAIMER OF DAMAGES - Except

for the “Right of Replacement or Refund” described in paragraph
1.F.3, the Project Gutenberg Literary Archive Foundation, the owner
of the Project Gutenberg™ trademark, and any other party
distributing a Project Gutenberg™ electronic work under this
agreement, disclaim all liability to you for damages, costs and
expenses, including legal fees. YOU AGREE THAT YOU HAVE NO
REMEDIES FOR NEGLIGENCE, STRICT LIABILITY, BREACH OF
WARRANTY OR BREACH OF CONTRACT EXCEPT THOSE
PROVIDED IN PARAGRAPH 1.F.3. YOU AGREE THAT THE
FOUNDATION, THE TRADEMARK OWNER, AND ANY
DISTRIBUTOR UNDER THIS AGREEMENT WILL NOT BE LIABLE
TO YOU FOR ACTUAL, DIRECT, INDIRECT, CONSEQUENTIAL,
PUNITIVE OR INCIDENTAL DAMAGES EVEN IF YOU GIVE
NOTICE OF THE POSSIBILITY OF SUCH DAMAGE.
1.F.3. LIMITED RIGHT OF REPLACEMENT OR REFUND - If you

discover a defect in this electronic work within 90 days of receiving it,
you can receive a refund of the money (if any) you paid for it by
sending a written explanation to the person you received the work
from. If you received the work on a physical medium, you must
return the medium with your written explanation. The person or entity
that provided you with the defective work may elect to provide a
replacement copy in lieu of a refund. If you received the work
electronically, the person or entity providing it to you may choose to
give you a second opportunity to receive the work electronically in
lieu of a refund. If the second copy is also defective, you may
demand a refund in writing without further opportunities to fix the
problem.
1.F.4. Except for the limited right of replacement or refund set forth in
paragraph 1.F.3, this work is provided to you ‘AS-IS’, WITH NO
OTHER WARRANTIES OF ANY KIND, EXPRESS OR IMPLIED,
INCLUDING BUT NOT LIMITED TO WARRANTIES OF
MERCHANTABILITY OR FITNESS FOR ANY PURPOSE.
1.F.5. Some states do not allow disclaimers of certain implied

warranties or the exclusion or limitation of certain types of damages.
If any disclaimer or limitation set forth in this agreement violates the
law of the state applicable to this agreement, the agreement shall be
interpreted to make the maximum disclaimer or limitation permitted
by the applicable state law. The invalidity or unenforceability of any
provision of this agreement shall not void the remaining provisions.
1.F.6. INDEMNITY - You agree to indemnify and hold the

Foundation, the trademark owner, any agent or employee of the
Foundation, anyone providing copies of Project Gutenberg™
electronic works in accordance with this agreement, and any
volunteers associated with the production, promotion and distribution
of Project Gutenberg™ electronic works, harmless from all liability,
costs and expenses, including legal fees, that arise directly or
indirectly from any of the following which you do or cause to occur:
(a) distribution of this or any Project Gutenberg™ work, (b)
alteration, modification, or additions or deletions to any Project
Gutenberg™ work, and (c) any Defect you cause.
Section 2. Information about the Mission of

Project Gutenberg™
Project Gutenberg™ is synonymous with the free distribution of
electronic works in formats readable by the widest variety of
computers including obsolete, old, middle-aged and new computers.
It exists because of the efforts of hundreds of volunteers and
donations from people in all walks of life.
Volunteers and financial support to provide volunteers with the

assistance they need are critical to reaching Project Gutenberg™’s
goals and ensuring that the Project Gutenberg™ collection will
remain freely available for generations to come. In 2001, the Project
Gutenberg Literary Archive Foundation was created to provide a
secure and permanent future for Project Gutenberg™ and future
generations. To learn more about the Project Gutenberg Literary
Archive Foundation and how your efforts and donations can help,
see Sections 3 and 4 and the Foundation information page at
www.gutenberg.org.
Section 3. Information about the Project
Gutenberg Literary Archive Foundation
The Project Gutenberg Literary Archive Foundation is a non-profit
501(c)(3) educational corporation organized under the laws of the
state of Mississippi and granted tax exempt status by the Internal
Revenue Service. The Foundation’s EIN or federal tax identification
number is 64-6221541. Contributions to the Project Gutenberg
Literary Archive Foundation are tax deductible to the full extent
permitted by U.S. federal laws and your state’s laws.
The Foundation’s business office is located at 809 North 1500 West,

Salt Lake City, UT 84116, (801) 596-1887. Email contact links and up
to date contact information can be found at the Foundation’s website
and official page at www.gutenberg.org/contact
Section 4. Information about Donations to

the Project Gutenberg Literary Archive
Foundation
Project Gutenberg™ depends upon and cannot survive without
widespread public support and donations to carry out its mission of
increasing the number of public domain and licensed works that can
be freely distributed in machine-readable form accessible by the
widest array of equipment including outdated equipment. Many small
donations ($1 to $5,000) are particularly important to maintaining tax
exempt status with the IRS.
The Foundation is committed to complying with the laws regulating

charities and charitable donations in all 50 states of the United
States. Compliance requirements are not uniform and it takes a
considerable effort, much paperwork and many fees to meet and
keep up with these requirements. We do not solicit donations in
locations where we have not received written confirmation of
compliance. To SEND DONATIONS or determine the status of
compliance for any particular state visit www.gutenberg.org/donate.
While we cannot and do not solicit contributions from states where

we have not met the solicitation requirements, we know of no
prohibition against accepting unsolicited donations from donors in
such states who approach us with offers to donate.
International donations are gratefully accepted, but we cannot make

any statements concerning tax treatment of donations received from
outside the United States. U.S. laws alone swamp our small staff.
Please check the Project Gutenberg web pages for current donation
methods and addresses. Donations are accepted in a number of
other ways including checks, online payments and credit card
donations. To donate, please visit: www.gutenberg.org/donate.
Section 5. General Information About Project

Gutenberg™ electronic works
Professor Michael S. Hart was the originator of the Project
Gutenberg™ concept of a library of electronic works that could be
freely shared with anyone. For forty years, he produced and
distributed Project Gutenberg™ eBooks with only a loose network of
volunteer support.
Project Gutenberg™ eBooks are often created from several printed

editions, all of which are confirmed as not protected by copyright in
the U.S. unless a copyright notice is included. Thus, we do not
necessarily keep eBooks in compliance with any particular paper
edition.
Most people start at our website which has the main PG search
facility: www.gutenberg.org.
This website includes information about Project Gutenberg™,

including how to make donations to the Project Gutenberg Literary
Archive Foundation, how to help produce our new eBooks, and how
to subscribe to our email newsletter to hear about new eBooks.

(Download PDF) Development of The Nervous System 3rd Edition Sanes Test Bank Full Chapter

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

(Download PDF) Development of The Nervous System 3rd Edition Sanes Test Bank Full Chapter

Uploaded by

Copyright:

Available Formats

Development of the Nervous System

3rd Edition Sanes Test Bank

Muscular System Manual The Skeletal Muscles of the

Money Banking and the Financial System 3rd Edition

Understanding the Australian Health Care System 3rd

Basics of the U.S. Health Care System 2nd Edition Niles

American Political System 3rd Edition Kollman Test Bank

Essentials of Life Span Development 3rd Edition

Essentials of Life-Span Development 3rd Edition

Basic Immunology Functions And Disorders Of The Immune

a. Yes, it doubles in weight

a. Synaptic inputs from other neurons

[5] The purpose of TUNEL labeling is

a. To label DNA in dying neurons before fragmentation

d. To detect pyknosis in dying neurons

[7] In necrosis as opposed to apoptosis neurons ________ as they degenerate.

[9] In addition to the PCD of neurons, about ______ percent of oligodendrocytes

[10] Difficulty in obtaining an accurate count of the number of neurons during

a. PCD and neurogenesis overlapping in time

a. Change in target size is the sole determinant of neuron survival

a. There was a diffusible chemical that influenced sensory neuron survival*

a. NGF was not a protein because venom breaks down proteins

a. All sympathetic and DRG to increase in size*

[17] Injecting an antibody directed against NGF in neonatal rodents demonstrated

a. NGF is necessary for sympathetic neuron survival

[18] NGF antibody treatment at an early embryonic stage of development will

[23] Neurotrophin ligands bind selectively to the tyrosine kinase family of

[27] If a Trk receptor is activated in the absence of a neurotrophin, the process is

[28] Each TrK receptor has a high specific affinity for

[31] What is transactivation?

[32] The observed pattern of NT-3 expression is that it is typically found

d. None of these are correct

b. Retrogradely to the cell nucleus along microtubules*

[38] Neurotrophins released as uncleaved pro-peptides, which bind with high-

[42] The convention for naming a cytokine is

[45] Glial cell line-derived neurotrophic factor (GDNF)

[50] A factor suggesting that steroid hormones widely influence naturally-

[54] If chick embryos are treated with either cycloheximide or actinomycin-D at

[55] Protein synthesis must occur in order for cells to die.

[56] Gene transcription must occur in order for cells to die.

[57] Which set is the correct sequence of neurotrophin signal transduction:

[58] Following the first phosphorylation of an adaptor protein (Shc), two

[60] When neurotrophin-dependent neurons are deprived of NGF, what happens?

[61] Which is an example of a pro-apoptotic protein?

[66] Free radicals such as O2.- and mitochondrial flavoproteins (AIF)may be

[67] A neuron’s mitochondrion outer membrane becomes permeable and

[68] In mammals, the Bcl-2 family of membrane-associated proteins

[69] Transgenic mice that overexpress the Bcl-2 protein,

b. Is the normal movement of this transporter in a healthy cell

[74] Contrary to the prediction that the formation of functional synapses

[77] The N-methyl D-aspartate (NMDA) receptor, is activated by the

[78] It is believed that calcium-dependent neuron survival happens because the

To protect the Project Gutenberg™ mission of promoting the free

Section 1. General Terms of Use and

1.B. “Project Gutenberg” is a registered trademark. It may only be

1.E. Unless you have removed all references to Project Gutenberg:

1.E.1. The following sentence, with active links to, or other

1.E.2. If an individual Project Gutenberg™ electronic work is derived

1.E.3. If an individual Project Gutenberg™ electronic work is posted

1.E.4. Do not unlink or detach or remove the full Project

1.E.5. Do not copy, display, perform, distribute or redistribute this

1.E.7. Do not charge a fee for access to, viewing, displaying,

1.E.8. You may charge a reasonable fee for copies of or providing