GUTS Ion Transport

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Consolidated Study Questions from the syllabi.
Enjoy.
1-2 GUTS Ion Transport
Study Questions (review of key concepts)
1. What is the relationship between osmolarity (or osmolality) and water
concentration?
2. What is the osmolarity of normal plasma?
3. What are the normal concentrations of Na+, K+, Ca2+, and Cl- in intracellular
and extracellular fluids?
4. What is active transport?
5. What is the difference between primary and secondary active transport?
6. How many Na+ and K+ ions are transported per molecule of ATP hydrolyzed
by the Na,K-ATPase?
7. What are the main functions of the Na,K-ATPase?
8. What are the functional differences between SERCA Ca-ATPases and
plasma membrane Ca-ATPases?
9. What is the difference between symport and antiport?
10. In which direction are substrates transported by the Na-glucose transporter?
The Na-Ca exchanger? The Na/K/Cl transporter?
11. Why is Cl- influx mediated by the Na/K/Cl transporter and the Na/Cl
transporter “uphill?” I thought Cl- concentration was higher outside than
inside, so influx would be “downhill.”
12. What are the main mechanisms by which cells maintain a low cytoplasmic
concentration of Ca2+?
13. What are the mechanisms by which cardiac glycosides increase cardiac
contractility?
14. What transporters are essential for neurotransmitter uptake and packaging
into synaptic vesicles?

Study Question Answers
1. There is an inverse relationship between osmolarity and water
concentration. The higher the osmolarity, the lower the concentration of
water.
2. The osmolarity of normal plasma is 290 mOsm/kg (or 290 mOsm/L).
3. The normal concentrations of Na+, K+, Ca2+, and Cl- in ICF are 15 mM, 120
mM, 10-4 mM and ~20 mM, respectively. In ECF, the concentrations are 145
mM, 4.5 mM, 1.2 mM, and 116 mM, respectively.
4. Active transport is the process of transporting a substrate against its
concentration gradient, from a region of lower concentration to a region of
higher concentration (i.e. uphill transport).
5. In primary active transport, ATP is hydrolyzed by the transporter itself to
provide the energy required for uphill transport of substrate. In secondary
active transport, the uphill transport of one substrate is coupled to the
downhill transport of another.
6. Three Na+ ions are pumped outward and 2 K+ ions are pumped inward for
molecule of ATP hydrolyzed by the Na,K-ATPase.
7. The three main functions of the Na,K-ATPase are (1) to create the Na+
gradients that are used by many secondary active transport processes, (2)
to create the Na+ and K+ gradients that are required for resting membrane
potentials and action potentials, and (3) to maintain cell volume by pumping
net solute (Na+) from the cytoplasm to the ECF.
8. SERCA Ca-ATPases have both high capacity and high affinity for Ca 2+
transport. Plasma membrane Ca-ATPases have high affinity for Ca2+ export,
but they do not have high capacity.
9. A symporter (co-transporter) transports two (or more) substrates in the
same direction across a membrane. An antiporter (exchanger) transports
two (or more) substrates in opposite directions across a membrane.
10. The Na-glucose transporter normally mediates the influx (transport from ECF
to ICF) of glucose (uphill or downhill) and the downhill influx of Na +. The Na-
Ca exchanger usually transports Ca2+ outward (from ICF to ECF, uphill) in
exchange for downhill Na+ influx (although this transporter sometimes runs
in reverse and allows Ca2+ influx in exchange for Na+ efflux). The Na/K/Cl
transporter mediates the uphill influx of K+ and Cl- along with the downhill
influx of Na+.
11. The answer to this question requires the information in the lecture on the
Resting Membrane Potential. The chemical gradient for chloride (116 mM
outside, 5-20 mM inside) favors chloride influx, so you'd think that chloride
influx would be downhill. However, the electrical gradient (negative voltage
inside relative to outside; see notes on Resting Membrane Potential) favors
chloride efflux because the inside negativity repels intracellular chloride. If a
cell’s membrane potential is more negative than the cell’s equilibrium
potential for chloride (calculated from the Nernst equation), then the
electrochemical gradient for chloride favors chloride efflux. In this case, any
chloride influx driven by a transporter would be “uphill.” If a cell’s membrane
potential is less negative than the equilibrium potential for chloride, then the
electrochemical gradient for chloride favors chloride influx, and any chloride
influx is “downhill.” If the membrane potential is exactly equal to the
equilibrium potential for chloride, then any chloride influx would be neither
uphill nor downhill.
The Na/Cl-cotransporter and the Na/K/Cl-cotransporter usually transport
chloride “uphill” because a cell's membrane potential is usually more
negative than the equilibrium potential for chloride. This is true for most
cells, most of the time. Another way to look at it is this: because of Na-
driven transporters like the Na/Cl-cotransporter and the Na/K/Cl-
cotransporter, the concentration of chloride inside a cell is usually higher
than it would be if chloride was at electrochemical equilibrium, so the
transport of chloride is usually “uphill.”
12. The main mechanisms by which cells maintain a low cytoplasmic
concentration of Ca2+ are (1) Ca2+ transport from the cytoplasm into the ER
or SR by the SERCA Ca2+-ATPases, (2) Ca2+ transport from the cytoplasm
to the ECF by the Na-Ca exchanger, and (3) Ca2+ transport from the
cytoplasm to the ECF by the plasma Ca2+-ATPases.
13. The mechanisms by which cardiac glycosides increase cardiac contractility
are (1) partial inhibition of the Na,K-ATPase, (2) increase in intracellular Na+
concentration and decrease in Na+ gradient, (3) decreased export of Ca2+
by the Na-Ca exchanger, (4) increased Ca2+ transport from cytoplasm to SR
by the SERCA Ca2+-ATPases, (5) more Ca2+ release from SR during
triggered contraction (systole).
14. Neurotransmitter uptake and packaging requires (1) Na,K-ATPase in the
surface membrane to create a Na+ gradient, (2) Na-driven cotransporter in
the surface membrane (specific for the neurotransmitter) to transport
neurotransmitter from extracellular fluid to cytoplasm, (3) V-ATPase in the
synaptic vesicle membrane to create a H+ gradient in synaptic vesicles (high
concentration of H+ inside the vesicles), and (4) H-driven exchange
transporters in the synaptic vesicle membrane (specific for the type of
neurotransmitter) to transport neurotransmitter from cytoplasm into the
lumen of the synaptic vesicles.

1-2 GUTS Resting Membrane Potentials

Study Questions (review of key concepts)
1. What forces create equilibrium potentials?
2. What is the Nernst equation for K+? For Na+? For Ca2+? For Cl-?
3. What are the normal equilibrium potentials for K+, Na+, Ca2+, Cl-?
4. Does the Nernst equation define the resting membrane potential of a normal
cell?
5. What equation describes the membrane potential of normal cells?
6. Why are the resting membrane potentials of most cells negative?
7. Why is the RMP of cardiac myocytes more negative than that of liver cells?
8. What would happen to the membrane potential of a cell if the permeability to
Na+ suddenly increased?
9. What would the membrane potential of a cell be if it was equally permeable
to Na+ and K+ and had no Cl- permeability.
10. What class of proteins mediate membrane potentials?

Study Question Answers
1. Equilibrium potentials are created by the balance between (1) the diffusion
of ions down their concentration gradients, and (2) the electric field created
by the movement of a single type of ion.
2. EK = (60 mV) * log ([K]out/[K]in)
ENa = (60 mV) * log ([Na]out/[Na]in)
ECa = (30 mV) * log ([Ca]out/[Ca]in)
ECl = (-60 mV) * log ([Cl]out/[Cl]in) = (60 mV) * log ([Cl]in/[Cl]out)
+
3. The normal equilibrium potentials for K , Na+, Ca2+, Cl- are -85 mV, +59 mV,
+122 mV, and -82 to -46 mV, respectively.
4. No, the Nernst equation does not define the resting membrane potential of a
normal cell. The Nernst equation defines the equilibrium potential for an ion.
5. The GHK equation describes the membrane potential of normal cells.
6. The resting membrane potential of most cells is negative because they have
a higher resting permeability to K+ than to other ions and the equilibrium
potential for K+ (EK) is negative.
7. The RMP of cardiac myocytes is more negative than that of liver cells
because cardiac myocytes have a high resting permeability to K+ and very
low resting permeabilities to other ions. Liver cells have a lower resting
permeability to K+ and a higher resting permeability to Na+ and Cl- than
cardiac myocytes.
8. If the membrane permeability to Na+ suddenly increased, the membrane
potential of a cell would depolarize.
9. Plugging PCl = 0, PK/PNa = 1 and normal internal and external concentrations
of Na+ and K+ into the GHK equation, one gets Vm = 2.7 mV in this case.
10. Ion channels are primarily responsible for creating and controlling
membrane potentials.

1-3 GUTS Action Potentials

Study Questions (review of key concepts)
1. What is threshold? What is an overshoot? What is an after-
hyperpolarization?
2. What is the duration of typical nerve action potential?
3. What happens if a nerve is depolarized, but not to threshold?
4. What happens when a nerve is depolarized past threshold?
5. In terms of channel behavior, what is threshold?
6. What role do voltage-gated Na channels play in action potentials?
7. What role do voltage-gated K channels play in action potentials?
8. Why are nerve action potentials “all-or-none?”
9. What is the difference between a closed Na channel and an inactivated Na
channel?
10. What allows inactivated Na channels to work again?
11. Are voltage-gated K channels required for repolarization?
12. What is the difference between the absolute and relative refractory periods?
13. Why is it “harder” for a cell to fire an action potential during the relative
refractory period?
14. What are the three types of ion flow (current) that is required for the
propagation of action potentials?
15. What are two factors that affect the speed at which action potentials
propagate?
16. Why do action potentials in myelinated nerves propagate faster than those
in unmyelinated nerve?

Study Question Answers
1. Threshold is the voltage at which an excitable cell has a 50% probability of
firing an action potential. Overshoot is the height of an action potential
above 0 mV. (The amplitude is the height of an action potential above the
RMP.) The afterhyperpolarization is the time after an action potential during
which the membrane potential is below the RMP.
2. The duration of typical nerve action potential is 1-2 msec.
3. If a nerve is depolarized but not to threshold, the membrane potential will
repolarize back to the RMP.
4. If a nerve is depolarized past threshold, it is very likely to fire an action
potential.
5. In terms of channel behavior, threshold is the voltage at which enough Na
channels are activated to initiate the positive feedback loop (Na channel
activation  Na+ influx  depolarization  more activation) that is
responsible for the action potential upstroke.
6. Voltage-gated Na channels are responsible for threshold and the upstroke
of action potentials.
7. Voltage-gated K channels accelerate the repolarization phase of action
potentials and participate in the afterhyperpolarization.
8. Nerve action potentials “all-or-none” because the positive feedback loop for
Na channels causes most or all of the available Na channels to be activated
during each action potential.
9. A closed Na channel can open if it is depolarized. An inactivated Na channel
cannot open until it recovers from inactivation to the closed (resting) state.
10. Inactivated Na channels recover from inactivation (to the closed resting
state) at polarized (or hyperpolarized) potentials. When they are in the
closed resting state, they are available to be activated again by a
depolarization.
11. Voltage-gated K channels are not required for repolarization, but they are
important for accelerating repolarization and keeping action potential
durations short.
12. During the absolute refractory period, it is impossible for a cell to fire
another action potential. During the relative refractory period, an excitable
cell can fire another action potential, but a larger-than-normal stimulus is
required, and the action potential may not have the same upstroke or
amplitude.
13. It is “harder” for a cell to fire an action potential during the relative refractory
period because the smaller number of available Na channels and the
increased K permeability raise the threshold.
14. The three types of ion flow (current) required for the propagation of action
potentials are (1) influx of Na+ through Na channels, (2) longitudinal
electrotonic current carried in the cytoplasm and in the extracellular fluid,
and (3) outward capacitative current.
15. Two factors that affect the speed at which action potentials propagate are
(1) the diameter of the axon and (2) whether the axon is myelinated. Large-
diameter axons propagate action potentials faster than do small-diameter
axons. Myelinated axons propagate action potentials faster than
unmyelinated axons.
16. Action potentials in myelinated nerves propagate faster than those in
unmyelinated nerve because the myelin insulates the membrane, which
allows the longitudinal electrotonic current to flow farther in the cytoplasm.
Thus, action potentials propagate rapidly from one node of Ranvier to
neighboring nodes (up to 1-2 mm away). Because the nodes are relatively
far apart, propagation is fast.

1-4 EXCITATION-CONTRACTION COUPLING IN SKELETAL MUSCLE

Study Questions (review of key concepts)
1. What is a motor unit?
2. What are the steps that lead from an action potential at the motor endplate to
the increases in intracellular Ca2+ in the muscle cytosol?
3. What are the steps that terminate a muscle contraction?
4. Does a single action potential in muscle cause a contraction?
5. Why is a muscle twitch so much longer than an action potential?
6. Is the peak level of intracellular Ca2+ during a twitch much smaller than during
a sustained contraction?
7. Why does a twitch generate less peak muscle force than a sustained
contraction?
8. Describe the two ways to regulate (grade) the strength of skeletal muscle
contraction.
9. Describe the three types of skeletal muscle.

Study Questions Answers
1. A motor unit is the group of muscle cells innervated by a single motor neuron.
2. The steps that lead from an action potential at the motor endplate to the
increases in intracellular Ca2+ in the muscle cytosol are: (1) Propagation of
action potentials from the surface into the T-tubules; (2) Activation of voltage
sensor proteins (DHP receptors) in the T-tubules; (3) Opening of Ca2+-release
channels (ryanodine receptors) in the SR membrane; (4) Efflux of Ca 2+ from
SR to the cytoplasm.
3. The steps that terminate a muscle contraction are (1) the de-activation of the
Ca2+-release channel and (2) the re-sequestration of Ca2+ into the SR.
4. A single action potential in muscle causes a twitch (a small, brief contraction).
5. A muscle twitch is much longer than an action potential because the Ca2+
release channel and Ca2+ re-uptake mechanisms are much slower than the
Na and K channels that are responsible for the action potential.
6. The peak level of intracellular Ca2+ during a single twitch is not much smaller
than during a sustained contraction. The peak level of intracellular Ca 2+
during a single twitch is ~80% of the maximal level attained during a
sustained contraction.
7. A single twitch generates less peak muscle force than a sustained contraction
because much of the contraction during a single twitch goes into stretching
the series elastic elements. Only after the series elastic elements are
stretched (during a sustained contraction) does muscle contraction reach its
maximal force.
8. The two ways to regulate (grade) the strength of skeletal muscle contraction
are by (1) temporal summation and (2) special summation. During temporal
summation, the frequency of action potentials in a single motor neuron is
changed. The higher the frequency, the greater the contractile force of the
motor unit. During spatial summation, the number of motor units is changed.
A stronger contraction will recruit more motor units. Typically, smaller motor
units are recruited first, then progressively larger motor units.
9. The three types of skeletal muscle are: (1) Slow-twitch (type I) muscle, with
slow myosin and an abundance of myoglobin; (2) fatigue-resistant fast-twitch
(type IIa) muscle, with faster myosin, an abundance of myoglobin, and an
abundance of glycogen and glycolytic enzymes; and (3) fatigable fast-twitch
(type IIb) muscle, with the fastest myosin, little myoglobin, and the highest
concentration of glycogen and glycolytic enzymes.

1-4 Synaptic Transmission at the NeuroMuscular Junction

Study Questions (review of key concepts)
1. What is the neurotransmitter at the NMJ?
2. What are the steps that trigger the release of ACh from the presynaptic
terminal at the NMJ?
3. What are the steps that trigger action potentials in muscle when a motor
neuron is stimulated?
4. Is Ca2+ influx through nAChRs in the motor endplate responsible for muscle
contraction?
5. What defect is present in patients with myasthenia gravis?

Study Questions Answers
1. Acetylcholine (ACh) is the neurotransmitter at the NMJ.
2. The steps that trigger the release of ACh from the presynaptic terminal are:
(1) An action potential propagates into the presynaptic terminal; (2) The
depolarization activates voltage-gated Ca channels in the presynaptic
terminal; (3) Ca2+ influx through the Ca channels increases the
concentration of Ca2+ in the presynaptic terminal; (4) Increased Ca2+
concentration triggers the fusion of docked, loaded vesicles with the surface
membrane, releasing ACh into the synaptic cleft.
3. The steps that trigger action potentials in muscle when a motor neuron is
stimulated are: (1) Activation of nicotinic receptors in the motor endplate; (2)
Influx of Na+ through AChRs depolarizes the motor endplate; (3)
Depolarization of the motor endplate activates voltage-gated Na channels,
initiating action potentials that propagate in the muscle cell.
4. Ca2+ influx through nAChRs in the motor endplate is not responsible for
muscle contraction. Nicotinic receptors at the motor endplate are sparingly
permeable to Ca2+, but Ca2+ influx is not important there. It is the influx of
Na+ through nAChRs and the resulting depolarization that is important for
triggering action potentials in the muscle cell.
5. Patients with myasthenia gravis have a low number of nicotinic receptors in
their motor endplates because their immune systems attacks and destroys
them. The paucity of nAChRs causes weakness and paralysis of the
affected muscle.

1-4 SYNAPTIC TRANSMISSION IN THE CNS.doc

Study Questions (review of key concepts):
1. What ion channel mediates ion flow between cells at electrical synapses?
2. What physiological function is served by electrical synapses between
neurons in the CNS?
3. What steps make up most of the delay in fast chemical synaptic
transmission?
4. In terms of the postsynaptic response, what is the difference between an
excitatory and inhibitory neurotransmitter.
5. What are the steps that follow the activation of metabotropic receptors?
6. Name two effectors and the 2nd messengers they make.
7. What are the three mechanisms for terminating synaptic transmission?
8. What terminates signaling in the G protein pathway?
9. What is temporal summation?
10. What is spatial summation?
11. Does synaptic location matter to the postsynaptic cell.

Study question answers:
1. Gap junction ion channels (connexons) mediate ion flow between cells at
electrical synapses.
2 .Synchronous firing of action potentials in neurons coupled by electrical
synapses. Coordination of responses by multiple glial cells coupled by
electrical synapses.
3. Synaptic delay in fast chemical synaptic transmission is due to (1) the time
needed for Ca channels to open, (2) the time required for SNARE proteins
to change conformation, and (3) the time reuired for synaptic vesicles to
fuse with the surface membrane.
4 Excitatory neurotransmitters cause depolarizations of postsynaptic cells.
Inhibitory neurotransmitters cause hyperpolarizations of postsynaptic cells.
5. Activation of GPCRs lead to (1) conformational changes in the coupled G
protein; (2) release of bound GDP from the  subunit and binding of GTP
to the  subunit; (3) dissociation of the GTP-bound  subunit from the
GPCR; (4) dissociation of the  subunit from the GTP-bound  subunit;
(5) activation of effectors by GTP-bound  subunits and  subunits.
6. One effector is adenylyl cyclase. It makes cAMP. Another effector is
phospholipase C. It makes IP3 and DAG.
7. Synaptic transmission is terminated by (1) re-uptake of neurotransmitter,
(2) hydrolysis of neurotransmitter (for ACh and peptides only), and/or (3)
desensitization of receptors.
8. G protein signaling is terminated by hydrolysis of GTP by the  subunit, re-
association of  subunits, and re-association of the G protein with the
unliganded GPCR.
9. Temporal summation is the integration of EPSPs or IPSPs following rapid
bursts of presynaptic action potentials. EPSPs and IPSPs are longer-
lasting than presynaptic action potentials and the time-course of synaptic
transmission, so high-frequency presynaptic stimuli will be summated by
the postsynaptic cell. A high frequency of sub-threshold EPSPs can add
up (in time) to a large, supra-threshold EPSP.
10. Spatial summation is the integration (summation) of multiple different inputs
by a single postsynaptic cell. Multiple different subthreshold stimuli can be
integrated by the postsynaptic cell to a supra-threshold EPSP. IPSPs and
EPSPs from multiple different presynaptic cells can cancel each other out.
11. Synaptic location does matter. A synapse that is close to the spike initiation
zone on an axon will have more influence on whether the postsynaptic cell
fires action potentials than a synapse that is far away on a distal dendrite.

1-5 GLIAL CELL FUNCTION

Study questions:
1. How does cell-cell signaling differ between neurons and glia?
2. Why might one expect most CNS tumors to be derived from glia instead of
neurons?
3. Are the biological functions of astrocytes well understood?

(Answers)
1. Most neurons are specialized for rapid (<sec) communication via action
potentials over often large distances to anatomically specific targets that they
physically contact at chemical synapses. Although our understanding of glial
signaling is limited, glial signaling is not based on action potentials or transmitter
release at morphologically defined chemical synapses. Glial release of factors
such as GDNF almost certainly affects many neurons or glia not in direct contact
with the secreting cell and has a much slower time course than synaptic
transmission. The calcium waves that can propagate in astrocytes represent
another potential system for glial based signaling.
2. Unlike neurons, which are generally produced early in development and are
fundamentally postmitotic, glia retain the ability to proliferate in response to a
variety of specific signals in the adult nervous system and thus may be more
vulnerable to disruptions in growth regulation. Schwannomas, oligodendromas,
astrocytomas, and ependymomas are all relatively common nervous system
tumors.
3. Probably not.
1-5 Neuroanatomy Session 1 Overview of Brain and Spinal Cord.doc

Exercises :

1. Fill in the following chart of brain regions and functions. How many can you
fill in from memory before referring to the list in the syllabus above?

Brain region Functions

Frontal lobe

Temporal lobe

Parietal lobe

Occipital lobe

Precentral gyrus

Postcentral gyrus

Dorsal horn

Ventral horn

Thalamus

Basal ganglia

Wernickes area

Broca’s area

Internal capsule

2. At right is a random-order list of the brain slices shown in the images above.
At left is a random-order list of the brain structures that are labeled in these
images. How many can you match from memory, before referring to the images?
Note: some structures are present in multiple sections.

a. Pons Pyramidal tract
Hypothalamus
Caudate nucleus
Septum pellucidum
b. Horizontal section of cerebrum Middle cerebellar
peduncle
Optic chiasm
Internal capsule
c. Caudal Medulla Inferior olive
Globus pallidus n.
Cerebral peduncle
Ventral horn
d. Mid-Medulla Thalamus
Corpus callosum
Caudate nucleus
Inferior colliculus
e. Spinal cord Hippocampus/uncus
Doral horn
Insula
Superior colliculus
f. Coronal section of cerebrum Cingulate gyrus
Putamen nucleus
Lateral ventricle
3rd ventricle
g. Midbrain Cerebral aqueduct
4th ventricle
Central canal

3 -4 Color / shade in the body region(s) which would be affected by the lesion.

3. Loss of blood to the right lateral parietal lobe.
What is the major functional deficit?

4. Tumor growing in the midline sagittal fissure in the area of precentral gyrus.
What is the major functional deficit?

3. 4.
5. List major differences in functional deficits between a right-sided and a left-
sided lesion of the cerebral hemispheres.

6.The upper MRI is a coronal or horizontal view?

The lower MRI is a coronal or horizontal view?

What structure(s) is/are damaged in the white lesions at the ends of the
arrows in the MRIs below?

Are these 2 MRIs likely from the same patient?

Are either of them the lesion causing Figure A’s deficits (shaded in red)?
A

Clinical Case : Select all correct choices in the following clinical history and
physical exam to best describe the patient in the MRIs below.

Mr. R.T. is a 65 year old man who describes 2 months of increasing headaches
and (right / left? ) (upper extremity / lower extremity / facial?) (weakness /
sensory loss?). You send him for neuron-imaging (see MRIs below). The
lesion is the entire round, white structure at the tip of the arrow. In the patient’s
chart you use the accompanying diagram of a person and shade in the region(s)
of deficits you find on physical exam.
1-5 Neurotransmitters and Their Receptors in the CNS.doc

Study questions (review of key concepts):
1. Do all neurotransmitters activate both ionotropic and metabotropic
receptors?
2. What is the most important excitatory neurotransmitter in the central
nervous system?
3. What are the most important inhibitory neurotransmitters in the CNS?
4. What is the primary difference between the synthesis of small-molecule
neurotransmitters and neuropeptides?
5. What neurotransmitters are catecholamines?
6. Catecholamines are derived from what amino acid?
7. Serotonin is produced from what amino acid?
8. Where do most dopaminergic neurons originate? Noradrenergic?
9. Which neurotransmitters are responsible for general arousal and
attention?

Study question answers:
1. No. Some neurotransmitters, such as ACh, glutamate, and GABA activate
both ionotropic and metabotropic receptors, but dopamine,
norepinephrine, epinephrine, histamine, adenosine, opioids (and several
other neurotransmitters) activate only metabotropic receptors. Glycine
activates only ionotropic receptors.
2. Glutamate is the most important excitatory neurotransmitter in the central
nervous system.
3. GABA is the most important inhibitory neurotransmitter in the brain.
Glycine is the most important inhibitory neurotransmitter in the spinal cord.
4. Small-molecule neurotransmitters are synthesized and specifically
packaged into presynaptic vesicles in nerve terminals. Neuropeptides are
synthesized and packaged into vesicles in the cell body, and then
transported to nerve terminals.
5. The catecholamines are dopamine, norepinephrine, and epinephrine.
6. Catecholamines are produced from tyrosine.
7. Serotonin is produced from tryptophan.
8. Dopaminergic fibers originate in the substantia nigra and ventral tegmental
area of the midbrain. Noradrenergic fibers originate in the locus ceruleus.
9. The neurotransmitters that are important for arousal are norepinephrine,
epinephrine, and histamine.

1-8 Autonomic Nervous System.doc

Study Questions.

1. Explain how sensory fibers participate in autonomic reflexes.
2. Explain the autonomic regulation of heart rate.
3. Explain the autonomic regulation of micturition.
4. Briefly outline the organization of the hypothalamus and explain how it regulates
autonomic function.

Answers.

1. Sensory fibers from the viscera arise from cell bodies in the dorsal root ganglia
and the sensory ganglia associated with the IX and X cranial nerves (just like
somatic sensory fibers). Visceral sensation may be diffuse and difficult to localize
because there are fewer visceral than somatic sensory neurons. Although for the
most part visceral input conveys limited information to consciousness, sensory
fibers participate in autonomic control by terminating on spinal cord neurons (or
brainstem nuclei) which in turn project to the preganglionic neurons at the origin
of the sympathetic and parasympathetic divisions. Some sensory fibers from the
viscera contact directly these neurons, in a manner reminiscent of muscle
afferents in the stretch reflex.

2. Heart rate may increase or decrease in response to sensory input from
essentially two classes of receptors, i.e. baroreceptors (conveying information
about pressure in the arterial system), and chemoreceptors (conveying
information about the levels of oxygen and carbon dioxide in the blood). These
afferents travel to the brainstem via the IX and X cranial nerves and terminate in
the nucleus of the solitary tract. From here, input is relayed to the cells of origin
of “motor” fibers of the vagus nerve (in the nucleus ambiguus and dorsal motor
nucleius of the vagus). Stimulation of the vagus reduces heart rate. Spinal reflex
arcs are also activated resulting in stimulation of postganglionic symapthetic
fibers which have the opposite effect.

3. The parasympathetic control of micturition originates from neurons in S2-S4
which innervate parasympathetic ganglia in or near the bladder. Neurons in S2-
S4 are under the control of sensory afferents from the bladder terminating in the
spinal cord and brainstem centers (including a “micturition” center in rostral
pons). In general, parasympathetic innervation produces contracvtion of the
bladder walls and relaxation of the sphincters. The sympathetic innervation of the
bladder originates in preganglionic neurons in the upper lumbar cord segments
whose axons run, directly or indirectly (i.e. after a synapse in the inferior
mesenteric ganglion), to the inferior hypogastric plexus. Sympathetic activity
inhibit the contraction of the bladder wall and closes the internal urethral
sphincter.

4. The hypothalamus is the upper center that regulates and controls body
homeostasis. It consists of a heterogeneous collection of nuclei and pathways at
the base of the diencephalon. Although some of the hypothalamic control on
autonomic preganglion neurons may be exerted via direct input, most of the
relevant outflow from the hypothalamus is relayed via “autonomic centers” in the
brainstem. These centers operate as premotor circuits that coordinate the
efferent activity of preganglionic motor neurons and organize specific visceral
functions of all major organs in the body.

Neuroanatomy Session 2 : CNS Vasculature

Exercises
Use images and information from this and the previous session to answer the
following.
1. Answer these questions about the cerebral cortex blood supply.
a. Which arteries supply the primary somatosensory and motor cortices?
b. Which artery supplies the region where the lower extremity is represented?
c. Which artery supplies the region where the face is represented?
d. Which artery supplies the region where the upper extremity is represented?
e. Which artery supplies the primary visual cortex?
f. Which artery supplies the primary auditory cortex?
2. Fill in the charts : Cerebral arteries
Abbreviations : UE = upper extremity LE = lower extremity

Cerebral artery Cerebral lobe(s) Function(s) of Function(s) of
perfused these regions in these regions in
LEFT brain RIGHT brain
Anterior cerebral Frontal- Medial Right LE motor Left LE motor
Parietal- Medial Right LE sensory Left LE sensory

Middle cerebral

Posterior cerebral

For MCA, be sure to consider speech areas.

Abbreviations : I = Ipsilateral B = Bilateral C = Contralateral
Important structures Function(s) Vascular supply
Internal capsule
Brocas’ area
Wernicke’s area

3. Answer the questions for vertebro-basilar system.
a. What arteries supply the pons? The mid-medulla? The caudal medulla?

b. In order to learn these vascular territories, you can draw outlines of each of
these brainstem levels, and practice drawing in the vascular territories.

4. Answer the questions for the spinal cord arterial supply.
a. Occlusion of which spinal artery in the spinal cord can result in bilateral
impairments?
b. Posterior spinal artery occlusion, in the spinal cord, results in which
type(s) of deficit(s)? Sensory Motor
c. Anterior spinal artery occlusion, in the spinal cord, results in which type(s)
of deficit(s)? Sensory Motor
Clinical Cases
1. A 64 year old male is brought to the Emergency Department. Physical exam
is noteworthy for slurred speech. He is sent for neuroimaging (see below) and
the diagnosis of stroke (= CVA = cerebrovascular accident) is made.
 The patient’s left is the right side of the image.
 When viewing images, first decide what the plane of section is.
 Next, when looking for lesions, compare right and left sides. Lesions often
are unilateral, so one side is normal, the other abnormal.
 Lesions will appear either as white areas or dark areas, depending on
factors used when making the image.
Which of these 3 images is horizontal and which coronal?
The lesion (CVA) in the 2 images to the left appears as abnormal white areas.
The lesion (CVA) in the image on the right appears as a dark area.
What cerebral area is involved?
What artery is occluded and causing his CVA?
Muscle weakness is present and causing slurred speech on which side, right or left?

2. An 83 year old woman presents to her physician with recent onset of severe
headache. She is sent for neuroimaging (see below). A diagnosis of CVA is made.
Which of the 3 images is horizontal and which coronal?
The lesion (CVA) in all 3 images appears as abnormal white areas.
Point out the lesion. What cerebral area is involved?
What artery is occluded and causing her CVA?
Given this location, in addition to headache, what is her other major symptom?
B

3. This is an autopsy specimen of a CVA. Could it be the brain of either of the
patients above (assuming they died)? Why / why not?

1-8 The enteric nervous system.doc

Study Questions
1. What is the main functional difference that distinguishes the submucosal
plexus from the myenteric plexus?
2. Describe the differences between “short loop” and “long loop” reflexes
3. In what ways do the slow waves observed in intestinal smooth muscle differ
from the action potentials observed in skeletal muscle?
4. Describe the peristaltic reflex. How is it generated? Why do peristaltic waves
occur at different frequencies in different parts of the GI tract?
5. In an experimental animal:
a) Parasympathetic and sympathetic nerves to the GI tract are cut
b) Ingestion of food stimulates secretion of enzyme X into the lumen of the
GI tract
c) Administration of intravenous atropine (a cholinergic antagonist) blocks the
secretion of enzyme X in response to ingestion
i) What could you conclude about the reflex mechanism controlling
secretion of enzyme X into the lumen in this experimental
animal?
ii) Could a hormone play a role in the secretion of enzyme X in this
experimental animal? If so, what additional experimental
evidence might support a role for a hormone?
6. What is the function of Interstitial Cells of Cajal?
Answers to Study Questions

1. The submucosal plexus primarily regulates mucosal physiology and the
myenteric plexus primarily regulates smooth muscle physiology.
2. Reflexes in the GI tract, like reflexes in any other part of the body, are
mediated by neurons. (a) Long loop reflexes are mediated by the autonomic
nervous system. The most important long loop reflexes that we have
discussed in the GI portion of this course are mediated by the parasympathetic
nervous system (usually by the vagus nerve). Parasympathetic reflexes
typically stimulate GI function. In contrast, the sympathetic nervous system is
inhibitory to the GI organs, and is called into play primarily during “fight or
flight” responses. Sensory information from the gut itself often triggers long
loop reflexes. This sensory information is carried by autonomic afferent fibers
from the gut to the brain, where it is processed to generate the reflexes that
then are returned to the gut by autonomic efferent fibers. (b) Short loop
reflexes are intrinsic to the gut itself, and are generated by the enteric nervous
system. Short loop reflexes are not eliminated when autonomic afferent and
efferent fibers are destroyed. Short loop reflexes are typically initiated and/or
modified by sensory information about the intraluminal environment that is
reported by chemo-, osmo- and mechanoreceptors. Although there are many
short loop reflexes, the only one we have considered in detail is the peristaltic
reflex.
3. The duration of the slow wave (4 - 6 sec) is much longer than that of the action
potential (3 - 4 msec). Smooth muscle slow waves occur spontaneously at a
regular frequency, under the control of oscillating “driver potentials” in
intestinal pacemaker cells (Interstitial Cells of Cajal), whereas skeletal muscle
action potentials are seen only in response to activity in spinal motor nerves.
The slow wave is initiated by depolarizing current that enters the smooth
muscle cell through gap junctions, and the slow upstroke of the slow wave is
due to passive spread of the current that enters though these gap junctions. In
contrast, the action potential is initiated by depolarizing current that enters the
skeletal muscle cell through acetylcholine-gated channels, and the rapid
upstroke of the action potential is driven by voltage-dependent sodium
channels.
4. The peristaltic reflex is a short-loop reflex that is intrinsic to the intestine (i.e.
occurs even when autonomic inputs have been cut). This reflex propels food in
the rostral-to-caudal direction. It is generated by a more complicated version of
the oversimplified circuit shown in figure 6. The basic idea is that circular
smooth muscle contracts upstream of the stimulus (driving the intestinal
contents forward), while circular smooth muscle relaxes downstream of the
stimulus (making it easier for the intestinal contents to advance). In addition,
longitudinal smooth muscle contracts downstream of the stimulus, shortening
the tube and pulling it over the material in the lumen (like a sock being pulled
over a foot). Peristaltic waves occur at different frequencies in different parts of
the GI tract because the output of the peristaltic reflex is superimposed on top
of slow-wave potentials that occur with different rhythms in different parts of
the gut. No one yet knows what causes the rhythm of the slow-waves to vary
from region-to-region; it must reflect different intrinsic properties of the
pacemaker cells that initiate the slow waves.
5. The fact that secretion of enzyme X is blocked with atropine suggests that the
secretion of enzyme X is induced by a reflex loop that requires participation of
an ACh-releasing cell (i.e. a neuron). Since the autonomic inputs have been
eliminated, it is apparent that the reflex pathway is a short loop, involving the
enteric nervous system. None of the data presented supports or rules out the
participation of a hormone either upstream or downstream of the enteric
neuron(s)... for example, food ingestion might activate an atropine-sensitive
neuron which then stimulates a hormone-releasing cell and the hormone might
in turn stimulate an enzyme-secreting cell. Appropriate experimental evidence
on this point could involve showing that (i) the stimulus (ingestion of food)
leads to an elevation of the plasma levels of a hormone (ii) a hormone receptor
antagonist blocks the secretion of enzyme X in response to the stimulus (iii)
injection of a hormone into the blood induces secretion of enzyme X even in
the absence of the stimulus.
6. Interstitial Cells of Cajal are the pacemaker cells of the GI tract. They
spontaneously exhibit waves of depolarization (called “pacemaker potentials”
or “driver potentials”). These waves of electrical activity propagate into smooth
muscle cells through gap junctions to evoke “slow wave” potentials in the
muscle cells. The slow wave potentials serve as “timing waves” that set the
frequency of rhythmic contractions in the gut. Neuronal activity can increase or
decrease the amplitudes of slow waves (and can also, to a lesser degree,
affect their frequency), and thus increase or decrease the amplitudes (and,
somewhat, the frequencies) of rhythmic contractions.

1-9 Ascending Pathways and Pain.doc

Study questions:

1. Can you think of at least two reasons why muscle contraction in response
to brisk tapping of the patella is a faster reflex than withdrawal from a
noxious stimulus?
2. What is the difference between hyperalgesia and allodynia?
3. What is the mechanism of action of aspirin?
4. What is the definition of neuropathic pain?
5. Can you think of some targets for the development of new analgesic
drugs?

Answers:

1. Muscle afferents are more rapidly conducting than nociceptive afferents
and have monosynaptic (direct) contact with motor neurons. (Access of
nociceptive afferents to motor neurons is by way of spinal interneurons).
2. Hyperalgesia is an increased response to a noxious (pain inducing)
stimulus; allodynia is a perception of pain in response to a stimulus which
is not ordinarily painful.
3. Aspirin, like other non-steroids analgesics, inhibits cyclooxygenase, thus
blocking the production of prostaglandins.
4. Neuropathic is triggered by a lesion of the peripheral or central
components of the nerve fibers or central pathways and nuclei involved in
the transmission of nociceptive input.
5. Peripheral targets include capsaicin receptors, TTX-resistant sodium
channels, and bradykinin receptors. Central targets include NMDA
receptors and NK-1 (for substance P) receptors.

1-9 CHEMICAL SENSES

Questions for Study or Review:

1. Why might neurodegenerative diseases like Alzheimer’s Disease or
Parkinson’s Disease have amongst their earliest symptoms decline in
olfactory and taste function?

Maintenance of neural stem cells in the olfactory epithelium and brain, and
ongoing genesis and growth of new olfactory receptor neurons—and
possibly, but still not definitively established—some new olfactory bulb
neurons may be compromised quite early by the same pathological
mechanisms that ultimately damage more stable neural populations.

2. Odorant receptor molecules are members of a larger family of signaling
proteins-What is that family, and why might this particular family of
proteins be provide evolutionarily advantageous mechanism for encoding
odorant information?

Odorant receptors are members of the G-protein coupled, 7
transmembrane (TM) family of cell surface receptors. This might provide
and evolutionarily advantageous mechanism because of the diversity of
structure that can be generated by varying the extracellular binding
domains of the receptors—this could be useful for creating unique binding
sites for a broad range of distinct odorants. Also, the signal amplification
capacity of 7TM receptors is functionally significant-most odorants are
present at very low concentrations in the air, so to have some
amplification of the external stimulus would be advantageous.

3. What is the major challenge for representing odor information in circuits in
the CNS? How might this differ from other sensory systems?
The olfactory system represents a wide range of chemically and
perceptually distinct odors, and is primarily concerned with identity and
discrimination. Thus there is no known topography of the representation
(i.e. no equivalent of the somatosensory homunculus), and no real
knowledge of the relationship between the peripheral encoding of
information in receptor cells via receptor proteins, and the central map of
odor information. The key challenge is to discern how such a broad range
of identities is encoded by the circuitry in the olfactory bulb.

4. How does the representation of taste stimuli differ from that of odorants?
What does this imply about the function of the taste system versus the
olfactory system?

All available information indicates that taste encodes a few basic classes
of stimuli (salty, sweet, sour, bitter, umami) through specific receptors, and
then relays and processes this information in distinct channels, or “labeled
lines” in the brain. Thus, damage to one subset of the receptors in the
periphery will lead to loss of the perceptual experience of that class of
taste stimuli. This is not known to be the case for olfaction.

5. What are the major differences in the primary relay pathways for olfaction
and taste? What is unique about the olfactory pathway? Does the taste
pathway resemble any other sensory system?

The taste pathway is basically a special case of a somatosensory
pathway. Peripheral sensory ganglion cells (cranial ganglia) innervate
specialized receptors in an epithelium (the tongue, or lingual epithelium).
The relay of the information is then through the brainstem, the thalamus
and to the cerebral cortex. The olfactory pathway receptor cells are
neurons, their axons project from the periphery directly to the brain, and
the relay of information thereafter is to specialized olfactory structures
(olfactory bulb, pyriform cortex) prior to any information reaching the
cerebral cortex via the thalamus.

1-9 Somatosensory Spinal Cord.doc

Study Questions:

1. What other sensations from the body may we perceive that are not
part of the somatosensory system?
2. Why is there no such thing as a pure “motor” nerve?
3. Can you mention a functional purpose for the existence of capsule
around some cutaneous receptors?
4. What is a compound action potential?
5. What might the conduction velocity of the fastest sensory cutaneous
fibers (Aβ) be compared with?
6. Are there receptive fields for muscles?
7. Are there synapses in the DRG? What type?
8. What are the major classes of molecules released by central afferents
of DRG neurons?
9. What does quadriplegia mean and what do the two words it is made of
(quadri-plegia) mean?
10. How would a spinal interneuron which is also a projection neuron look
like?
11. What transmitter is released by the interneurons in the dorsal column
nuclei that are involved in surround or lateral inhibition?
12. In which part would somatosensation be lost as a result of an
occlusion of the left anterior cerebral artery?

Answers:

1) Sensations from the viscera and specialized sensations from the head,
like olfaction, vision, hearing, etc.
2) Because muscles receive also a sensory innervation.
3) In the case of the Pacinian corpuscles, the presence of the capsule
determines the adaptation rate of the receptor.
4) It is the electrophysiological expression of the spread of conduction
velocity of different fibers in a peripheral nerve.
5) The conduction velocity of the fastest cutaneous sensory fibers (Aβ,
72m/sec) is comparable to the speed of a racing car. (The conduction
velocity of the fastest sensory fibers from muscles (Aα, 120m/sec) is
comparable to that of a jet plane).
6) It would be hard to define a receptive field for muscles.
7) There are no synapses in the DRG (There are synapses, though, in the
autonomic ganglia).
8) Amino acids (particularly glutamic acid) and neuropeptides.
9) It means paralysis and loss of sensation in all four limbs. Quadri- is Latin
for four, and -plegia is Greek for paralysis (paralysis of all four limbs).
10) It would have a long axon which gives profuse branching at short distance
from its origin from the soma.
11) The inhibitory amino acid gamma-amino butyric acid (GABA).
12) In the right leg.

1-10 Neuroanatomy session 3 Somatosensory Pathways.doc

Exercise 3: Lesions involving the trigeminal pathways involve symptoms relating to
fine touch, vibration, proprioception and pain and temperature for the face. Fill in
the table below.
3 Trigeminal System

Face Region of
Postcentral Gyrus

Mesencephalic Nuc. Of
V

Motor Principal Sensory
VPM Nucleus Nucleus of V
of V
2
2
Trigeminal
Ganglion

C.Nerve
V

Trigeminothalamic
Tract
1 1
Spinal Trigeminal
Tract & Nucleus

Lesion #1 Deficits Which Side Do Vascularized By?
Symptoms Affect

1. Spinaltrigeminal
nucleus & tract
2. Trigemino-thalamic
tract
3. Postcentral gyrus

Clinical Case: During the class session a case will be presented with symptoms relevant
to the pathways discussed. Students will be prompted to work together in small groups to
use their new-found knowledge to address questions related to the case study. Answers
to these questions will NOT be posted elsewhere.
Anatomy Related Study Questions:
1. Complete the chart below:
Cell Location Site of Site of Site of
Decuss
Tract bodies of axons at first second third Function
ation
of Origin entry synapse synapse synapse
DC-ML Medial
dorsal root
entry zone

AL/STT

Spinal
Trigmeminal
System-
Trigeminothalamic
Tract

Principal Sensory
System-
Trigeminothalamic
Tract

1. Large diameter primary afferent axons mediate __________________________
sensory information to the CNS.

2. Large diameter axons of primary afferent neurons enter the dorsal root entry zone
____________ (lateral/medial) to small diameter, unmyelinated axons.

3. The cell bodies of small diameter, unmyelinated primary afferent axons are
located where?

4. What blood vessel supplies the “leg region” of the postcentral gyrus?

5. Where in the CNS is the vascular supply different for the DC-ML pathway and
the spinothalamic tract?

6. What blood vessel(s) vascularize(s) pain and temperature pathways from the face,
but not fine touch, vibration and proprioception pathways from the face?

7. To what region of the postcentral gyrus do axons from VPM neurons terminate?

Clinically Related Study Questions:
1. A midline cyst (as in syringomyelia) in the cervical segments of the spinal cord
would result in
a. what type of somatosensory deficits?
b. affecting what region of the body?
c. which side of the body?

2. Tabes dorsalis is a condition involving the degeneration of primary afferent
neurons with large diameter axons. What symptoms would occur?

3. An anterior spinal artery occlusion at L1 would result in
a. what somatosensory impairments?
b. affecting what part of the body?
c. affecting which side of the body?

4. An anterior spinal artery occlusion in medulla would result in
a. what somatosensory impairments?
b. affecting what part of the body?
c. affecting which side of the body?

For the following lesions, consider only the
somatosensory consequences. Be sure to include affects
on the face. 5. 6.

5. Lesion to the right dorsal columns at ~ C4.
Description of deficits
_______________________________

_______________________________

6. Lesion to the right dorsal columns at ~ T10.
Description of deficits
_______________________________

7. Lesion of the right medial lemniscus in the midbrain.
Description of deficits 7. 8.
_______________________________

_______________________________

8. Lesion to the entire right postcentral gyrus.
Description of deficits
_______________________________

9 10
9. Lesion to the right cuneate nucleus.
Description of deficits
_______________________________

_______________________________

10. Lesion to the right anterolateral white matter at ~ T10.
Description of deficits
_______________________________

_______________________________

11. Damage to the right dorsal roots at ~ C5 to T1.
Description of deficits 11 12
_______________________________

_______________________________

12. Damage to the right dorsal roots at ~ L2 to S2.
Description of deficits
_______________________________

_______________________________

13. Damage to the right thalamus.
Description of deficits
_______________________________
13 14
_______________________________

14. Damage to the anterolateral system as it courses through
the brainstem on the right side.
Description of deficits
_______________________________

_______________________________

1-11 Neuroanatomy session 4 Optic Pathways.doc

Exercise 3: The right-hand panel indicates the normal response and three patient
responses to the command, “Look to the right.” The normal response is labeled “N.”
Using numbers 1-3, label the pathway diagram with the location of the corresponding
lesion site.
Right Left
Right Left

Lateral Lateral
Rectus
Medial
Rectus Response when patient is
Rectus requested to look to the right

Right Left

N
Oculomotor
Nucleus (III)

Abducens 1
Nerve (VI) MLF

2
Abducens
Nucleus
(VI)

3
PPRF
Input from
Frontal Eye Fields
Ventral view (Cerebral Cortex)

Clinical Case: During the class session a case will be presented with symptoms relevant
to the pathways discussed. Students will be prompted to work together in small groups to
use their new-found knowledge to address questions related to the case study. Answers
to these questions will NOT be posted elsewhere.
Anatomy Related Study Questions:
1. Optic fibers serving which regions of the retina cross at the optic chiasm?

2. Axons from which retinal cells form the optic nerve?

3. Transection of the optic chiasm précisely on midline would result in
chromatolysis of which cells? Be specific, please.

4. Input to the cuneus on the right represents what portion of the visual field?

5. The pretectal area receives synaptic input from which cells of the retina?

6. The neurotransmitter released by Edinger-Westphal axonal synapses on ciliary
ganglion neurons is?

7. The neurotransmitter released by ciliary ganglion neurons at synapses on
sphincter muscles of the iris is?

8. The parapontine reticular formation (PPRF) receives synaptic input from what
region of the cortex?

9. The vestibular input to the abducens is the sensory limb of which reflex?

Clinically Related Study Questions:
1. Scotomas affecting the visual fields in one eye, only, indicate a lesion in the
visual pathway ____________(rostral to/at/caudal to) the optic chiasm.

2. Scotomas affecting heterologous (different) visual fields in both eyes indicate a
lesion in the visual pathway ___________ (rostral to/at/caudal to) the optic
chiasm.

3. Scotomas affecting homologous (same) visual fields in both eyes indicate a lesion
in the visual pathways ___________(rostral to/at/caudal to) the optic chiasm.

4. A lesion of one side of the cervical spinal cord can result in a constricted pupil
and a drooping eyelid on that same side. Explain.

5. Why does a lesion of the N III result in a dilated pupil and a drooping eyelid?

6. Shine a light in a patient’s right eye and the left pupil constricts, but the right
pupil does not. Where is the lesion?

7. Which blood vessel supplies the left primary visual cortex? What type of
scotoma would occur if an occlusion occurred in this vessel?

1-11 The Visual Pathway.doc
Questions for Study or Review:

1. What is a receptive field? What sorts of information are represented in
receptive fields in the visual system?

A receptive field reflects the relationship between a distinct region of sensory space (in

this case the entire visual field), and the response properties of individual neurons in the

visual pathway from the retina to the cortex. For vision, the first relationship that is

represented by receptive fields is topography. Each cell in the visual pathway responds

maximally (either by increasing or decreasing the number of action potential responses

per unit time) to light in a particular small subregion of the visual field—this is called the

spatial receptive field for any visual system cell. Other aspects of vision that are

represented within the spatial receptive field are luminance, contrast, wavelength,

contour, and motion.

2. In what cells in the visual pathway is center/surround organization of
receptive fields first detected?What is the difference between and “on”
and “off” center/surround receptive field? How does that difference
reflect retinal circuitry?

The center/surround organization of a receptive field is seen first in retinal ganglion

cells. In an “On” center receptive field, the maximal response in a visual system neuron

is generated by a circular spot of light where the center is more brightly illuminated than

the flanking “donut”. In an “Off” center receptive field, the maximal response is

generated by the opposite relationship of “hole and donut”: the center is comparatively

dimly illuminated, while the flanking annulus (a fancier word for “donut”) is brighter.

On and Off center receptive fields are generated using different types of retinal bipolar

interneurons that either respond to photoreceptors with an excitatory (for generating
either the “on” center or the more brightly illuminated surround in and “off” center

cell), or inhibitory (the “off” center, or the “on” surround) response that is transmitted

to retinal ganglion cells.

3. What types of information remain segregated in the dLGN? How is this
segregation reflected in V1?

Inputs to the dLGN are segregated by eye of origin, by receptive field size (the “M” and

“P” streams), by “on” versus “off” center receptive fields, and by topography (in each

lamina, there is a continuous map of the visual field). Thus, all of the information about

distinct aspects of the visual scene (topography, depth/ocularity, contrast, form, motion)

is maintained in separate streams, and not further processed in the dLGN.

4. What is an ocular dominance column? An orientation column? How does
the organization of these two classes of cortical columns insure that each
point in visual space is analyzed for all aspects of visual information?

An ocular dominance column is the radial array of cells in V1 (the primary visual cortex)

that are maximally or preferentially excited by light illuminating the spatial receptive

fields of cells in one eye or the other. Eye segregation is completely maintained in layer 4

of the cortex, which provides anatomical definition for the ocular dominance columns. In

layers 2/3 and 5/6, there is a range of ocular dominance that varies from one eye-driven

cells to truly binocular cells. An orientation column is a radial array of cortical neurons

(from layer 2/3 through layer 5/6) in which all of the cells respond maximally to a

light/dark edge oriented at a particular angle. Remember that because of the direct input

from the dLGN to layer 4, cells in layer 4 do not have orientation selectivity. Thus,
orientation selectivity is generated by the connections between layer 4 cells and layer 2/3

or 5/6 cells. Ocular dominance and orientation columns guarantee that information from

all points of space, seen by both eyes, and all possible contours that might be seen at

those points, will be analyzed by a contigouous array of cells in the primary visual

cortex.

5. What areas of the parietal lobe are specialized for the representation of
motion in the visual field? What areas of the temporal lobe are specialized
for the representation of form or color? How does the specific nature of
visual information relayed to the parietal versus temporal lobe match the
general functional identity of these two cortical regions?

Area “MT” in the parietal lobe is specialized for representing motion, as well as other

parietal visual association cortices. Area “V4” in the temporal lobe is specialized for

color and form, and other temporal cortical areas have cells that respond to particular

classes of visual stimuli whose form is key for their identification. This makes sense

because the parietal lobe is concerned with attention mechanisms (thus, having cells that

can detect moving objects in the visual field—like predators or moving cars as you cross

the street—is good to alert the organism to watch out for specific stimuli that might have

an impact on well-being. Similarly, the temporal lobe is specialized for identification

generally (including for language). Thus, it makes sense that visual form information,

which is key for identification, should be represented in the temporal lobe.

1-12 Auditory System Cochlear Function and Hearing.doc

Study Questions:
1. Presbyacusis is the loss of high frequency hearing in older people.
Which part of the basilar membrane is affected?
2. If half of the basilar membrane is affected, to what frequency level would this
reduce the upper limits of hearing?

3. Would the person suffering from presbycusis tend to confuse the words "cat"
and "bat" or "cat" and "cut"?

4. If you have killed some of your hair cells by chronically playing your iPod at
high intensity, will new hair cells grow back?

5. Can an eighth nerve fiber whose critical frequency is at concert A (440 Hz)
"hear" a neighboring note like A-flat (396 Hz)? Explain.

6. What two precise properties must a sound have in order to excite a specific
cell of the medial superior olivary complex?

7. The ability to distinguish the words "brat" and "brought" rely primarily on:
a. which portion of the basilar membrane?
b. what structure(s) in the brainstem?
c. what other auditory structures in the CNS?

(Answers)
1) Higher frequencies are encoded in the basal portion of the basilar membrane
and higher frequencies are lost first in presbyacusis.

2) Losing the basal half of the cochlea would lead to loss of frequencies over
roughly 1000 Hz. Although a healthy young person can hear from 20-20,0000
Hz, frequency is mapped logarithmically along the basilar membrane.

3) People with presbyacusis would confuse "cat" and "bat" because consonants
consist primarily of high frequencies while vowels consist primarily of low
frequencies.

4) No. Like most neurons, once hair cells die, they are gone forever.

5) Yes. This is like the question "can a green cone see red light?" The 8th nerve
fiber's tuning curve shows us that it hears A-flat, just not as well. That is, A-flat
has to be played louder than A to elicit firing in this fiber.

6) A specific frequency and a specific delay in the arrival time between the two
ears.

7) a. apical b. dorsal cochlear nucleus, inferior colliculus
c. medial geniculate, auditory cortex
1-12 The Vestibular System and Mechanotransduction by Hair Cells.ppt

Study Questions:
1) How do hair cells compare to photoreceptors with respect to transduction
speed. Give an approximate time range over which each cell type responds to its
stimulus--seconds, milliseconds, microseconds?
2) Aminoglycoside drugs such as streptomycin can damage hair cells by
entering the transduction channels. Where are these channels located?
3) The very loud noise at a basketball game or band concert can leave one
temporarily deaf to very quiet sounds. This phenomenon is called the “temporary
threshold shift.” What is thought to be the cellular basis of this temporary
damage to the hearing?
4) The transduction channels in a hair cell have a rather large opening that will
let most cations pass through. Which ions do normally pass through the
channels, and why?

(Answers)
1) Hair cells can respond in less than 10 microseconds. Photoreceptors are
several orders of magnitude slower, sometimes requiring up to a tenth of a
second.
2) The transduction channels are located near the tips of the stereocilia.
3) It is thought that loud noises cause such large movements of the hair bundles
that tip links between stereocilia break, thus leading to temporary threshold shift.
Tip links in this situation can reform, and do so with a time course similar to the
recovery of normal hearing.
4) It is primarily K+, and, to a smaller degree, Ca++ ions that enter because they
are the predominant cations in endolymph.