LEVELS OF ORGANIZATION



INTRO TO PHYSIOLOGY, TISSUES, MEMBRANES

READING: p. 2-23; 61-68; 72-85

Physiology is the study of the functions of the body. It is a very logical science that employs a few basic mechanisms to explain and predict what will happen in an organism. What will happen to heart rate just before the onset of exercise? Will it return to resting levels immediately after exercise stops? These are all typical questions a physiologist would pose. Finding the answer to them highlights the other characteristic of physiology: it is a mechanistic science. Physiologists ask “how” something occurs, and try to explain the mechanism behind various events. For example, How does drinking alcohol increase urinary output? How does muscle get bigger when it’s put under mechanical stress (i.e. weightlifting)?

In this course, you will learn the basic “rules” that govern the functions of the body, so that you will be able to explain and predict what the body will do in different situations. You may even be able to enlighten your friends as to what’s really happening to them when they exercise, or feel faint, or startle. In fact, the more fun you can have with this material, the better. Because you will be learning about yourself and the way your body functions, the more personal you can make the information, the more you will enjoy it. So observe the way your body responds when you run or eat or hold your breath and try to figure out what’s going on. Two favorite questions can help to guide your logic:

“Does this make sense?” “Would the body ‘want’ to do this?”

BIO 131 is called “Systemic Physiology”, which is a subdivision of physiology that studies how the organ systems of the body are integrated to sustain life. They communicate and cooperate with each other in a myriad of ways, and have one goal in common: the maintenance of homeostasis, a relatively stable internal environment for the cells. (Think about why this might be important functionally).

“Systemic” also means that we will be touring the body one organ system at a time, and integrating as we go along. To begin this process, you first need to learn about the basic building blocks of the body: the cells and how they organize into tissues. From there we will enter the nervous system, and then we are on our way. Please keep in mind that every step of the process is important, and that most of the concepts learned in these early chapters will be seen again and again – they really are crucial to your later understanding, so learn them!!

The following questions are designed to “guide” you through the reading material, and you will see this type of set-up (area summary followed by questions) for each section.

The right margin is larger to allow you to practice Cornell note taking – try it!

** Also pay attention the “mapping” demo in this chapter (pg. 6-7) – we will do a lot of this! In fact, mapping will become the only real source of extra credit in the class.

LEVELS OF ORGANIZATION

1. Living organisms are comprised of many different levels of organization. In this course, we will focus on the levels from cells to organ systems. Name these levels. (p. 3)

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2. You should be able to name all of the physiological systems of the body. In the following spaces, list the appropriate organ system next to its functional description. (Fig. 1.2, p. 4)

Maintenance of water/solute levels in the body ________________

Defense against foreign invaders ________________________

Support and movement ________________________

Coordination of body function via molecules traveling through blood/body fluids ________________________

Coordination of body function via electrical signals ________________________

Transport of substances between cells/tissues _________________

Exchange of CO2 and O2 with environment __________________

3. Name three of the above systems that could be considered “communicating” systems.

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FUNCTION AND MECHANISM

4. It is very important for you to be able to distinguish between function and mechanism. Your book describes that thinking about function explains “why” something happens, whereas thinking about mechanism explains “how” something happens (p. 5). Practice: Describe how each approach would explain the formation of ATP by the mitochondria ("why" it is formed vs. "how" it is formed)

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*NOTE: On exams for this class you will almost always be asked to describe HOW something happens (i.e. the mechanism).

THEMES IN PHYSIOLOGY

5. List four key themes in physiology (p. 5, 8-9). Give one example of the importance of each in the study of physiology.

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6. Define homeostasis, using words and a level of explanation that a non-science person would be able to understand.(p. 9-10)

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7. Disease happens when homeostasis fails. Describe (with examples) internal vs. external sources of failure (p. 10)

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8. Requirements for cells (oxygen, nutrients, waste removal) are met by their immediate environment (internal environment). What is the “internal environment” cells of the body? (p. 10)

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9. Give an example of how the law of mass balance would be observed in the human body (p. 11-12)

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10. What are the two primary organs that act to clear substances from the body? (p. 12)

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11. How does clearance rate play a role in the development of therapeutic drugs by pharmaceutical companies? (p. 12)

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12. How is homeostasis different from equilibrium? (p. 13)

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13. Distinguish between local control and reflex, or “long-distance” control (p. 13-14)

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14. Why is negative feedback so important in maintaining homeostasis? (p. 15-16)

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15. When might you see a positive feedback loop? (p. 17)

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16. How do biorhythms associated with body temperature affect an individual’s function? (p. 17)

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17. Use the idea of biological rhythms to explain something that changes for you in a different environment (p. 17-18)

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THE SCIENCE OF PHYSIOLOGY

18. What is the difference between an independent and a dependent variable? (p. 19)

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19. Why should every experiment have a control?

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20. How does a scientific theory differ from a hypothesis? (p. 18)

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21. What is the advantage of having a crossover study (vs. one in which the experimental and control groups are different)?

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Although we will be conducting some minor experiments on you, human experimentation is really tricky!

22. Describe the placebo and nocebo effects. (p. 22)

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LOOK AT THE GRAPHS AND THEIR ASSOCIATED QUESTIONS ON PAGES 20-21; PLEASE ANSWER THE GRAPH QUESTIONS FOR EACH.

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BRIEF HIGHLIGHTS OF… CELLS, MEMBRANES

23. What are the three fluid compartments of the body? (p. 61)

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24. What are the two primary functions of the cell membrane? (p. 61)

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25. Membranes are composed mostly of ____________________ and ____________________________. (p. 62)

26. What is the role of cholesterol in the cell membrane? (p. 67-68) ________________________________________________

NOTE: Much of this chapter (e.g. organelle function), as well as the roles of membrane proteins, should be a review from intro biology (I assume you know it). Need more review: pgs 65-72.

TISSUES OF THE BODY

27. Name two body tissues with lots of extracellular matrix. (p. 72)

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28. What are cell adhesion molecules and why are they important?

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29. Cells are held together by cell junctions to form tissues. Give a primary function for each of these junctions. (p. 72-75) Place a star next to those you'd expect to find in skin.

Tight junctions: ______________________________________________________

Gap junctions: ______________________________________________________

Anchoring junctions (e.g. desmosomes): ______________________________________________________

30. How might anchoring junctions (or their lack) play a role in cancer? (p. 74) _____________________________________

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There are four basic tissue types: epithelial, connective, muscle, and nervous. Their characteristics are described in detail on pgs. 76-84. It is not necessary to read these pages intensively; rather, skim to get an overview.

31. List two basic functions for each of the tissue types listed.

Epithelial tissue _______________________________________________

Connective tissue _______________________________________________

Muscle tissue _______________________________________________

Nervous tissue _______________________________________________

32. Which tissue types are “excitable tissues”? What does that term mean? (p. 84)

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TISSUE REMODELING

33. When might it be useful to have apoptosis? (p. 84)

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Read the information on stem cells, but realize that this area of research is moving so rapidly that the information in this book does not reflect the current research. We have a Regenerative Medicine speakers series. More talks will come up this semester – please attend!

COMMUNICATION AROUND THE BODY

READING: p. 166-170; 180-189; 197-209; 236-250

The ways in which cells communicate with each other are highly complex and are included in an area of scientific discovery that is rapidly growing; however, they essentially boil down to two basic signal types: electrical signals (changing the MP), or chemical signals that bind to targets on cells. Local electrical signals can pass from cell to cell, and electrical signals can travel long distances as action potentials. Chemical signals (responsible for the bulk of communication) come in a wide variety of classifications, but in all cases the chemical doing the signaling is called a ligand. Ligands and include paracrines, cytokines, and hormones (among others), and obey the general rules for protein interactions – specificity, affinity, competition, and saturation (please refer to pg. 46 of the text for a review of these if needed).

It can be very confusing to sort everything out, but for this class, we will primarily cover the big ideas, as there’s another course that will cover it in detail (BIO 121).

1. Local communication between cells can be electrical (gap junctions) or chemical (contact-dependent signals, among others). How do these two differ from each other? (p. 166)

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2. How do paracrine and autocrine signals differ? (p. 167-8)

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3. Describe histamine’s role as a paracrine. (p. 168)

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It might not make the most sense now, but come back to this bit on neurotransmitters, neurohormones, & hormones soon!

4. Differentiate between the following: (p. 168)

Neurotransmitter

Neuromodulator

Neurohormone

5. How are cytokines different from hormones? (p. 168)

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6. Why do only cells of the thyroid gland respond to the hormone Thyroid Stimulating Hormone (TSH), when it’s floating around in the blood and comes in contact with all kinds of cells? (p. 169)

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7. What determines if a signal molecule binds on the outside of the cell or the inside of the cell? If it only binds on the outside, can it still cause things to change intracellularly? How? (p. 169)

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8. Describe the role of a second messenger (p. 170)

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*details of signal transduction will be left to other classes; we will skip to how those signals may be modulated, p. 180*

9. How does competition affect signaling? Give an example

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10. Differentiate between an agonist and an antagonist (p. 180)

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11. In lung tissue, the hormone epinephrine causes smooth muscle cells to relax, whereas in the blood vessels of the stomach, epinephrine causes smooth muscle to contract. How can this same chemical cause different effects in different places? (p. 180-81)

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12. If a patient had high circulating levels of Hormone X (assume this is going on for a while), would you expect that person to have a normal, down-regulated, or up-regulated number of receptors for X? Explain your reasoning. (p. 181)

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13. How is down regulation different from desensitization? (p. 181) ______________________________________________________

14. Use the portion of the Running Problem at the top of p. 182 to explain how insulin receptors differ in Type 1 and Type 2 diabetes.

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15. Once a cell has received a signal from another, how does it stop the signal pathway from continually progressing? (p. 182) _____________________________________________________

** Review homeostatic reflex pathways described on p. 182-187

16. Look carefully at the comparison of neural (electrical) and endocrine (chemical) control pathways in Table 6.2, p. 188. Given these parameters, decide if the following would be mediated by a neural pathway or an endocrine one. Then, come up with at least a few of their own examples.

You smell smoke and look for a fire

You lift weights and your muscles increase in size

If you haven’t eaten in a while, your liver releases glucose

You step on a sharp object and start hopping on the other foot

17. How is signal intensity encoded in the nervous system? What about the endocrine system? (p. 189)

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SKIP TO THE NEXT CHAPTER – THE ENDOCRINE SYSTEM

**We first introduce the Endocrine system here, but we’ll see it all semester long!

A hormone is a chemical released into the blood that acts on a distant target. It is effective in very low concentrations, and its specificity is due to the receptors on the target tissue. Chemically, hormones fall into one of three classes: peptide, steroid, or amine. They are generally distinguished according to how they are synthesized, stored, and released; how they are transported in the blood; and the mechanisms by which they cause a cellular response. Hormones can also interact with other hormones, and in doing so, alter cellular response. Three types of hormone interaction are discussed in the book: synergism, permissiveness, and antagonism.

Remember the ideas of negative feedback control systems when reading this material! While studying endocrine pathologies, really try to understand the concepts of hypersecretion, hyposecretion, up- and down-regulation, and abnormal tissue responsiveness.

18. Hormones act on their target cells by controlling…..(p. 197)

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19. What are the four classic steps for identifying an endocrine gland? (p. 198)

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20. Based on the evidence (p. 199), do you think human pheromones exist?

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21. What is meant by “the cellular mechanism of action” of a hormone? (p. 199)

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22. How can different cells have variable responsiveness to a single hormone? (p. 199)

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23. What is the half-life of a hormone? (p. 199-201)

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24. What are the three chemical classes of hormones? (Table 7-1, p. 202)

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25. Which two hormone types are transported in the blood bound to carriers? (Table 7-1)

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26. Which hormone type is synthesized on demand? What does that tell you about its response time?

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27. What do steroid and thyroid hormones have in common? (Table 7-1)

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28. MOST hormones are ________________________ (p. 201).

29. What is the function of the preprohormone? (p. 202)

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30. Are prohormones active molecules? __________ (p. 202-3)

31. What does “post-translational modification” mean? Could the inactive fragments be useful? (p. 202-3)

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32. How long does the effect of a peptide hormone last? (p. 202)

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33. Steroid hormones are derived from _____________________(p. 204)

34. Why can’t steroid hormones be stored? (p. 204)

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35. Two common hormones released during stress are cortisol (a steroid) and epinephrine (an amino acid-based hormone). Which gives you that instant “rush”? Which would you expect to be in the blood longer, and why? (p. 204)

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36. Given the cellular mechanism of action of steroid hormones (p. 204), why would it be dangerous for someone to take “extra” (exogenous) steroids?

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37. The catecholamines, all derived from the amino acid tyrosine, include ____________________________________________ (list all three, p. 206).

38. Describe how insulin is involved in a reflex pathway (Fig 7-7, p. 208)

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39. Draw a reflex pathway for parathyroid hormone in the space below (see p. 208 for the description)

40. Describe at least one way in which the nervous system can affect hormone release (p. 209)

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SKIP TO THE NEXT CHAPTER: ELECTRICAL SIGNALS

Electrical communication will be the topic of the next few sections as we cover the Nervous System. The Nervous System is specialized for rapid communication of signals throughout the body, and is composed of two primary cell types: neurons and glial cells. Neurons are responsible for producing and transmitting electrical and chemical signals to cells throughout the body, whereas glial cells are the support cells for the system. We will focus our attention on neurons, which have three basic parts: the cell body, the axon, and the dendrites.

As you have learned, electrical signaling along the neuron is due to ion movement across its membrane. Different portions of the neuron conduct electrical signals differently. The conduction of action potentials occurs only on the axon. The cell body and dendrites lack the fast Na+ channels necessary for the initiation of an action potential, and instead exhibit smaller electrical changes called graded potentials. Graded potentials are summed, and if they surpass the threshold for the membrane, an action potential is created. Action potentials cannot be summed, and are called “all or none” phenomena.

I assume you know basic neuronal anatomy!

ELECTRICAL SIGNALS IN NEURONS

1. Neurons and muscle cells are called excitable tissues because they do what? (p. 236)

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2. What two factors influence membrane potential? (p. 236)

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3. _________ is the major ion contributing to the resting membrane potential.

4. Which ion is more concentrated in the ECF: Na+ or K+ ? Which is more concentrated in the ICF?

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5. If the cell membrane is made suddenly permeable to Na+, in which direction will it move? What is causing this movement? (p. 238)

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6. When the membrane potential moves from –70 mV to +10 mV, what happens to the existing concentration differences across the membrane? (p. 238)

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7. If the cell membrane suddenly becomes more permeable to K+, what happens to the state of the membrane? Why?

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8. How do cells alter their permeability to ions? (p. 238-39)

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9. How are ion channels classified? Describe each type briefly (p. 239)

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10. What is a graded potential? (p. 240)

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11. How are action potentials different from graded potentials?

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12. Where on the neuron do graded potentials occur? Action potentials? (p. 240-41)

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What determines the magnitude of the graded potential? (p. 240)

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13. Describe two ways in which ion movement can hyperpolarize a cell.

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14. Where is the trigger zone? (p. 241) ________________________________________

15. If a graded potential reaches threshold at the trigger zone, what happens? (p. 241-42)

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16. If several graded potentials reach the trigger zone at the same time, what do you think will happen? Explain.

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17. Define an action potential. (p. 242)

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18. What does “all-or-none” mean when referring to action potentials? (p. 242)

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19. Action potentials specifically involve the movements of what two ions? In which direction are they moving? (p. 243)

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20. For each phase of the action potential listed below, indicate what is happening to ion permeability, which ions are moving, and in what direction (in or out of cell).

Rising phase:

Peak:

Falling phase:

After-hyperpolarization:

21. Name the two gates of the voltage-gated Na+ channels. (p. 245)

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22. In the resting neuron, which of these gates are closed and which are open?

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23. Depolarization opens the _____________________________ gate.

24. When do inactivation gates close? Why do they close? (p. 245)

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25. What must happen to the gates before the next action potential can take place?

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26. Define refractory period. (p. 245-46)

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27. How do the absolute & relative refractory periods differ?

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28. Why might the absolute refractory period be a “good thing”? (p. 246)

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29. Describe the role of the Na+/K+ ATPase pump in the action potential. (p. 246)

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30. What is meant by the conduction of action potentials? (p. 246)

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31. When Na+ channels in the middle of an axon open, depolarizing current flow will spread in both directions along the axon. Why then don’t action potentials ever reverse and move back toward the cell body?

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32. List two factors that affect the speed of action potential conduction. (p. 247-49)

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33. Explain saltatory conduction. (p. 249)

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34. What happens to conduction through axons that have lost their myelin? (p. 249)

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THINGS TO TRY:

1. Lidocaine inactivates voltage-gated Na+ channels on the neuronal membrane. If lidocaine is placed on the axon of a nerve that normally transmits signals from a pain receptor to the brain (to be interpreted by the brain as “pain”), the pain is not “felt” by the individual. Explain why.

2. Draw/label a neuron. Indicate on your picture exactly where graded

potentials would be generated and where action potentials would be generated

3. Drug Z prevents sodium inactivation (“h”) gates from moving from their resting position (“resting” refers to their position when the membrane is at its RMP). How would administration of Drug Z affect the function of a neuron?

SYNAPSES

READING: p. 253-

An action potential can travel down the length of the neuronal membrane and communicate the electrical information to another cell. This transmission occurs via a synapse. A synapse is a junction between a neuron and a target cell, which could be another neuron, a muscle cell, or a gland. At a synapse, the axon of the presynaptic neuron passes information to receptors on the dendrites or cell body of the postsynaptic target cell(s). Most synapses are chemical junctions, and involve the release of neurotransmitter from the presynaptic neuron onto the postsynaptic cell. Neurotransmitters are manufactured in the cell bodies of neurons (where the organelles are located) and travel down to the axon terminal where they are housed in vesicles until signaled for release. When the appropriate signal (action potential) arrives, neurotransmitter is released via exocytosis. The neurotransmitter then travels by diffusion to the postsynaptic membrane where it opens ion channels, resulting in some type of electrical potential change. Because this electrical change occurs on the dendrites or cell body, it is a graded potential. The overall postsynaptic potential change will determine whether or not an action potential will be fired.

Synaptic transmissions that bring the postsynaptic membrane closer to threshold are called excitatory postsynaptic potentials, or EPSPs. Inhibitory postsynaptic potentials, or IPSPs, take the membrane further from threshold. As mentioned, it is the overall postsynaptic potential that will determine if an action potential is fired on the postsynaptic cell.

1. Name the seven classes of neurotransmitters. (p. 254-57) ____________________________________________________________________________________________________________

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*Note: we will spend a lot of time in class on specific NT’s, so just read over the info on pg. 255 to get familiar with them.

2. What are the possible places for neurotransmitter synthesis? Where is it stored? (p. 257) ______________________________________________________

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3. At a chemical synapse, describe the sequence of events that leads to neurotransmitter release, beginning with an action potential traveling along the presynaptic membrane. (p. 258)

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4. What is the chemical trigger for neurotransmitter release?

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5. How does the new “kiss and run” pathway compare to regular exocytosis? (p. 258)

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6. What happens to Ach after it is released into the synaptic cleft? (Fig. 8-19, p. 259)

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7. How, using the same neurotransmitter, might an olfactory neuron alert you to a stronger smell? (p. 260)

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8. Draw a picture of neurons converging and another of neurons diverging. (p. 262)

9. Name one advantage of convergence. (Fig. 8-22, p. 262)

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10. A slow synaptic potential would likely cause what type of effect? (Fig 8-23, p. 263)

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11. What is spatial summation of graded potentials? (p. 264-65)

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12. Describe postsynaptic inhibition (p. 266)

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13. Describe temporal summation (Fig. 8-24, p. 264)

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14. Define long-term potentiation (p. 267)

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15. When might long-term potentiation be useful?

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16. List some pharmacological agents that can alter synaptic transmission. (p. 268)

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17. Neuron A, Neuron B and Neuron C are all presynaptic to Neuron F. If A and B fire, F fires. If A and C fire, nothing happens. Draw this scenario below.

What can you conclude about the synapse between C and F? Between A and F? What other information might you need?

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18. Neuron J, Neuron K, and Neuron L are all presynaptic to Neuron T. J and K are both excitatory to T, whereas L is inhibitory to T. Assume that T needs a net input of +2 (one EPSP is +1; one IPSP is -1) to fire an action potential. Describe how temporal summation could result in an action potential on T. Describe how spatial summation could result in an action potential on T.

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THINGS TO TRY:

1. Neuron A, Neuron B and Neuron C are presynaptic to Neuron D. When A fires an action potential, D fires an action potential. When A and B fire simultaneously, D does not fire. When A, B, and C fire simultaneously, D fires. This is an example of...

A. inhibition by D and temporal summation by A and B.

B. inhibition by B and temporal summation by A and C.

C. inhibition by B and spatial summation by A and C.

D. inhibition by B and spatial summation by A and D.

E. inhibition by A and spatial summation by B and C.

Defend your choice.

2. Black widow venom causes an explosive release in acetylcholine from the axon terminals of neurons leading to skeletal muscle. Discuss why this might be problematic to the victim.

3. Botulism toxin blocks the release of acetylcholine from these same neurons. How would the effects of this toxin compare to black widow venom? Can you explain why the victim would experience respiratory distress in both cases?

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