last updated 28 March 2002 at 1:00 pm
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|Paul Atkinson||Aundie Bishop||William Bohlem||Ashley Costa|
|Jason Elwell||Ryan Gilreath||Omar Javery||Chris Kandl|
|Kelly Moore||Brad Nesmith||Blair Smith||Rebecca Terry|
1. What are the differences between a chemical and electrical synapse? What are the advantages to each? Would a drug that affects a chemical synapse have the same affect on an electrical synapse? Why or why not?
2. What is quantal release and why is this important when considering how to treat conditions associated with release of neurotransmitters?
3. How does Clostridium toxin affect a person? In your answer be sure to explain the two ways that the toxin can affect a person and where the infection takes place to produce these affects.
4. What 3 criteria define a neurotransmitter?
5. How do neurotransmitters differ from other messenger molecules? Can a neurotransmitter act as anything else?
6. What is the advantage to having multiple NTs at an axon terminal?
7. Why would some NTs be broken down in the synaptic cleft while others are transported inside of cells before enzymes act on them?
8. What is the relationship between ischemia and excitotoxicity?
9. What are the different kinds of NTs and how do they differ? Which ones are excitatory and which are inhibitory? What are the advantages of having many different kinds of NTs?
10. What is the relationship between drugs like cocaine and dopamine? How does this relate to addiction?
11. Proteolytic processing of peptide NTs is advantageous because
12. If a cell was deprived of tyrosine hydroxylase, which NTs could it not
What if the cell was supplied with an abundant supply of tyrosine? If the cell was supplied with dopamine, could it produce epinephrine without hydroxylase?
13. Give an overview of the lifecycle of acetylcholine. Where is this NT involved?
What drugs interfere with ACh action? How do these drugs interfere with ACh?
1. Compare and contrast electrical and chemical synapses. Where might electrical
synapses function more effectively?
2. Explain Katz's study of the frog neuromuscular junction in the 1950s and 60s. How did he figure out this "quantal release" business?
3. How did Heuser and Reese use electron microscopy to expand on Katz's findings in the 1970's?
4. Why have neurons devised a method for local recycling of synaptic vesicles? How was HRP used to elucidate their secret?
5. How does blocking voltage-gated calcium channels in the pre-synaptic membrane affect the post-synaptic membrane potential?
6. How do we know, experimentally, that calcium is crucial for vesicle release from the pre-synaptic terminal?
7. Is there an action potential when calcium is not allowed entry into the pre-synaptic cell?
8. Explain how vesicular and plasma membrane SNARE proteins orchestrate neurotransmitter release. Discuss the 4 SNAREs that we must learn.
9. How would adding a-Latrotoxin (black widow spider venom) and calmodulin to the pre-synaptic membrane affect vesicle release?
10. What does myasthenia mean? How are calcium channels involved in Lambert-Eaton myasthenic syndrome?
11. Neuroscientist Synapt O. Brevin is trying to determine if a certain neurotransmitter is present in the axon terminal he is studying. What might he look for to answer his question?
12. What are some characteristics of the two categories of NT's? Which properties are used to classify NT's?
13. Describe the appearance of the "active zone" under electron microscopy.
1. What ion, moving in what direction, is responsible, ultimately, for the
release of neurotransmitters from the presynaptic terminal?
2. Suppose an electrode is placed in the axon of a motor neuron. If a depolarization is noted in the presynaptic motor neuron, what is this change in membrane potential known as? Under what conditions will this change in membrane potential in the presynaptic neuron cause muscle contraction?
3. Explain how the HRP (horseradish peroxidase) enzyme gives us an idea of how synaptic vesicles are recycled What new technique has augmented our understanding of how this same system operates and how does it work?
4. Tetrodotoxin blocks sodium channels, effectively preventing action potentials. When presynaptic terminals are treated with tetrodotoxin, and a voltage clamp is applied at 0 mV a prolonged action potential occurs. What is the likely answer to this biological riddle and what effect do presynaptic action potentials have on the release of neurotransmitters?
5. If a substance is injected into a presynaptic neuron which chelates Calcium, what effect will it have on: 1. action potentials 2. neurotransmitter release.
6. What proteins, located on both the vesicle and the membrane allow for the "docking" of the vesicle?
1. What are the three criteria that classify a chemical as a neurotransmitter?
2. In a typical presynaptic terminal, there are 2 types of neurotransmitters-one is big, the other smaller. What are the two different types of neurotransmitter, their contents, and under what circumstances is each one released? What advantage is gained by having two types of neurotransmitters for different circumstances?
3. Organophosphophate insecticides are used to control insect populations. They work by blocking acetylcholinesterase. If this same substance were to find its way into a human, what effect would blocking acetylcholinesterase have on the person?
4. A given neuron is CAT positive. What does this mean?
5. A person has accidentally ingested a poison which inhibits the release of glycine. What clinical manifestations would present themselves and what would be an appropriate course of treatment?
1. You are studying a particular synapse. How would you determine what kind of synapse you are dealing with (electrical/chemical)?
2. Describe why EPP's are reduced to the amplitude of MEPP's when the neuromuscular junction is bathed in low Ca++ concentrations.
3. What experimental evidence is there that MEPP's and EPP's are related?
4. Describe an experiment that would allow you to show that each vesicle causes a single quantal event on the postsynaptic vesicle. What is the significance of such an experiment?
5. Why is it that when presynaptic terminals are treated with tetrodotoxin they can still produce prolonged action potentials?
6. How does LEM's affect EPP's and neurotransmitter release? What are some ways to treat this disorder?
7. How do tetanus and botulism work? What problems result from these two disorders?
8. What is the fundamental difference between hormones and neurotransmitters?
9. What are three criteria that define a neurotransmitter?
10. What advantage is there to having 2 different populations of synaptic vesicles?
11. You are studying a neuron and its neurotransmitter is unknown. How would you go about determining which neurotransmitter is released by that particular neuron?
12. Describe how brain cancer affects synaptic transmission.
13. Describe the mechanism for differential release of neurotransmitters. Why is this significant for synaptic transmission?
1. In what ways do the two general classes of (synapses) in the brain differ?
2. What is the significance of having presynaptic neurons that are upstream and postsynaptic neurons that are downstream?
3. Why don't gap junctions display a delay in transmission that is characteristic of chemical synapses?
4. How does lowering calcium concentration effect end plate potential?
5. The fusion of synaptic vesicles causes new membrane to be added to the plasma membrane of the presynaptic terminal, but the addition is not permanent. Why is this so?
6. Where are the precursors to synaptic vesicles originally produced? During continuous neural activity, where do synaptic vesicles come from? Why is this so?
7. What neurological deficits would be present in one who has a contamination of a puncture wound by Clostridium bacteria?
8. Katz observed that presynaptic terminals treated with tetrodotoxin could still produce a peculiarly prolonged type of action potential. How is this possible?
9. What protein found in the membrane of synaptic vesicles is the leading candidate for calcium regulation of neurotransmitter release? How does this protein regulate neurotransmitter release?
10. What neurological deficits would be present in one who has suffered a bite from a female black widow spider?
1. What are the two broad categories of neurotransmitters and how do they differ from each other?
2. Why would one classify a neurotransmitter as "putative"?
3. How can a substance act both as a neurotransmitter and a hormone? Give an example of one such substance.
4. When more than one transmitter is present in a nerve terminal, why aren't both released simultaneously? By what mechanism is this achieved?
5. Would substance P be transported by slow or fast axonal transport? Why is this so? How is transport accomplished?
6. What neurological defects are present after one has came into contact with Sarin? By what mechanism does this occur?
7. Why is glutamate generally acknowledged to be the most important transmitter for normal brain function?
8. Why is vitamin B6 such an important vitamin in regards to neural activity? What deficits occur due to a deficiency in vitamin B6?
9. In Parkinson's disease, the dopaminergic neurons of the substantia nigra degenerate. Therefore, one would treat a Parkinson's patient using dopamine, right? Why or why not?
10. Why are selective serotonin reuptake inhibitors (SSRI) valuable in the treatment of depression. By what mechanism is this achieved?
1. Although rare, electrical synapses are present in humans. What structure joins two neurons in an electrical synapse? What is the significance of the pore of these channels being much larger than voltage gated ion channels? Why is it important for some neurons in the hypothalamus to be connected by electrical synapses?
2. If Juana la Loca is performing an experiment on frog muscles to record electrical responses in a postsynaptic cell from stimulating a presynaptic cell and she doesn't want the muscle contraction to break her recording electrode, what could she do?
3. How do you account for the small blips that occur sometimes and not at others when recording postsynaptic responses but have you have elicited no presynaptic stimulation?
4. How did Bernard Katz and colleagues discover the phenomenon known as Quantal Release?
5. If one vesicle elicits an EPP of 0.6 mV, how many vesicles would have to be released for a cell at -72 mV to be reach depolarization at +5 mV?
6. Mr. Astro Sietz notices that he is getting many more "no responses" in his postsynaptic membrane recordings than he should (during some quantal release experiments)? What could be the problem with the presynaptic or postsynaptic cell?
7. Using an transmission electroscopy, how was it first discovered that vesicles docked and released their contents? Where does the vesicle content come from and how does it get to the vesicle?
8. Describe an experiment using an enzyme to test the idea of synaptic vesicle recycling.
9. Mr. Strong Bone wants to determine if Ca++ is the ion responsible for synaptic vesicle release. What could he do to see that is Ca++ and not Na+ or K+?
10. Which three 3 proteins comprise the SNARE complex? What do the SNARE proteins do? Do SNARE proteins bind Ca++? If not, what does bind Ca++ and what does the Ca binding cause?
11. Why aren't hormones considered neurotransmitters? Which two criteria of being a NT do hormones meet?
12. What is the relationship between a synthetic enzyme and an NT? How can we tell if a neuron has a particular NT?
13. What kind of NT is packaged into small vesicles and what kind of NT is packaged into large vesicles typically? Which type(s) of vesicle(s) does high frequency stimulation cause the release of? How does this type of stimulation/release process allow for more flexibility in the effects on target cells?
14. Typically, what type of NT do neurons with long axons release? What type of NT do neurons with short axons release? Why would neurons be set up like this?
15. If Harry Pene wants to test to see if a neuron uses ACh as an NT, how would he do this? After ACh is broken down, how is choline transported back into the axon terminal? What would be the effect on a post-synaptic cell of applying an organophosphate to a synapse?
16. An individual was detected to have a slightly high level of free radicals. Relating to glutamate, what could be the problem with the individual? What treatments would you suggest?
17. Why are GABA agonist good for treating epilepsy and used as sedatives and anesthetics? If there is no GABA present in a neuron but you know it has inhibitory action, what other neurotransmitter would you propose the neuron to use?
1. What are some benefits of electrical synapses over chemical synapses? How
can you determine if a cell has an electrical synapse?
2. In an experiment measuring spontaneous MEPPs, data collected on a test subject showed that this subjects MEPPs often registered magnitudes of 0.3mV, 0.6mV, 0.9mV compared to readings from a normal individual of 0.4mV, 0.8mV, 1.2mV Firstly, why do we see such peaks? Secondly, what can explain the smaller MEPPs of the test subject?
3. What would happen if a normal individual suddenly showed a lack of clathrin in neurons? How would this affect signal transmission at a chemical synapse?
4. Describe an experiment that shows that synaptic vesicles are recycled.
5. Would injecting BAPTA into a presynaptic terminal on the NMJ result in tetany or paralysis? Explain.
6. Tetrodotoxin is injected into and remains in the presynaptic terminal. What is the effect on signal transmission and an AP?
7. Compare and contrast the mechanism by which the toxins from Clostridium botulinum and Clostridium tetani work. What visible effects can be observed in a human who has either toxin in his/her body?
8. Describe the method is used to determine the type of NT utilized by a particular cell.
9. Explain the pathway that leads to cell death during an episode of ischemia involving a NT that leads to cell death. What is a way to treat this?
10. How is it that benzodiazepines can be used to produce anterograde amnesia?
11. How would you expect an MAO inhibitor to affect the fight or flight response?
12. Compare and contrast small NTs and peptide NTs concerning where they are synthesized, their rate of transport, their fate after release, and how this relates to the type of axon with which they are associated.
13. A neuron tests positive for the presence of tyrosine hydroxylase, DOPA decarboxylase, and phenylethanol-amine N-methy-transferase. What NT will this cell utilize?
14. An individual has a mutation in the gene coding for opioid receptors. How would this effect the individual?
What are 2 features of electrical synapses that arise from their arrangement?
How can a neuromuscular junction and EPP be studied so that the electrode is not dislodged by muscle contraction?
Explain the significance of EPPs occurring in units of single MEPPs.
In patients with Lambert-Eaton myasthenic syndrome there is a loss of volage-gated Ca++ channels. What would be the effects of this regarding EPPs and MEPPs?
List the criteria that define a neurotransmitter.
What is the advantage of having more than one neurotransmitter within a presynaptic terminal?
What is the fate of glutamate once it is released into the synaptic cleft?
What are the effects of organophosphates?
What is the action of MAO and what effects would MAO inhibitors have?
What areas of the brain are involved in emotional reinforcement and what role do they play in addiction?
What type of transmitters mediate synaptic transmission when a rapid response is essential?
Name 2 major inhibitory neurotransmitters and their clinical importance.
1. Compare and contrast electrical and chemical synapses. What do they involve?
What is their structure? Which conducts faster?
2. Describe an experiment that could prove that an EPP is really made up of many MEPPs.
3. If one synaptic vesicle were released, how much depolarization would it cause? What does this therefore infer about synaptic transmission and action potentials?
4. Are used synaptic vesicles replaced by freshly synthesized ones from the cell body? If not, how are they replaced? How was HRP used in the demonstration of vesicle replacement?
5. If a presynaptic terminal is treated with tetrodotoxin, will it still be able to produce an action potential? Why or why not?
6. What are the 4 main proteins (that we have to know) involved in transmitter secretion, and what are their individual functions?
7. What are the 3 main criteria that define a neurotransmitter?
8. Substance X, thought to be a neurotransmitter, has been found to be present in the presynaptic terminal and to have receptors on the postsynaptic cell, though it is not sure whether Ca++-dependent release is involved? What (term is used to describe this) type of NT?
9. What are the two major categories of neurotransmitters and what are some examples and subcategories of each?
10. It is suspected that the presynaptic cell you are working with may contain small NTs and neuropeptides. If this is true, what will happen with low frequency stimulation? With high frequency stimulation?
11. Compare and contrast synthesis of small NTs and synthesis of neuropeptides.
12. What is the most common excitatory NT in the nervous system? The most common inhibitory NT in the nervous system? Which can cause excitotoxicity, and how does this come about?
13. What is the difference between NTs and neuromodulators/neuropeptides? (What effects do they cause?)
1. Why do LEMS patients have weak inactive muscles?
2. How does alpha-Latrotoxin work? Why is there a brief period of tetanus and then paralysis?
3. What are the three criteria for a substance to be considered a neurotransmitter?
4. What neurotransmitter did Otto Loewi discover? How did he discover it using frog hearts? What was it originally called?
5. Compare and contrast the type of vesicles released during a high frequency and a low frequency action potential. How do these synaptic vesicles differ in appearance under (electron) microscopy?
6. Compare and contrast the difference in the contents of the small vesicles and larger vesicles.
7. What is a neuromodulator? Are these released at high or low frequency action potentials? What affects do they have in synaptic transmission?
8. Where are peptide neurotransmitters synthesized? How are they transported to the axon terminal?
9. You have been drafted into the army. You notice that when people are exposed to a type of Nerve gas they have extreme initial tetanus. What could the gas be and what affects does it have in the synaptic cleft?
10. Glutamate is the most exciting neurotransmitter in the nervous system. (Describe) the process in which it is released, taken up and recycled.
11. Ischemia can lead to cell death. (Describe) the process in which this occurs.
12. Explain the difference between scanning and transmission electron microscopy in reference to how they are obtained.
13. How was horseradish peroxidase used to show that the axon terminal recycles its vesicle membranes?
14. What are two possible reasons for why Clostrum bacteria have toxins?
15. How is BoTX classified? How does BoTX affect the strength of the docking of neurotransmitters?
1. What are the general classes of synapses in the brain, and how do they differ in terms of structure and function?
2. You are mesmerized by the pulsing motion your pet jellyfish makes in your bathtub. Synaptically speaking, how is he able to move like this?
3. Your uncle, Bernard Katz, is using Hoppy, the family frog, to study end plate potentials. However, he just can't figure out how to stop the Hoppy's sartorius muscle from contracting, so he solicits your help. Make at least 2 suggestions to help out poor Uncle Bernard.
4. Would you observe changes in muscle cell membrane potential even if stimulation of the presynaptic motor neuron was absent? Fully explain your reasoning.
5. Briefly outline how you would prepare a sample for both a transmission electrograph and a scanning electrograph.
6. Describe how a scanning electromicrograph of the plasma membrane of an unstimulated presynaptic terminal would differ from a scanning electromicrograph of the same terminal when it is stimulated y an action potential. What accounts for these visible differences?
7. How does HRP assist the visualization of local recycling of synaptic vesicles in presynaptic terminals?
8. Why did Bernard Katz choose to experiment on the frog neuromuscular junction? Why didn't he use something else?
9. If given the choice, would you use HRP or florescent dyes to study vesicle recycling? What are the benefits and drawbacks of both methods?
10. When Katz & Miledi treated presynaptic terminals with tetrodotoxin, why could it still produce a peculiarly prolonged type of action potential?
11. What happens when BAPTA is microinjected into squid giant presynaptic terminals?
12. How were the presynaptic protein implicated in neurotransmitter release discovered experimentally?
13. During a muscle tissue biopsy of your patient, you decide to practice your abilities in making intracellular recordings. While stimulating his motor neurons, you notice that the number of quanta contained in individual EPPs is greatly reduced. However, the amplitude of spontaneous MEPPs is normal. What do you think is wrong with your patient, & why do you see such curious results?
1. You discover a new chemical and hope it is a neurotransmitter so that you can name it after your girlfriend for her birthday present. What 3 criteria should you use to see if Jessica-choline is truly a neurotransmitter?
2. If small-molecule neurotransmitters were racing against neuropeptides in a track and field sprinting event, who would you pick to win and why?
3. Briefly outline the 5 major steps in the life cycle of a neurotransmitter.
4. Why does the word "organophosphate" send chills of happiness down the spines of RAID manufacturers?
5. During a routine physical, your physician suddenly has a stroke. During his fall to the floor, he mumbles something about the glutamate blockers he keeps in the cabinet. Is he speaking trauma-induced gibberish, or is there actually some sense to his mumbling?
6. Why is it that people think Huntington's Syndrome is somehow related to glutamate?
7. Why is klonopin referred to as a date rape drug?
8. You are the owner of Pet Plus, an emergency veterinarian clinic. One night, a hysterical owner brings in their bulldog that appears to be violently seizing. You quickly administer phenobarbitol, and the pup has its final seizure. What is phenobarbitol, and why did you choose this particular drug?
9. If you wanted to fix membrane potential at -50mV, but your voltage clamp was broken, how else could you achieve a "clamped" membrane at this particular voltage?
10. What would you look for in a neuron if you wanted to see if it was catecholaminergic or not? Why?
11. What are the differences between metabotrophic and ionotrophic receptors?
GABA-A is what type of receptor?
1. Explain why electrical synapses are important in the hypothalamus? What would result from damage to this type of synapse in this region?
2. Explain the advantages and disadvantages of a "dye-coupled cells."
3. What affect does bathing a neuron in a solution with a low amount of Ca++
have on this neuron's production of end plate potentials when stimulated?
4. What are some of the explanations that could explain an experiment producing few, fairly small EPP's even when the neuron is bathed in a solution with normal calcium concentration?
5. How does the anatomy of a neuron contribute to the importance of local recycling of synaptic vessicles? How does this differ for large and small vessicles?
6. How is the inward presynaptic Ca++ current affected during a voltage clamp experiment when Cadmium is added to the extracellular fluid? What happens to the membrane potential of the postsynaptic cell?
7. What would be the defect in a presynaptic terminal lacking an endosome? What type of neurotransmitter (small or peptide) would this effect most and why?
8. What does a 1:1 ratio infer about vesicles and quantal release? How would a graph look if there was a 1:1 ratio between the two?
9. Why is it that Benadryl makes you sleepy?
10. What are some advantages of co-transmitters?
11. The main ingredient in Farmer Joe's pesticide is some type of organophosphate. Explain to him why this product is necessary for his farm.
12. How do you explain the change in membrane potential from -70 mV to -50 mV when GABA binds to a postsynaptic cell?
13. Explain the defect in Parkinsonism and explain how it is treated. Would dopamine aid in this treatment?
1. Why are electrical synapses much faster at conducting signals than their
chemical- synapse counterparts? Where might one find such synapses?
2. When Katz performed his experiment that led to the discovery of quantal release, why did he not want the myofiber to twitch? How did he perform the experiment in order to keep it from twitching?
3. Why must clathrin be present in an axon terminal of a neuron that has a chemical synapse with a neighbor?
4. How did neuroscientists learn that Ca++ cations are responsible for neurotransmitter release at the axon terminal? What substances were used? What are their effects?
5. In a freeze-fracture scanning electron micrograph of a presynaptic terminal, what are the small bumps? Also, what is one observing by seeing the large round crevices?
6. Explain both the locations and the roles of synaptobrevin, syntaxin, SNAP-25, and synaptotagmin in the presynaptic terminal.
7. How does the a-latrotoxin of black widow spiders work? What effect, then would this toxin have on the spider's victim? How is this mechanism advantageous for the black widow?
8. Otto Loewi identified acetylcholine as the first neurotransmitter (only he called it something else). What two important anatomical structures did he use in his experiment, and what effect was elicited on the effector structure by stimulation of the efferent pathway structure?
9. A specific neurotransmitter is not inherently excitatory or inhibitory. What, then, determines whether or not a neurotransmitter will have excitatory or inhibitory effects? Give an example of a neurotransmitter (and its target cells) that can be both excitatory and inhibitory.
10.If one observes small dense-cored vesicles in a transmission electron micrograph of an axon terminal, what type of neurotransmitter is probably contained in those vesicles? State the three subtypes of this neurotransmitter type and an exemplar molecule of each subtype.
11.What broad category of neurotransmitter would one expect to find in the terminals of long axons? What about local circuits? Why?
12.What results of ischemia, in relation to the neurotransmitter glutamate, contribute to excitotoxicity? How does excitotoxicity contribute to postsynaptic cell death? How might one treat excitotoxicity?
13.Neurotransmitters themselves are difficult to identify within the axon terminal. Rather, many neurons are identified as releasing a particular neurotransmitter by testing positive for an enzyme that helps to produce or process the neurotransmitter in question. What method would an experimenter use to identify such an enzyme? Give two specific examples of such a procedure being used.
14.Why are Klonopin and Rohypnol regularly used as the so-called "date rape" drugs?