Bio42

Midterm 2 Exam

Feb 23, 2015

Name:________________________________________________

Student ID Number:_____________________________________

Student email:__________________________________________

Section TA Name:_______________________________________

Section Day & Time:_____________________________________

DO NOT OPEN YOUR EXAM UNTIL YOU ARE TOLD TO DO SO!

You have 2 hours to complete this exam.

This is a CLOSED BOOK exam: you may NOT use any material other than that contained in this

exam paper.

You can write this exam in ink or pencil. You CAN ask for a re-grade on an exam written in

pencil. Exams will be photocopied at random right after grading is completed.

Make sure you follow the directions given. If you are asked to circle the correct response, you

must do so to receive credit.

Please make sure that your answers are brief, specific, and limited to the lines provided. If

incorrect information is included in your answer, you can lose points even if the correct

information is also there. Answers outside of boxes or lines will NOT be read.

All cell phones and electronic devices apart from calculators must be switched off: No text

messaging!

At the conclusion of this exam, please sign the honor code statement on the last page.

TOTAL FOR THIS EXAM= 100 points.

Point allocation (sorry, for graders only!)

Q 1. ___________/3

Q 2. ___________/6

Q 3.___________/12

Q 4. ___________/7

Q 5. ___________ /8

Q 6. ___________/5

Q 7. ___________ /14

Q 8. ___________ /4

Q 9. ___________/6

Q 10. __________/8

Q 11. __________/3

Q 12. __________/4

Q 13. __________/4

Q 14. __________/10

Q 15. __________/6

Total __________/100

Question 1 (3 points)
Lisa tries to determine cell fate of cells from various parts of the blastula of the frog.

a) (1 pt) At the end of gastrulation, what tissue layer will form from cells that originated from the top of the
animal pole of the blastula? ___________________________________________

b) (1 pt) At the end of gastrulation, what tissue layer will form from cells that originated from the bottom of the
vegetal pole of the blastula? ___________________________________________

c) (1 pt) Cells in which area of the blastula will eventually differentiate into blood cells? Be specific.
___________________________________________________________________________________

Question 2 (6 points)
We studied two cloning experiments in class: the creation of a frog from an intestinal nucleus (in the 1960s)
and the creation of Dolly the sheep (in the 1990s).

a) (2 pts) What is the name of the common technique/procedure used in both experiments? Briefly describe the
technique. Be sure to mention the important features of the cell types and components used in both experiments.
__________________________________________________________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________

b) (2 pts) What is totipotency? _________________________________________________________________

c) (2 pts) What fundamental principles in developmental biology do these cloning experiments tell us about the
somatic cell nucleus? _______________________________________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________

Question 3 (12 points)

Even-skipped (eve) is a pair-rule gene required for early segmentation in
Drosophila. It is expressed in a pattern of seven stripes across the embryo.
Expression of even-skipped in stripes 2, 3, and 7 can be seen in the sketch of
the normal embryo to the right. Anterior Posterior

In normal embryos, the even skipped promoter has binding sites for hunchback, bicoid, giant, and
krppel. Expression of even-skipped in stripe 2 is due to activation by hunchback and bicoid and repression by
giant and krppel. The expression pattern of these proteins with regard to the AP axis can be seen in the
diagram below.
expression levels

anterior
posterior


You generate 3 Drosophila mutants. In each mutant, the binding sites for one of the transcription factors has
been deleted from the even-skipped promoter region as follows:

Mutant 1: Binding sites for Giant have been eliminated Even-skipped expression pattern

Mutant 2: Binding sites for Krppel have been eliminated

Mutant 3: Binding sites for Bicoid have been eliminated

A. WT/Normal

a) (6 pts) Based on the rule we discussed in class for stripe 2, what

B. Mutant ________
will happen to expression of even-skipped in each of the three

mutants? Match each mutant (1-3) with the expected protein

C. Mutant ________
expression pattern in the diagram on the right by writing the correct

mutant number in each blank in the diagram.

D. Mutant ________

b) (4 pt) The above experiments suggest that even-skipped expression is not simply due to the presence of the 2
activators and absence of the 2 repressors. Propose ONE plausible hypothesis as to why there is no expression
of even-skipped in the far-most anterior pole of the mutant in D of the previous figure.
__________________________________________________________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________

d) (2 pts) Besides even-skipped itself, the expression of what other broad category of developmental genes will
be affected in these three mutants?

i) Name one such category of genes. ____________________________________________________________

ii) Explain why this category of genes will be affected: _____________________________________________

__________________________________________________________________________________________
__________________________________________________________________________________________

Question 4. Innate vs. adaptive immunity (7 points)

For each of the following, indicate whether it is a property of innate immune responses, adaptive immune
responses, both innate and adaptive responses, or neither. (Circle the ONE correct answer)

a) Responds to all types of pathogens (i.e., viruses, bacteria, parasites, and fungi).

Innate Adaptive Both Neither

b) Activates cellular responses by binding to receptors expressed on some types of leukocytes.

Innate Adaptive Both Neither

c) Can respond to anything foreign that enters the body.

Innate Adaptive Both Neither

d) Clonal selection by antigen.

Innate Adaptive Both Neither

5


e) Provides protective responses during the first few days after the initial infection with a pathogen.

Innate Adaptive Both Neither

f) Phagocytosis is an important effector mechanism.

Innate Adaptive Both Neither

g) Can be harmful if not adequately and appropriately regulated.

Innate Adaptive Both Neither

Question 5. Immunoglobulin deficiencies (8 points)

Much has been learned about mechanisms of immune responses from inherited immunodeficiencies (i.e., those
resulting from genetic mutations) in humans and animals. Answer the following questions about selective
immunoglobulin immunodeficiencies (i.e., deficiencies in production of specific classes of immunoglobulins).

a) (4 pts) IgA deficiency

i) What component of immune responses would be deficient in people deficient in producing IgA antibodies?
__________________________________________________________________________________________

ii) Give one example of a tissue that would have decreased protection against pathogens:
__________________________________________________________________________________________

iii) Briefly describe how IgA is uniquely able to function at this site:
__________________________________________________________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________

b) (2 pts) IgG deficiency

i) What is one form of immunological protection that would be defective in people unable to produce IgG
antibodies? ________________________________________________________________________________
__________________________________________________________________________________________

ii) Briefly describe how IgG uniquely functions in this role: __________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________

c) (2 pts) IgE deficiency

i) Name a class of harmful antigens to which people deficient in IgE antibodies would be particularly
susceptible: _____________________________________________________________________________

ii) Based on what you know about IgE functions, briefly propose a mechanism by which IgE might mediate this
protection: _____________________________________________________________________________
_______________________________________________________________________________________
_______________________________________________________________________________________

Question 6. Antibodies vs. T-cell receptors (5 points)

a) (3 pts) List three (3) ways in which antibodies and T-cell receptors, two key elements of adaptive immune
responses, are similar in their genetics, structure and/or function (notes: one similarity should be related to
antigen recognition. Answers such as both are on the cell surface, both bind antigen, both are diverse,
both are specific, etc. are not sufficiently detailed).

1) ________________________________________________________________________________________
________________________________________________________________________________________

2) ________________________________________________________________________________________
________________________________________________________________________________________

3) ________________________________________________________________________________________
________________________________________________________________________________________

b) (2 pts) List two (2) ways in which these proteins are different in their genetics, structure, and/or function.
(note: one difference should be related to antigen recognition).

1) ________________________________________________________________________________________
________________________________________________________________________________________

2) ________________________________________________________________________________________
________________________________________________________________________________________

Question 7. Protective responses to Mobola virus (14 points)

A new respiratory virus, Mobola virus, has infected your colony of inbred (i.e., genetically-identical) BLAB
mice, killing about half of the mice. While all mice get sick from the virus, half recover. You want to
determine how half of the mice are able to defeat the virus infection, i.e., what type of immune response they
generate that eventually allows them to eliminate the virus. You hypothesize that the surviving mice may have
been able to generate antibodies, helper T cells, and/or cytotoxic T cells (CTL) that enabled them to eliminate or
control the viral infection.

a) (2 pts each; 6 pts total) For each of the following components of immune responses, briefly describe an
experiment you could do (with BLAB mice that had not previously been exposed to Mobola virus plus BLAB
mice that had recovered from infection, and using the kinds of techniques covered in class), that would test the
hypothesis that this component contributes to protection against the virus, that enables the mice to recover.

i) Antibodies:______________________________________________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________

ii) Helper T cells: __________________________________________________________________________

__________________________________________________________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________

iii) Cytotoxic T cells: ________________________________________________________________________

__________________________________________________________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________

b) (6 pts) True/False. The following statements describe possible steps leading to the generation of anti-
Mobola virus antibodies in mice that recover from the infection. Indicate whether a statement is true or false by
circling True or False. Note: Evaluate each statement independently. The statements do not have to be in
correct order relative to each other. Also, the generation of memory cells is occurring along with plasma cells,
but memory cells are not mentioned to simplify the statements.

i) Virus binds to the B-cell receptor on nave B cells in lymph nodes and activates them to proliferate and
differentiate into antibody-secreting plasma cells making anti-Mobola antibodies.

True False

ii) Effector TH cells recognize viral peptide:MHC class II complexes on B cells and stimulate them to proliferate
and differentiate into antibody-secreting plasma cells making anti-Mobola antibodies.

True False

iii) B cells in the lungs bind Mobola virus and carry it through lymphatic vessels to draining lymph nodes, where
the B cells become activated by the virus and by TH cells to differentiate into plasma cells making anti-Mobola
virus antibodies.

True False

iv) In lymph nodes, nave TH cells recognize viral peptides bound to MHC class I proteins on macrophages or
dendritic cells and are activated to proliferate and differentiate into effector TH cells that can help activate B
cells.

True False

10


v) Virus binding to the B-cell receptor on nave B cells in lymph nodes partially activates them, and triggers
receptor-mediated endocytosis, viral degradation in endosomes/lysosomes, and the loading of viral peptides on
MHC class II proteins.

True False

vi) Free Mobola virus particles and virus carried by dendritic cells travel through lymphatic vessels to lymph
nodes where Mobola virus can be internalized and degraded by macrophages and dendritic cells into peptides
that bind to MHC class II proteins and activate nave TH cells.

True False

c) (2 pts) Boris, a freshman who has not taken Bio42, asks the fundamental question of how antibodies help to
rid the mice of Mobola virus infection. For simplicity, you decide to describe just the mechanism of protection
that can be mediated by antibodies of any heavy chain class. What is that mechanism and how does it work to
end the viral infection?
__________________________________________________________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________

11


Question 8 (4 points)
You are studying LTP in the hippocampus of a rat. For each of the following, circle whether the action would
increase the strength of LTP, decrease LTP, or have no effect. (1 pt. each, 4 pts total)

a) You overexpress the gene for nitric oxide synthase in the hippocampus.

Increase Decrease No effect

b) You overexpress a protease inhibitor that is specific to dendritic spines in the hippocampus.

Increase Decrease No effect

c) The rat has just eaten a large meal resulting in high concentrations of neuronal ATP.

Increase Decrease No effect

d) The rat has just drunk alcohol.

Increase Decrease No effect

12


Question 9 (6 points)

Experiment 1

Stimulate Record membrane

voltage

Presynaptic terminal Post Synaptic dendritic spine

The diagram above shows a synapse in a region of the brain where LTP could occur. When the presynaptic
terminal is stimulated, it releases a LOT of glutamate into the synapse. However, even with repeated stimulation
of the presynaptic terminal over a long period of time, you see no change in membrane voltage in the post-
synaptic spine (Experiment 1 above).

Next you stimulate the presynaptic terminal repeatedly as before, but at the same time, you also electrically
stimulate the post-synaptic spine directly (see Experiment 2 below).

Experiment 2

Stimulate Stimulate

Presynaptic terminal Post Synaptic dendritic spine

Several days after Experiment 2, you stimulate just the presynaptic terminal, without stimulating the post-
synaptic spine. This time, you see significant post-synaptic membrane depolarization.

a) (2 pts) What relevant type of receptors were already present on the post synaptic spine prior to Experiment 2?
______________________________________________________________
b) (2 pts) What were the immediate consequences of electrical stimulation of the post-synaptic spine in
experiment 2?
__________________________________________________________________________________________
__________________________________________________________________________________________
13


c) (2 pts) In experiment 1, repeated stimulation of the presynaptic neuron did not result in any post-synaptic
membrane depolarization. After experiment 2, what is the ONE most important long-term change that has
occurred in the post-synaptic neuron, which allows presynaptic neuronal stimulation to trigger post-synaptic
membrane depolarization? Explain briefly. _______________________________________________________
__________________________________________________________________________________________
__________________________________________________________________________________________

Question 10 (8 points)
(2 pts) Part 1. Theres no free lunch part 1.
Numerous neurotransmitter biosynthetic pathways are efficient in that two different neurotransmitters are made
from the same precursor. Which downside of this efficiency was discussed in class? Circle the ONE BEST
choice.
A. Loss of function mutations in the rate-limiting enzyme impairs the synthesis of two
neurotransmitters.
B. Hallucinogens (i.e., drugs that can mimic the action of a neurotransmitter because of their close
structural resemblance) are particularly potent, because they can mimic two neurotransmitters.
C. If there is an excess of precursor, there will be shortages of both neurotransmitters.
D. The receptors for the two neurotransmitters have to be particularly sensitive, in order to
distinguish between the neurotransmitters which, despite being structurally similar, are not
necessarily functionally similar.

(2 pts) Part 2. Theres no free lunch part 2.

A particular neurological disease involves a shortage of Neurotransmitter-A (NT-A), due to a lesion in a
particular brain region. Thus, you treat people with this disease with a drug that activates the receptor for
NT-A. What is the most common downside of this treatment? Circle the ONE BEST choice.
A. By temporarily increasing signaling via the receptor for NT-A, you ultimately trigger long-term
potentiation, making disease symptoms worse.
B. There will be side effects, due to the fact that the drug also activates receptors for other
neurotransmitters.
C. There will be side effects, due to the fact that you will have boosted signaling via the NT-A
receptor into abnormally high levels in other brain regions.
D. The increased NT-A receptor signaling will cause the post-synaptic neuron to fire so much as to
deplete the neuron of energy, killing it.

14


(2 pts) Part 3. The dangers of too much of a good thing.

The release of the neurotransmitter glutamate is central to LTP. If glutamate levels get too high,
however: (Circle the ONE BEST choice)
A. There is down-regulation of all classes of glutamate receptors (i.e., a decrease in their
numbers), so that subsequent LTP is blocked.
B. There is non-specificity to memory formation (i.e., function is impaired because everything, in
effect, is remembered indiscriminately).
C. Neurons are killed due to excitotoxicity.
D. There is inhibition of neurogenesis (i.e., the birth of new neurons), in adults.

(2 pts) Part 4. Nothing is ever quite perfect.

No pump or channel is 100% efficient. This helps account for which of the following? Circle ALL that apply:
A. The fact that the Nernst equation does not perfectly predict the resting potential.
B. The fact that the side effects of treating individuals with Parkinsons Disease include symptoms
related to schizophrenia, and that the side effects of treating individuals with schizophrenia
include symptoms related to Parkinsons Disease.
C. The existence of spontaneous action potentials in the absence of presynaptic input.
D. The inconsistency of the threshold of the axon hillock.

Question 11 (3 points)
The nervous system evolved to maximize contrasts. That helps explain which of the following? Circle ALL
that apply:
A. In the absence of excitation, theres charge separation across the neuronal membrane.
B. The resting potential evolved to be negatively, rather than positively charged.
C. That chloride channels open at the peak of the action potential.
D. That potassium channels open at the trough of the refractory period.
E. Spatial sharpening of neuronal signaling, brought about by neurons sending inhibitory
collatoral projections back onto themselves.
F. Temporal sharpening of neuronal signaling, brought about by lateral inhibition of parallel
circuits.

15


Question 12 (4 points)
(2 pts) Part 1.
The activation of the visual cortex in blind individuals when they read Braille is due to: (Circle the ONE BEST
choice)
A. Birth of new neurons in the (adult) visual cortex.
B. The fact that, as Braille is learned, synapses connecting tactile neurons in fingertips with
neurons in the visual cortex undergo LTP.
C. The fact that, as Braille is learned, tactile neurons in fingertips remap to include the visual
cortex as targets for their projections.
D. The migration of retinal photoreceptors to fingertips.

(2 pts) Part 2.

A
B

Above is a diagram of a three neuron circuit in which Neuron A sends an excitatory projection onto Neuron B,
and Neuron C sends an inhibitory GABA-ergic axo-axonic projection onto Neuron A. Thanks to a mutation,
when GABA binds to its receptor in this circuit, sodium channels open. As a result: (Circle the ONE BEST
choice)

A. Neuron A can never cause depolarization in Neuron B.

B. Neuron C is potentially able to promote LTP between Neurons A and B.
C. Neuron C negatively modulates the excitability of Neuron B.
D. Neuron A is able to alter the excitability of Neuron C through retrograde signaling.

16


Question 13 (4 points)
For each statement below, assume that apart from the defect mentioned, all other aspects of neuronal function
are normal.

(2 pts) Part 1. In a neuron, which of the following will increase the contrast between the excited state and the
silent state? Circle ALL that apply:
A. Maximum permeability to potassium occured at +50 mV instead of +30mV.
B. The first voltage-gated sodium channels in the axon hillock opened at 65 mV instead of 40
mV.
C. Potassium channels closed at 80 mV instead of 90 mV.
D. The resting potential was 80 mV instead of 70 mV.

(2 pts) Part 2. In a neural circuit, which of the following will increase the contrast between the excited state
and the silent state? Circle ALL that apply:
A. Decreasing the amount of neurotransmitter released by inhibitory collaterals that mediate self
inhibition of neurons.
B. Increasing the amount of neurotransmitter released by inhibitory collaterals that mediate lateral
inhibition.
C. Flattening dendritic spines in neurons throughout the circuit.
D. Allowing each neuron in the circuit to form synapses with every other neuron in the circuit.

17


Question 14 (10 points)

Below is the sharp pain/dull pain circuitry diagram discussed in class. Refer to the diagram to answer the
questions below.

1 Pain traveling up spine
2

For each of the following i-v, write the one correct consequence from the list of possible consequences A-E
below. Note: Each letter choice (A-E) should be used once.

i) ______ A drug is administered which blocks the reuptake of the neurotransmitter released by
Neuron 1.
ii) ______C fiber activation causes excitation, rather than inhibition of Neuron 1.
iii) ______C fibers became myelinated.
iv) ______A fibers became unmyelinated.
v) ______The axon of Neuron 2 has sprouted collaterals that axo-axonically inhibit A fibers
projecting onto Neurons 1 and 2. Neuron 2 continues to signal up the spine as usual.

List of possible consequences:

A. A sharp pain is followed by an even longer period of no pain afterward than usual.
B. There would be a longer latency period until you experience sharp pain.
C. Stimulating A fibers no longer transiently blocked throbbing pain.
D. There would be a shorter latency period until you experience dull pain.
E. What would typically be a dull, throbbing pain is experienced as sharp pain.

18


Question 15 (6 points)
Consider the following neurotransmitter/receptor/ion channel relations:
Receptor A is coupled to a sodium channel.
Receptor B is coupled to a chloride channel.

Neurotransmitter 1 has a high binding affinity for Receptor A and a weak binding affinity for Receptor B.
Neurotransmitter 2 has a high binding affinity to Receptor B and does not bind Receptor A at all.

In all cases, once the neurotransmitter binds the receptor, the channel will open.

You now begin to look at the effect of each neurotransmitter on neurons expressing one or both types of
receptors on their surface to see how excitable the neuron is (i.e., how likely the neuron is to have an action
potential). See table below.

INSTRUCTIONS: Based on the neuronal receptors that are on the surface, circle how the neuron will respond
to each neurotransmitter applied to the synapse. NOTE: For each cell in the table, circle ONE response.

Receptor type on Neurotransmitter Applied

dendritic surface
1 only 2 only

A alone Highly Excited Highly Excited

Highly Inhibited Highly Inhibited
No Effect No Effect

B alone Highly Excited Highly Excited

Weakly Excited Weakly Excited
Highly Inhibited Highly Inhibited
Weakly Inhibited Weakly Inhibited
No Effect No Effect

A and B Highly Excited Highly Excited

Weakly Excited Weakly Excited
Highly Inhibited Highly Inhibited
Weakly Inhibited Weakly Inhibited
No Effect No Effect

19


Honor Code Statement:
I have followed the Stanford Honor Code while taking this exam.

Signature:_____________________________________

20


Developmental Biology Term List:

The Cycle of Life Sperm and Egg
Fertilization Sperm
Cleavage Acrosomal Vesicle
Gastrulation Midpiece
Neurulation Flagellum
Organogenesis Egg
Gametogenesis Zona Pellucida
Ovum
Spermatogenesis & Oogenesis Gastrulation
Spermatogenesis Ectoderm
Germ Cell Mesoderm
Spermatogonium Endoderm
Primary Spermatocyte Blastopore lip
Secondary Spermatocyte Animal hemisphere
Spermatids Vegetal hemisphere
Mature Sperm Marginal zone
Oogenesis
Germ cell
Oogonium
Primary Oocyte
Secondary Oocyte
Mature Egg
Neurulation Types of Stem Cells
Neural plate Totipotent
Notochord Pluripotent
Neural fold Multipotent
Nervous system Unipotent
Embryonic Stem (ES) Cells
Adult Stem Cells
Induced Pluripotent Stem (iPS) Cells
Regulatory Hierarchy in Fly Embryos Brain Wiring
Egg-polarity Genes Functional Selection of Exuberant
Bicoid Connections
Nanos Predetermination
GAP genes Retinal Ganglian Cell (RGC)
Hunchback Optical Nerve
Kruppel Retina
Pair-rule Genes Tectum
eve EphA3
Segment Polarity Genes Ephrin-A5
Wingless Nasal (anterior)
Hedgehog/Sonic Hedgehog Temporal (posterior)
Homeotic Selector (HOX) Genes

21


Immunology Term List:

Cells and tissues of the immune system Innate Immunity
Blood cells and hematopoiesis: Phagocytosis
Hematopoietic stem cells Pathogen-Associated Molecular Patterns
Myeloid progenitor cell (PAMPs)
Leukocytes Pattern Recognition Receptors (PRRs)
Granulocytes Toll-like Receptors (TLRs)
Phagocytic cells NF-B
Lymphoid progenitor cell Inflammation
B lymphocytes
T lymphocytes

Lymphoid tissues:
Bone Marrow
Thymus
Spleen
Lymph Nodes & lymphatic vessels
Mucosal Tissues

Adaptive Immunity T cells
B lymphocytes T cell receptor
Plasma cells MHC class I and class II proteins
Primary and Secondary Immune Response Antigen processing and presentation
Neutralization CD4 and CD8 proteins
Enhancement of phagocytosis Activation Phase
Complement activation Effector Phase
Poly Ig receptor Effector Cells
Clonal selection by antigen Memory Cells
Cytotoxic T lymphocytes (TC, CTL)
Perforin
Helper T lymphocytes (TH)
Cytokines
Antibodies/Immunoglobulins/B cell AIDS (not responsible for material not
receptors covered)
Light Chains: and ; V, C regions HIV
Heavy Chains: (IgG), (IgM), (IgA), Retrovirus
(IgD), and (IgE); Constant region CD4
domains CH1, CH2, CH3
Hypervariable regions/complementarity-
determining regions (CDRs)
Fab and Fc
Hinge region
V, D, and J gene segments
Gene rearrangement
Membrane immunoglobulin/B cell receptor
Heavy chain class switching

22


Neurobiology Term List:

Nervous System and Neuronal Anatomy Ion Channels, membrane potentials,
electrical flow of information
VNS (Voluntary Nervous System) Receptor-Gated Ion Channel
ANS (Autonomic Nervous System) Voltage-Gated Ion Channels
SNS (Sympathetic Nervous System) Resting Membrane Potential
PNS (Parasympathetic Nervous System) Nernst Equation
Hypothalamus Goldman Equation
Cortex Saltatory conduction
Limbic System Depolarization, Hyperpolarization,
Anterior Pituitary Repolarization
Posterior Pituitary Refractory period
Neuron Resting Potential
Soma Action Potential
Dendrite Temporal summation
Axon Hillock Spatial summation
Axon Delayed rectification
Myelin Sheath
Nodes of Ranvier
Synapse

Neural Networks LTP (Long Term Potentiation)
Lateral geniculate NMDA receptors
Stellate cells Non-NMDA receptors
Fast Pain Fiber Calcium
Slow Pain Fiber Magnesium
Temporal sharpening Sodium
Spatial sharpening Nitric Oxide
Lateral Inhibition Carbon Monoxide
Collateral Arachidonic Acid
Feedforward Inhibition Ethanol
Interneuron Adenosine
Axo-axonic communication ATP
Intestinal peristalsis
Contrast enhancement
Center/surround
Neurotransmitters and hormones
Glutamate
GABA
Dopamine
L-DOPA
Acetylcholine
Serotonin
Norepinephrin
Ephinephrin

23


Neurotransmitters and hormones (Cont.)

Serotonin
Melatonin
Adrenaline
Glucocorticoids
Estrogen
Progestins
Androgens
Mineralocorticoids
Atrial natriuritic factor
Steroid hormones
Peptide hormones
ATP
Nitric Oxide
Carbon Monoxide

24