Exam 1: Friday 5/10 in person (the lecture hall 8402)

Details:

~30 MC or T/F style questions (still writing up the exam, but somewhere in this range!)

Dr. Y will bring scantrons, you don't need to purchase those.

~5 short response where you will explain your answer to 5 of the MC’s above

Remember you have seen these questions in lecture during our class discussions OR on handouts

That means you have practiced this question and we’ve reviewed it together. The exam is the 2nd or even 3rd time you’ve practiced the idea

The wording might change a bit but the concept tested is the same

The exam is designed to take around 1 hour, but you have the full 1hr and 50 minutes so you can take your time

 

What should I study?

Remember that you’ve been consistently reviewing each week during your post-class assignments so hopefully the questions below will be review/familiar!

You should take a careful look at all our in-class handouts & any questions I posed during our lectures. The majority of questions are based on those handouts and in-class questions. In addition, short response/explain your answers will always be pulled from questions we discussed/debriefed together in lecture so you should feel comfortable explaining your answer or reasoning.

You should also take a look at post-class questions as well

Please don't memorize. Focus on being able to do the process/answer the question. If I told you about ion "A"'s concentration gradient and charge (instead of mentioning K+ or Na+), can you still answer the question about which direction the ion moves and what effect this will have on the membrane potential?

Compiled questions from lecture to review here.Download Compiled questions from lecture to review here.

Updated for Spring 24!!!

(Final version, it is not pretty, but it is compilation of nearly all the activities/questions we went through in lecture together in one place). If you can tackle these questions again but this time on your own, without having to go back to your notes then you probably have a pretty solid understanding of the material we covered. Be prepared to be able to explain your thinking too as there are some short response questions.

Practice Quizzes (were posted weekly for each week resource page):

Week 2 Practice Quiz

Week 3 Practice Quiz

Week 4 Practice quiz

No practice quiz for Week 1

 

What can I bring?

Summary sheets from Weeks 1-5. You will turn these in with your exam.

NO questions & answers (I would consider this a form of cheating and you would have a penalty placed on your midterm)

For example from the Lecture 8 Handout,

Parasympathetic NS would release Ach to Type 1 Muscarinic Receptors on cardiac muscle cells.

For example from Post-Class 3 Quiz, 

What is the effect of the SSRIs on the serotonin concentration in the synaptic cleft?

The serotonin concentration in the synaptic cleft will decrease.

The serotonin concentration in the synaptic cleft will increase.

 

Guiding questions

In the ideal case, you have been regularly reviewing these questions weekly (these are the same Guiding Questions from each week, I just copied and pasted so they are all in once place). If at this point you are just starting to look at the questions, then only use the questions below to identify areas you need to review. In other words, for efficient studying, I don’t recommend sitting down and answering all the questions (that will take a long time and potentially distract you away from reviewing in-class questions/handouts).  

Rather, you should read through the questions below, and highlight or circle the ones you can’t answer. Then, you can revisit your notes/lecture slides that you need to spend more time on. Please reach out to Dr. Y if that didn’t make sense! Please don’t get overwhelmed, the list is meant to be a comprehensive list of questions that review everything we covered the last 4 weeks.

 

Membrane dynamics & membrane potential

Describe several ways that intracellular fluid (ICF) differs from extracellular fluid (ECF). What ions are higher in the ICF vs ECF?

Describe what a concentration gradient is and how it leads to diffusion and the establishment of a dynamic Can you identify the flow of ions in/out of cells based on concentration gradients?

Describe the mechanism of the Na+/K+ pump and explain how it contributes to the resting membrane potential of a cell.

What would happen to the resting membrane potential if the Na+/K+ pump was mutated and not working?

Describe the mechanism of Na+ and K+ leak channels. How do they contribute to the resting membrane potential of a cell? How do they contribute to membrane permeability?

What is the resting membrane potential? What voltage value is it typically for most cells in your body?

If the concentration gradient of K+ decreases across the cell membrane, what happens to the membrane potential?

If the cell all the sudden became permeable (think gated membrane channels opening) to K+, what would happen to membrane potential? What about Ca2+? Na+?

What is hyperpolarization vs depolarization of the membrane potential? What ion channels should be opened to cause either?

 

Graded Potentials

Draw and describe the structure of a neuron.

Identify each of the following structures on your drawing and describe their structures: dendrites, dendritic spines, cell body, axon, axon hillock, collateral, axon terminal, synapse, postsynaptic cell

Where are the sensory receptors located on a neuron? From where on the neuron are neurotransmitters released?

Where do graded potentials occur?

What type of stimuli causes a graded potential? How does the strength of the stimulus affect the amplitude of the graded potential?

As a graded potential travels through the cell body, they lose amplitude. Explain why.

What is an EPSP? What is an IPSP? What ion channels contribute to each? Are each caused by depolarizations or hyperpolarizations?

How does an EPSP contribute to triggering an action potential? What about an IPSP?

 

Action Potentials

Differentiate between graded potentials and action potentials.

Where in the neuron do action potentials occur?

How does the strength of the stimulus effect the amplitude of the action potential? Why are they all-or-none?

Explain how ion permeability changes during the rising phase and falling phase of an action potential.

What is the stimulus for opening EACH of the channels used during an action potential?

What is the order of stimulus, opening and closing of all of these channels?

How is the resting membrane potential reestablished after an action potential?

Hint, we did this for our in-class activity! Can you visualize what’s happening with each of the channels?

Voltage gated Na+ channels in the axon contain two gates. What are they? How are they triggered?

What are the absolute and relative refractory periods?

How does the inactivation gate on the Na+ channel cause the absolute refractory period?

What causes the relative refractory period?

How are action potentials conducted along the length of the neuron?

Why don’t action potentials lose amplitude along the length of the axon?

If action potentials all have the same amplitude, how do action potentials transmit the intensity of the signal (to phrase it a different way, how do neurons alter the amount of neurotransmitter release based on the size of the stimulus?)?

Explain how myelin increases conduction speed down the length of an axon.

Explain the mechanism of salutatory conduction

What is the effect of demyelination? What are the symptoms of demyelination diseases (multiple sclerosis).

  

Synaptic Transmission

Draw and label the components of a synapse. Be sure to label the following structures: presynaptic cell, axon terminal, synaptic cleft, and postsynaptic cell (either neuronal or non neuronal)

What is the difference between a chemical and electrical synapse?

What is the trigger for neurotransmitter release from a synapse? Outline the steps of synaptic transmission.

How is neurotransmitter release terminated?

How is synaptic activity terminated (be sure to talk about all three mechanisms)?

Differentiate between “FAST” receptors and “SLOW” receptors on a post synaptic cell.

Explain how neurotransmitter binding to a fast receptor might cause an EPSP in the post synaptic cell. How about and IPSP?

Explain how a neurotransmitter binding to a slow receptor might cause an EPSP in the post synaptic cell. How about an IPSP?

What is long-term potentiation (LTP)? What is the neurotransmitter that governs LTP?

What are the neurotransmitter receptors involved in LTP?

What is the result of glutamate binding to AMPA? Is this a fast response or a slow response?

What about NMDA receptors?

Describe the sequence of events that occurs when glutamate is released from the presynaptic cell. How do these events lead to LTP?

Describe the structure of the synapse of the neuromuscular junction.

What is the neurotransmitter released from a somatic motor neuron?

What is the receptor on the muscle cell? Does triggering this receptor with neurotransmitter trigger a fast response or a slow response?

Describe the sequence of events that occurs when an action potential reaches the axon terminal of a somatic motor neuron.

How is synaptic transmission terminated at a neuromuscular junction?

What is AChE and what does it do at the synaptic cleft?

What is an agonist and how does it affect synaptic transmission? Give examples of both direct and indirect agonists.

What is an antagonist and how does it affect synaptic transmission? Give examples of both direct and indirect antagonist

Explain how GABA work to inhibit post-synaptic cell response.

How would blocking GABA receptors affect response in the post-synaptic cell?

Hint, remember our in-class handout!

Make a list of all of the ion channels we have discussed. Make sure you indicate where you find the channel, how it is gated, which way ions will travel through it and their effect on membrane potential and when it is used.

Make a list of all of the neurotransmitter-receptor pairs we have discussed. Make sure you indicate where the neurotransmitters are used and how they are regulated

Hint, we did a lot of this in our in-class handouts!

 

Peripheral Nervous System

Describe the organization of the nervous system.

Be sure to use the following terms: efferent neurons, afferent neurons, sensory receptors, autonomic neurons, somatic motor neurons, parasympathetic neurons, sympathetic neurons, somatic motor neurons, skeletal muscles, central nervous system, peripheral nervous system.

What does the somatic motor division of the efferent nervous system control?

Describe the structure, target, neurotransmitter and receptor and enzyme used in the somatic motor division.

What are the two divisions of the autonomic nervous system?

What are the targets of the autonomic nervous system?

How are pre and postganglionic neurons similar and different in the sympathetic vs parasympathetic divisions?

Describe how the two divisions of the autonomic nervous system maintain homeostasis through antagonistic control.

Give several examples of antagonistic control carried out by the autonomic nervous system.

Describe how the preganglionic neuron and the postganglionic neurons are arranged in the sympathetic and parasympathetic systems.

What neurotransmitter-receptor pair is used in the autonomic ganglion of BOTH divisions of the autonomic nervous system?

How are the postganglionic autonomic synapses similar and different than the synapses in the neuromuscular junction?

Hint, a lot of this work is summarized by your in-class handout!

In the sympathetic division, what neurotransmitter-receptor pair is used in the ganglion? What about at the postganglionic synapse?

Give several examples of how the parasympathetic system affects different tissues (for example, how does it affect heart rate, salivation, rate of digestion, airways)

Describe how different types of adrenergic receptors can cause different responses to the same neurotransmitter.

As an example, explain how this works to modulate the diameter of arteries in the digestive system and blood vessels in the skeletal muscles during a systemic sympathetic response.

Hint, this is summarized in your in-class handout!

You can review the adrenal medulla material (it will be relevant in 40C as well), but note I won’t ask you any questions about it!

In the parasympathetic division, what neurotransmitter-receptor pair is used in the ganglion? What about at the postganglionic synapse?

Compare and contrast nicotinic receptors and muscarinic receptors.

Give several examples of how the parasympathetic system affects different tissues (for example, how does it affect heart rate, salivation, rate of digestion, airways)

Again, this is summarized by our in-class activity!

 

Pyramidal Cells

Large neurons with long axons that travel through the spinal cord and form huge voluntary tracts.

• Central Sulcus
• Pyramidal Cells
• Projection Fibers
• Premotor Cortex

https://www.cleverlysmart.com/right-brain-and-left-brain-what-are-the-differences/ 

Pyramidal cells, or pyramidal neurons, are a type of multipolar neuron found in areas of the brain including the cerebral cortex, the hippocampus, and the amygdala. Pyramidal cells are the primary excitation units of the mammalian prefrontal cortex and the corticospinal tract.

 Brain Folds (Cerebral Gyri):

The human brain’s outer layer, known as the cerebral cortex, exhibits intricate folding patterns. These folds, called gyri, significantly increase the brain’s surface area within the limited space of the skull.

Brain folding typically begins during the second trimester of pregnancy and continues after birth. Researchers from Harvard have studied the mechanics of brain folding using hydrogel models. They found that folding reduces instability caused by differential growth rates between the inner and outer layers of the brain1.

These folds play a crucial role in accommodating a large number of neurons and enhancing neural connectivity.

Intestinal Villi:

In the small and large intestines, circular folds (also known as plicae circulares) increase the surface area for nutrient absorption.

Within these circular folds, there are small, hairlike projections called villi. Each villus is vascularized and covered with epithelial cells.

The presence of villi significantly enhances the surface area available for nutrient exchange, allowing efficient absorption of nutrients from digested food2.

Skin Wrinkles:

Wrinkles on human skin are another example of surface area enhancement. As we age, our skin naturally develops wrinkles due to changes in collagen and elastin fibers.

These wrinkles increase the skin’s surface area, allowing it to accommodate movement and stretching while maintaining its protective function.

Tumor Buckling Protrusions:

Tumors can develop buckling protrusions on their surfaces. Although these are pathological, they demonstrate how surface irregularities can increase the effective area for tumor invasion.

Researchers study these features to understand tumor behavior and develop targeted treatments3.

In summary, creases and folds that increase surface area are essential for efficient functioning in various biological systems. Whether it’s the brain, intestines, or skin, nature has ingeniously designed these structures to optimize space and functionality. 🧠🌟🌿

I’ve provided a brief overview of different examples related to surface area-enhancing folds. If you’d like more details or have any other questions, feel free to ask! 😊

14.2 Population Growth

 Population Growth

 14.2 Explain why the Least Industrialized Nations have so many children, consequences of rapid population growth, population pyramids, the three demographic variables, and problems in forecasting population growth. Even if starvation is the result of a maldistribution of food rather than overpopulation, the Least Industrialized Nations are still growing much faster than the Most Industrialized Nations. Without immigration, it would take several hundred years for the average Most Industrialized Nation to double its population, but just 50 years for the average Least Industrialized Nation to do so. Figure 14.5 puts the matter in stark perspective. Figure 14.5 World Population Growth, 1750–2150

14.1.4: Why Are People Starving?

14.1.4: Why Are People Starving? 

Pictures of starving children gnaw at our conscience. We live in such abundance, while children and their parents starve before our very eyes. Why don’t they have enough food? Is it because there isn’t enough food in the world to feed them or because the abundant food the world produces does not reach them? 458 The Anti-Malthusians make a point that seems irrefutable. As Figure 14.4 shows, there is much more food for each person in the world now than there was in 1950. Despite the billions of additional people who now live on this planet, improved seeds and fertilizers have made more food available for each person on Earth. With the breakthroughs that bioengineers are making in agriculture, even more food is on the way. Figure 14.4 How Much Food Does the World Produce per Person?

NOTE: 2004–2006 equals 100. Projections by the author.​ SOURCES: Based on Simon 1981; Statistical Abstract of the United States 2010:Table 1335, 2019:Table 1391; UN FAO 2019.

 The vertical axis represents “Per capita food production” ranging from 0 to 120 in increments of 10, while the horizontal axis represents “Year” ranging from 1950 to 2020 in increments of 5. The curve begins at 64, in the year 1950, which is shown to increase till 112 in the year 2015. Further, the curve is represented through a dotted line, increasing till 115, in the year 2020. Note: All data is approximate. 2004 to 2006 equals 100. Projections by the author. 459 If the Earth is so productive, why do people die of hunger? From Figure 14.4, which you just viewed, we can conclude that people don’t starve because the Earth produces too little food, but because particular places lack food. Droughts and wars are the main reasons. Just as droughts slow or stop food production, so does war. In nations ravaged by civil war, opposing sides confiscate and burn crops, and farmers flee to the cities (Bariyo 2017; Mednick 2018). The New Malthusians counter with the argument that the world’s population is still growing and that we don’t know how long Earth will continue to produce enough food. They add that the recent policy of turning food (such as corn and sugar cane) into biofuels (such as gasoline and diesel) poses a threat to the world’s food supply. A bushel of corn that goes into someone’s gas tank is a bushel of corn that does not go on people’s dinner plates. Both the New Malthusians and the Anti-Malthusians have contributed significant ideas, but theories will not eliminate famines. Starving children are going to continue to peer out at us from our televisions and magazines, their tiny, shriveled bodies and bloated stomachs nagging at our consciences, imploring us to do something. Regardless of the underlying causes of this human misery, the solution is twofold: first, to transfer food from nations that have a surplus to those that have a shortage, and second, to teach more efficient farming techniques. The pictures of starving Africans leave the impression that Africa is overpopulated. Why else would all those people be starving? The truth, however, is far different. There are 37 people per square kilometer in Africa, only slightly more than the 33 people per square kilometer in the United States. At 136 people per square kilometer, Asia’s population is three-and-a-half times as concentrated as Africa’s, and people there are not starving (Kaneda et al. 2019). Africa even has vast areas of fertile land that have not yet been farmed. The reason for famines in Africa, then, cannot be too many people living on too little land. Gallery Famine and Feast

Photos of starving children, such as this child in South Sudan, haunt Americans and other members of the Most Industrialized Nations. Many of us wonder why, when some are starving, we should live in the midst of such abundance, often overeating and even casually scraping excess food into the garbage. As in this photo from Toronto, Ontario, Canada, we even have eating contests to see which “competitive eater” can eat the most food in the least amount of time. Credits: Jenny Matthews/Alamy Stock Photo; Daniel Zuchnik/FilmMagic/Getty Images Watch 

Does the World's Top Weed Killer Cause Cancer

14.1.3: Who Is Correct?

 14.1.3: Who Is Correct? 

As you can see, both the New Malthusians and the Anti-Malthusians have looked at historical trends and projected them onto the future. The New Malthusians project continued world growth and are alarmed. The Anti-Malthusians project Stage 3 of the demographic transition onto the Least Industrialized Nations and are reassured. There is no question that the Least Industrialized Nations are in Stage 2 of the demographic transition. The question is, Will these nations enter Stage 3? After World War II, the West exported its hybrid seeds, herbicides, and techniques of public hygiene around the globe. Death rates plummeted in the Least Industrialized Nations as their food supply increased and health improved. Because their birth rates stayed high, their populations exploded. This alarmed demographers, just as it had Malthus 200 years earlier. Some predicted worldwide catastrophe if something were not done immediately to halt the population explosion. We can use the conflict perspective to understand what happened when this message reached the leaders of the industrialized world. They saw the exploding populations of the Least Industrialized Nations as a threat to the global balance of power they had so carefully worked out. With swollen populations, the poorer countries might demand a larger share of Earth’s resources. The leaders found the United Nations to be a willing tool, and they used it to spearhead efforts to reduce world population growth. The results have been remarkable. The annual growth of the Industrializing Nations has dropped by close to half (44 percent), from 2.5 percent a year in the 1960s to 1.4 percent today (Kaneda et al. 2019). The New Malthusians and Anti-Malthusians have greeted this news with incompatible interpretations. For the Anti-Malthusians, this slowing of growth is the signal they were waiting for: Stage 3 of the demographic transition has begun. First, the death rates in the Least Industrialized Nations fell; now, just as they predicted, birth rates are also falling. Did you notice, they would say if they looked at Figure 14.2, that it took 12 years to add the fifth billion to the world’s population—and also 12 years to add the sixth billion—and also 12 years to add the seventh billion? Despite millions upon millions of more women of childbearing age, population growth has leveled off. The New Malthusians reply that the growth is slower than it was, but a slower growth rate still spells catastrophe; it will just take longer for it to hit. 457 Then the Anti-Malthusians drop a bombshell, making the New Malthusians moan in disbelief. They say that our future will be the opposite of what the New Malthusians worry about: There are going to be too few children in the world, not too many. The world’s problem will not be a population explosion, but population shrinkage—populations getting smaller. Europe points to the future. If it weren’t for immigration from Africa, all the countries of Europe would fill more coffins than cradles (Kaneda et al. 2019). Population shrinkage has also reached Asia, with Japan’s population dropping by about 400,000 people a year (Kaneda et al. 2019). With their need for future workers and their dislike of immigrants, to say that Japan’s politicians are worried would be an understatement. Some Anti-Malthusians even predict a demographic free fall. As more nations enter Stage 4 of the demographic transition, the world’s population will peak and then begin to grow smaller. Two hundred years from now, they say, we will have a lot fewer people on Earth. Who is right? It simply is too early to tell. Like the proverbial pessimists who see the glass of water half-empty, the New Malthusians interpret changes in world population growth negatively. And like the eternal optimists who see the same glass half-full, the Anti-Malthusians view the figures positively. Sometime during our lifetimes, we should know the answer.

14.1.2: The Anti-Malthusians

 14.1.2: The Anti-Malthusians 

All of this seems obvious, and no one wants to live shoulder-to-shoulder and fight for scraps. How, then, can anyone argue with the New Malthusians? To find out, let’s turn to a much more optimistic group of demographers, whom we can call the Anti-Malthusians. For them, the future is painted in much brighter colors. They believe that Europe’s demographic transition provides a more accurate picture of the future. This transition is diagrammed in Figure 14.3. During most of its history, Europe was in Stage 1. Europe’s population remained about the same from year to year, because its high death rates offset its high birth rates. Then came Stage 2, the “population explosion” that so upset Malthus. Europe’s population surged because birth rates remained high while death rates went down. Finally, Europe made the transition to Stage 3: The population stabilized as people brought their birth rates into line with their lower death rates. Figure 14.3 The Demographic Transition

Hearing from the Author: The Demographic Transition Listen to the Audio This, say the Anti-Malthusians, will also happen in the Least Industrialized Nations. Their current surge in population growth simply indicates that they have reached Stage 2 of the demographic transition. Hybrid seeds, medicine from the Most Industrialized Nations, and purer public drinking water have cut their death rates, while their birth rates have remained high. When they move into Stage 3, as surely they will, we will wonder what all the fuss was about. In fact, their growth is already slowing.

Large families on U.S. farms used to be common. Children helped plant and harvest crops, take care of animals, and prepare food. As the country industrialized and urbanized, children became nonproducers, making them expensive to have around. Consequently, the size of families shrank as we entered Stage 3 of the demographic transition. This photo was taken in 1887 near Comstock, Nebraska. Credit: Everett Collection/SuperStock