Download 1 Biology 13100 Problem Set 7 Components and functions of all

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Biology 13100 Problem Set 7
Components and functions of all nervous systems
Master regulation of development in plants and animals depends on patterns of responses to
signals that are shared among very different kinds of organisms. One of the earliest systems to
develop in most animals is the nervous system. Sensory neurons (afferent neurons) transmit
information from sensory cells to the central nervous system (CNS) whereas autonomic and
motor neurons (efferent neurons) transmit information from the CNS to muscles, glands, and
organs (effectors). Interneurons transmit information from sensory to motor neurons and between
other interneurons within the CNS. Spinal and cranial nerves transfer information to/from
specific tissues. Regions of the cerebral cortex have a receptive field and are responsible for
certain functions (the sensory and motor homunculus). To understand how this system works,
remember that cell membranes have ion channels. Some are ligand-gated. Others, called voltagegated channels, open and close with changes in the cell membrane potential. A membrane will
become more permeable if ion channels open, but the flux of ions across a membrane depends
not only on the concentration gradient but also on the electrical membrane potential.
A neurite is an extension of a neuron (a nerve cell). It may later become either an axon or
dendrite. A ganglion is a collection of nerve cell bodies (the part of the cell with the nucleus).
During development, neural crest cells collect in ganglia near the spinal cord (the dorsal root
ganglia) and send out neurites to the periphery and to the spinal cord. These sensory neurons
convey information to CNS. Motor neurons have their cell bodies in the ventral part of the
spinal cord and send long neurites to the muscles. They are not derived from neural crest cells.
In order to form axons, the cell body sends out neurites and these can grow long distances to find
their targets. The end of the neurite has a growth cone, which explores the environment and
selects the direction of growth. We can generate normal human neurons from stem cells and they
survive transplantation but we have no idea how to promote accurate axonal outgrowth to long
distance targets.
Human stem cells can come from four sources: embryonic stem cells (ESCs), nuclear transfer of
unfertilized cell cells (or other types of gene transfer), direct infusion of transcription factor
proteins to convert a cell to a stem cell, or other forms of transdifferentiation. One example of
transdifferentiation would be to convert bone marrow cells into myocytes and coronary cells that
line the walls of a blood vessel. A stem cell is an undifferentiated cell found in a differentiated
tissue that can renew itself (replicate) and differentiate to give rise to all the specialized cell types
of the tissue from which it originated. It is important to note that scientists do not agree about
whether or not adult stem cells may give rise to cell types other than those of the tissue from
which they originate. An important and useful property of stem cells is that of self-renewal
(replication). Similar signaling pathways may regulate self-renewal in stem cells and cancer
cells. In fact, cancer cells may include ‘cancer stem cells’ — rare cells with indefinite potential
for self-renewal that cause growth of tumors. A stem cells glossary for biol13100 is online at
https://wiki.bio.purdue.edu/biol13100/index.php/Stem_cells_including_cancer#Glossary
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Properties of excitable cells
Electrical signals are used to transmit information within cells through changes in membrane
potential (Vm). Depolarization is an increase in Vm relative to resting Vm and Hyperpolarization
is a decrease in Vm relative to resting Vm. Neuron cells communicate via two basic forms of
electrical signals: graded potentials (small amplitude, short-distance signals) and action
potentials (APs): larger amplitude, long-distance signals Action Potentials. An AP is a large and
rapid (1-2 msec) all-or-none change in Vm involving depolarization of the membrane due to
changes in permeability of the membrane to ions and currents carried primarily by sodium and
potassium ions via voltage-gated channels (voltage-gated ). The AP uses energy stored in the
membrane potential. What occurs with regard to ion movements (currents) is due to diffusion via
specific ion channels, and different specific ion channels open during each phase which is
reflected in membrane permeability changes as follows:
1. upswing (depolarization): voltage-gated Na+ channels open by positive feedback
(activation gate opens), Na+ influx makes Vm increase
2. peak of AP: just before the peak, voltage-gated Na+ channels have started to close
(inactivation gate closes) and voltage-gated K+ channels have started to open, so both
K+ efflux and Na+ influx are occurring; thus, peak approaches but does not reach the
Eeq for Na+.
3. downswing (repolarization): all voltage-gated Na+ channels are closing, all voltagegated K+ channels are open, K+ efflux dominates
4. after-spike hyperpolarization: all voltage-gated Na+ channels are closed and
inactivated, all voltage-gated K+ channels are open, K+ efflux brings Vm below
resting Vm (hyperpolarizes)
5. return to resting Vm: inactivation gates of voltage-gated Na+ channels begin to open
but activation gates close, voltage-gated K+ channels are closed, cell returns to
resting conditions
Only cells with a resting nonequilibrium Vm and voltage-gated Na+ and K+ channels can
generate and propagate APs. These are called excitable cells. Excitable cells exhibit a
refractory period when the membrane is “refractory” to stimuli – no AP can be generated in
response to the same stimulus. A refractory period is composed of the Absolute Refractory
Period and Relative Refractory Period
Speed of AP propagation along the cell depends on how far in advance of the point where the AP
is present does the current spread to bring the membrane to threshold. Speed may be increased
by increasing the amount of current flow within the cytoplasm relative to the amount of current
flow across the cell membrane. A squid giant axon does this by having a large diameter so it
has more cytoplasmic volume relative to the amount of membrane surface area, thus increasing
the proportion of current flow in the cytoplasm relative to the current flow across the cell
membrane. Vertebrates increase AP speed by increasing the membrane resistance by “insulating”
it with a myelin sheath made of many layers of cell membrane from another cell. The layer of
cells that wrap around the myelin sheath, creating many layers, are called Schwann cells.
Schwann cells are derived from Neural crest cell origins. Myelination results in saltatory
conduction of APs between Nodes of Ranvier.
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Transfer of signals between cells within the nervous system at synapses
Most neuron-neuron junctions in nerve networks do NOT contain gap junctions through which
APs are propagated between cells. Instead, at chemical synapses between a pre-synaptic cell
and a post-synaptic cell, chemical messengers (neurotransmitters, NTs) must be used to
communicate between cells. There is a synaptic delay of 0.5 - 1 msec for transmitting signals
between cells. NTs are produced in the cell body, enclosed in membrane-bound vesicles, and
transported to the axon terminals, where the vesicles await the appropriate signal for release.
There are up to 100,000 synapses within the CNS; Only one type of neurotransmitter is released
at a given synapse but different receptors can cause different neurons to respond to the same NT
in different ways. (See powerpoint table for types of neurotransmitters).
At the axon terminals, depolarization of the axon terminal membrane, due to AP propagation,
opens voltage-gated Ca2+ channels located there, thus causing exocytosis and secretion of the
NT vesicles into the synaptic cleft. The NT diffuses to the post-synaptic cell membrane and
binds with specific receptors. NT-receptor binding results in opening or closing of specific
ligand-gated (or chemical-gated) ion channels in the post-synaptic cell membrane, allowing a
change in ion flux across the membrane and changing Vm (e.g., synapse between a motor neuron
and a skeletal muscle cell). An increase in Vm = depolarization = excitatory post-synaptic
potential (EPSP), whereas a decrease in Vm = hyperpolarization = inhibitory post-synaptic
potential (IPSP). These are graded potentials; the magnitude change is proportional to the
amount of ion flux resulting from NT-receptor binding. Enzymes rapidly degrade
neurotransmitters so signal stops relatively rapidly (e.g., acetylcholinesterase). The net result on
the post-synaptic cell is determined by spatial and temporal summation of PSPs . If the axon
hillock reaches threshold, an AP is generated and propagated along the post-synaptic cell. A
given cell may receive hundreds of synapses, from many different cells, and may allow
convergence and divergence, or inhibition.
The somatic motor system
Spinal motor neurons control skeletal muscles. Cell bodies of motor neurons are in the ventral
horn of spinal cord. Only one neuron from the spinal cord has the effector skeletal muscle (once
this motor neuron is stimulated to initiate an AP, it propagates along the cell to the muscle). All
somatic motor neurons release ACh at axon terminals, which binds to nicotinic AChRs. All
synapses with skeletal muscles are excitatory (neuromuscular junctions): Motor neuron releases
ACh, binds to nicotinic AChRs, causes excitation and contraction of muscle with this mechanism
for activation of muscle contraction:
1. start at the neuromuscular junction, with the arrival of a motor neuron AP
2. AP to the terminal button (axon terminal) near motor-end plate
3. Voltage-gated Ca2+ channels open, Ca2+ influx
4. Release of ACh from vesicles
5. ACh diffuses across synaptic cleft
6. ACh binds to ACh-gated Na+ K+ channels on muscle
7. Muscle cell membrane depolarizes
8. Voltage-gated Na+ channels open, generating a muscle cell AP
Note that skeletal muscle is specialized to respond only to ACh. It responds only by contracting.
Unlike cardiac or smooth muscle, there are no adrenergic receptors in skeletal muscle.
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Skeletal Muscle Excitation-Contraction Coupling
Muscles are grouped according to antagonistic pairs, e.g. extensors/flexors. Whole muscle is
made of many multinucleated muscle cells (muscle fibers), composed of myofibrils and
myofilaments (with actin and myosin contractile proteins). A motor unit includes the muscle
fibers connected to a single motorneuron. To get larger force production, more motor units are
recruited, more individual fibers contract. Muscle fibers contain myofibrils, composed of
myofilaments that include thick filaments with myosin and thin filaments with actin. For force
production, the sarcomere shortens in response to cross-bridge formation; shortening of entire
myofibril is achieved by increasing degree of overlap of thick and thin filaments in each
sarcomere. The muscle cell membrane, called the sarcolemma, extends with a Transverse tubule
system to spread the action potential into cell interior where it comes in close proximity to the
sarcoplasmic reticulum to trigger release of calcium. The sarcoplasmic reticulum, like the
endoplasmic reticulum of other types of cells, has calcium pumps that take up free Ca2+ from the
cytoplasm. Remember that cells generally have a very low concentration of Ca2+ in the
cytoplasm.
When a motor neuron releases ACh at neuromuscular junction, it binds the Nicotinic AChR, a
ligand-gated cationic channels that can be blocked by toxins/drugs. The action potential spreads
through the sarcolemma to the T-tubule system where a voltage-sensitive protein on T tubules
(dihydropyridine receptor) changes conformation. Somehow, this opens Ca2+ channels of the
sarcoplasmic reticulum (SR), causing release of Ca2+ from sarcoplasmic reticulum into the
cytoplasm. Intracellular Ca2+ rises and opens more Ca2+-gated Ca2+ channels of the SR. When
intracellular Ca2+ rises, it binds to troponin C of thin filaments; Ca2+ plays a key role in
initiating/terminating contractile events by causing a shape change in the troponin-tropomyosin
complex. In the non-contractile state, the troponin-tropomyosin complex shields actin sites from
binding myosin. However, when Ca2+ binds to troponin complex, specifically troponin C,
topomyosin undergoes conformational change to reveal myosin binding sites on actin. If
activated, myosin head binds to actin and pivots, causing filament sliding, sarcomere shortening,
and muscle fiber contraction.
The sliding-filament theory of contraction explains how this happens by formation of crossbridges by myosin heads. At a molecular level, you should know myosin structure to understand
how the myosin ATPase works. The myosin head binds ATP and it hydrolyzes ATP, but ADP +
Pi remain attached; this activates the myosin head for binding to actin. When the myosin head
can bind to actin, ADP + Pi are released, the myosin head rotates, and the power stroke moves
actin toward center of A-line. Then new ATP binds to myosin, myosin detaches from actin and
the cycle repeats if ATP and Ca2+ available.
Receptive Fields and Lateral Inhibition in the Visual System
Unlike a motor neuron that releases ACh, the neurotransmitter released by a photoreceptor is
glutamate. Its release always declines in response to light. Bipolar cells are the post-synaptic
cells. Two types of bipolar cells have different receptors for glutamate, so that a reduction in
glutamate causes opposite reactions. In one case, the bipolar cell depolarizes, and in the other, it
hyperpolarizes.
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In general, the physical area of the primary sensory cells to which a neuron responds is called the
receptive field. In the case of the visual system, the receptive field of a neuron in the visual
pathway is the area comprising the photoreceptors whose stimulation by light leads to a
detectable response in the neuron, generally a change in the rate of firing action potentials.
The Hermann-Hering grid illusion shows how receptive fields work. It consists of dark illusory
spots perceived at the intersections of horizontal and vertical white bars viewed against a dark
background. The dark spots originate from processing by cells in the retina. Perception depends a
lot on assessing local differences in illumination as demonstrated by this example. Think of
retinal organization as consisting of two major systems: the
through system and the lateral system. Starting with the
photoreceptors, the through system connects to the retinal
ganglion cells via the bipolar cells. There are two lateral
systems that are produced by the horizontal cells and the
amacrine cells. These lateral networks give rise to the surround
organization of receptive fields as seen in the retinal ganglion
cells. The information from the retina is sent to the brain by the
axons of the retinal ganglion cells. There are several different
classes of retinal ganglion cells that differ in their response
characteristics. The two classes are the ON and OFF which will
be discussed below.
The Hermann-Hering Grid
Consider the receptive field of a ganglion cell in the retina. The field can be mapped by
impaling a ganglion cell with a microelectrode, to record its membrane potential (and thus its
action potentials) and then stimulating the photoreceptor cells by shining light on different areas
of the retina. When those experiments were done, it was found that the receptive fields of
ganglion cells are concentric circles of photoreceptor cells and the circle for a ganglion cell is
centered on the ganglion cell. Some are activated when photoreceptors detect light, while others
are activated in the absence of light. These two types usually encircle each other and are spread
throughout the retina creating receptive fields. It was also found that there are two types of
ganglion cells in terms of their receptive fields. One type, the on-center ganglion cell, is
maximally stimulated when a spot of light is place at the center of its receptive field, and is
strongly inhibited if an annulus of light, with the center dark, is shined on the receptive area.
The other type, the off-center ganglion cell, is maximally stimulated (that is, maximally increases
its rate of firing action potentials) if an annulus of light is shined on the receptive field, and is
maximally inhibited if a spot of light shined on the receptive field.
This organization can be understood in terms of the bipolar cells that connect the photoreceptors
to the ganglion. The on-center ganglion cell is connected to the photoreceptors in the central
spot by ON-bipolar cells and to the surrounding annular region via OFF-bipolar cells. The
situation is reversed in the case of the off-center ganglion cells. The next Figure illustrates the
two arrangements. Only a few of the photoreceptors that feed into a ganglion cell are shown.
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It is important to understand that this arrangement of receptive fields is completely dependent on
the existence of two kinds of bipolar cells and the
function of those two kinds of cells. ON-bipolar
cells depolarize in response to the hyperpolarization
of the photoreceptor cells to which they are
connected, and they pass on the depolarization to
the ganglion cells, which causes increased rate of
action potentials. OFF-bipolars, on the other hand,
hyperpolarize in response to photoreceptor
hyperpolarization (photoreceptors ALWAYS
hyperpolarize in response to light) and pass that
hyperpolarization on to the ganglion cells, which
causes reduced rate of action potentials. Using ONCenter receptive fields as an example, when your
eyes are focused on the Hermann grid (except at an intersection) the dark surrounding
photoreceptors counteract the activity of the light center photoreceptors.
The axons of the ganglion cells form the optic nerve. They make synapses in the lateral
geniculate nucleus (LGN) of the thalamus. LGN neurons also have receptive fields arranged in
concentric circles, but they have better contrast between the center and the annular areas.
Convergence of the ganglion cells on the LGN cells leads to a sharpening of the receptive fields.
LGN neurons project to simple cells of the cerebral cortex via stellate cells, and most simple
cells have rectangular receptive fields. Almost all simple cells demonstrate spatial selectivity,
meaning that they respond most strongly to rectangles of light in a particular orientation. This
occurs though the convergence of adjacent circular receptive fields of the LGN cells onto one
simple cell. For further detail, see Neural Control of Vision at
http://web.mit.edu/bcs/schillerlab/research/A-Vision/A.htm
Problem Set 7
1. Suppose that you have in culture an isolated motor unit from a vertebrate; that is, an intact
motor neuron and its associated muscle fiber. If you were to replace the Ringer’s solution in
which the motor unit was bathed with a Ca-free Ringer’s solution, what would you predict
the effect would be on the functioning of the motor unit? For example, could you elicit an
action potential in the neuron by stimulating it with a current source? Would the muscle
fiber contract in response to an action potential? Explain your predicted result.
2. The snake toxin, bugarotoxin, binds to nicotinic ACh receptors and irreversibly blocks the
binding site on the receptor for ACh. What would be the effect of bungarotoxin on the
isolated motor unit described above? Would the muscle contract if the neuron were
stimulated? Why or why not? (Note: the use of various toxins has proved exceedingly
valuable for the study of ion channel physiology. The toxins have often been engineered
through evolution to have an astonishing degree of specificity for a particular ion channel,
sometimes for a subtype of a particular channel.)
3. The puffer fish toxin, tetrodotoxin (TTX), completely blocks voltage gated sodium channels,
thus it blocks the generation and propagation of action potentials in neurons. Suppose the
motor unit describe above were bathed in TTX so that stimulating the neuron did not cause
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an action potential, thus preventing the neuron from secreting ACh at the synapse. If you
added ACh (it is a readily available chemical) to the bathing medium, would this cause the
muscle to contract? Why or why not?
4. Ouabain is a plant alkaloid that inhibits the Na-K ATPase. What would you predict the
effect on action potentials to be if ouabain were applied to a neuron? (Hint: remember what
was mentioned early in the course about the relative number of ions that cause electrical
changes and that cause changes in ion concentrations.)
5. Describe the ionic basis for a typical action potential, including all steps (in sequence) that
occur in an action potential (including the subsequent refractory period): what happens in
terms of ion flow across the membrane (which ions, which direction, when), conductance (or
permeability) changes, alterations in membrane gated ion channels. Also be able to discuss
what would happen if, at any specific time during the action potential (AP), alterations were
made to intra- or extra-cellular concentrations of specific ions, gated channels were blocked
or opened sooner than normal (consider several different scenarios that you create).
6. Explain why the Nernst potential for Na+ can closely predict the peak amplitude of an action
potential.
7. Explain the importance of voltage-gated Na+ channel inactivation (closing of the inactivation
gate) for an AP and for the refractory period.
8. Explain why APs are called “all-or-none” electrical signals.
9. Explain what graded potentials are.
10. Explain how an action potential is propagated in an unmyelinated nerve and in a myelinated
nerve.
11. Explain the difference between APs and post synaptic potentials, both of which are changes
in membrane potential.
12. The equilibrium potential for Ca is +130 mV and that for K is -100 mV, in a typical
mammalian neuron. Which type of ion channel would most likely underlie a hyperpolarizing
IPSP response? Give your rationale.
13. Explain how EPSPs and IPSPs are generated in a post-synaptic membrane, and how both
temporal and spatial summation occur. If a neuron receives an IPSP of -20 mV and an EPSP
that is +35 mV that are spatially and temporally close to each other, would the resulting
integrated response be a negative or positive response? What would happen if the two
responses occurred at places in the neuron that were long distances from each other?
14. Would a drug that blocks the reuptake of a neurotransmitter have a potentiating or inhibiting
effect on the synaptic response to that neurotransmitter? Give a rationale for your choice.
15. Explain convergence and divergence in neuron networks, and the significance of each.
16. List the components of a reflex arc and relate them to how the nervous system maintains
homeostasis for the whole organism.
17. Explain why information about the strength of stimulation to a neuron cannot be encoded in
the size of the action potential. How is the information encoded?
18. Suppose that an action potential is started simultaneously at two different places on an axon.
Describe the propagation of the two action potentials.
19. A newly discovered element, Purduonium, exists in solution as a monovalent cation, Pm+. It
is found that the concentration of Pm+ in neurons is 10 mM and the concentration in the
outside solution is 1 mM. If a neurotransmitter opens a Pm+-specific channel in the neuron,
is that neurotransmitter inhibitory or excitatory in this situation? Why?
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20. Explain why the depletion of ATP following the death of an organism leads to rigor mortis,
the stiffening of all of the skeletal muscles.
21. Consider the preparation described in Problem 1 above. What could you do to the Ringer’s
solution that bathes the neuron in order to alter the amplitude of the action potential?
22. Shown in the diagram below are three cross-sections of a sarcomere. Identify the location of
each cross-section within the sacromere
23. If you touch a very hot skillet, your hand jerks away before you sense the pain of the burn.
Explain.
24. A certain (fictional) bacterial toxin inhibits the cGMP-specific phosphodiesterase. What
would be the effect of the toxin on vertebrate photoreceptor cells in the dark? In the response
of photoreceptors to light? (By the way, cGMP-specific phosphodiesterase inhibitors do
exist. Viagra is such an inhibitor.)
25. Retinal is the molecule that actually absorbs light in rod cells and all three types of cones.
How, then, do different cones respond to different wavelengths of light?
26. If the rhodopsin molecules in each of 10 rod cells absorbs one photon of light at about the
same time, a perceptible flash is sensed by the brain. This is the lowest level of light that
produces a detectable signal in the mammalian visual system. Assuming that the light is
green (say, 500 nm), how much energy is imparted to the system by the absorption of the ten
photons? How does this energy compare to the energy required to lift a 1 Kg mass 1 meter
against gravity? [The energy required to lift the mass is equal to the work done. Work and
energy have the same units, Joules
(1 Joule = 1 Kg m2/s2). The work done is equal to
force times distance, and the force required is equal to mass times acceleration of gravity (g ≈
10 m/s2).]
27. What is the receptive field of an on-center ganglion cell? An off-center ganglion cell?
28. Describe the receptive field of the simple cells in the visual cortex. Explain how the simple
cell receptive field arises from the convergence of inputs from cells with concentric receptive
fields.
29. This graph was generated by students in a physiology lab. The top trace shows contraction
force of a frog leg muscle, the bottom shows the electrical stimulus. What is happening to the
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muscle and why?
30. You are a member of a team of scientists that recently discovered a previously unknown
animal species, which is not a mammal. You have been assigned the task to determine whether a
given motor efferent system in the animal is functionally similar to or different from that in
humans using any combination of the following tools to find out if it works like the motor
efferent system to a skeletal muscle cell (motor neuron - muscle fiber). Are the
neurotransmitters and receptors at the neuromuscular synapse in this animal the same as in the
human system?
Experimental tools:
for adrenergic receptors:
EPINEPHRINE is an agonist of all types of adrenergic receptors
DRUG H is an agonist of beta1-adrenergic receptors
SALBUTAMOL is an agonist of beta2-adrenergic receptors
CARMINE is an agonist of alpha-adrenergic receptors
PROPANOLOL is an antagonist of both beta1- and beta2-adrenergic receptors
PHENOXYBENZAMINE is an antagonist of alpha-adrenergic receptors
COMPOUND Q is an antagonist of beta2-adrenergic receptors
for cholinergic receptors:
SUCCINYLCHOLINE is an agonist of nicotinic cholinergic receptors
MUSCARINE is an agonist of muscarinic cholinergic receptors
CURARE is an antagonist of nicotinic cholinergic receptors
ATROPINE is an antagonist of muscarinic cholinergic receptors
for ion channels:
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DRUG A blocks ligand-gated Ca2+ channels within the muscle plasma membrane
DRUG B blocks ligand-gated Na+ channels within the muscle plasma membrane
DRUG C blocks ligand –gated K+ channels within the muscle plasma membrane
DRUG D blocks ligand-gated Cl- channels within the muscle plasma membrane
DRUG E blocks ligand-gated Na+/K+ channels in the muscle plasma membrane
other tools you may use:
use RADIOACTIVELY LABELLED IONS of any type
ALTERING THE EXTRACELLULAR CONCENTRATION of any ion
VIAGRA inhibits phosphodiesterase
AEQUORIN fluoresces in the presence of free Ca2+
FLUORO-X fluoresces in the presence of free Na+
PEPTIDE-K fluoresces in the presence of free K+
Describe the experiments you would do, using any of the above tools, to answer the question
completely (is this animal similar to the human?). First state how the system works in humans,
for comparison (what is the neurotransmitter and receptor type at each synapse, and what
happens when the receptor binds the neurotransmitter, in humans?) Be sure to include in your
answer a description of the experimental set-up or design and the appropriate controls. If you
need help,
you may want to consult a library to find research publications where these drugs
were used in experiments with muscle.
31. Explain in detail ONE specific effect, within the specified cell type, of a mutation in the gene
that codes for ONE of the following (A or B); assume that the mutation renders the gene product
nonfunctional. Then describe ONE thing you could do to counteract that effect on the cell (other
than replace the gene, mRNA, or protein it codes for).
A. cell membrane voltage-gated Ca2+ channel in a skeletal muscle fiber
B. calmodulin in a multi-unit skeletal muscle
C. Ca2+ATPase in a skeletal muscle cell
Vocabulary for the BIOL13100 lectures related to Problem Set 7
absolute refractory period
acetylcholine
actin
action potential
adrenergic receptor
axon
axon hillock
axon terminal
bipolar cell
brain
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Ca2+ channels
Ca2+ pump
Ca2+ release channels
central nervous system (CNS)
cerebral cortex
cGMP
contraction
convergence
cross-bridge cycling
dendrite
depolarization
dihydropyridine receptor
divergence
excitable cell
excitation-contraction coupling
excitatory neuron
excitatory post-synaptic potential (EPSP)
excitatory signal
extensor
fatigue
flexor
ganglion
glutamate
graded potential
hyperpolarization
inhibitory neuron
inhibitory post-synaptic potential (IPSP)
inhibitory signal
integration of signals
interneurons
lateral inhibition
LGN
ligand-gated
M line
membrane potential
motor end plate
motor neuron
motor unit
motor unit
muscle
muscle fiber
muscle shortening
myelinated axon
myosin
Na+ channel inactivation
Na+/K+ channel
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Na+/K+ pump
nervous system
neurite
neuron
neurotransmitter
nicotinic receptor
OFF-bipolar cell
Off-center receptive field
ON-bipolar cell
On-center receptive field
opsin
optic nerve
perception
permeability
phosphodiesterase
photoreceptor
photoreceptor
phototransduction
pigmented epithelium
postsynaptic receptor
presynaptic terminal
receptive field
receptor
reflex
relative refractory period
relaxation
repolarization
retina
retinal cones
retinal rods
rhodopsin
rigor mortis
saltatory conduction
sarcolemma
sarcomere
sarcoplasm
sarcoplasmic reticulum
Schwann cell
sensory neuron
Sliding filament theory
sodium permeability
spinal cord
synapse
synaptic cleft
synaptic vesicle
T-tubule
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thick filament
thin filament
transducin
trigger zone
tropomyosin
troponin
voltage-gated
voltage-gated Ca2+ channel
voltage-gated Cl- channel
voltage-gated K+ channel
voltage-gated Na+ channel