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Understanding Neuron Membrane Potentials and Neurotransmission, Exams of Neuroscience

The concepts of neuron membrane potentials, including resting potential, action potentials, and synaptic potentials. It also covers the role of ions such as k+ and na+, and the effects of removing certain ions from the external medium. The document further discusses the voltage sensitivity of k+ conductance and the differences between unmyelinated and myelinated axons. Hodgkin and huxley's discovery of ion channels and the techniques of voltage and patch clamping are also touched upon.

Typology: Exams

2023/2024

Available from 03/26/2024

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Download Understanding Neuron Membrane Potentials and Neurotransmission and more Exams Neuroscience in PDF only on Docsity! FUNDAMENTAS OF NEUROSCIENCE REVIEW EXAM Q & A 2024 What is the magnitude of a typical neuron’s resting membrane potential? Why do neurons and other cells have a negative resting membrane potential? Typical resting membrane potential Is around -80 to -60 mV This is because they have more K+ inside the cell and more Na+ outside of the cell, giving them a negative potential. Negative due to the high relative K+ permeability, and high internal concentration of K+. Explain the difference between action potentials (all-or-none) and synaptic potentials (graded). Synaptic potentials are generally smaller depolarizations that don’t necessarily generate an action potential while an action potential is the summation of graded potentials that occurs when the neuron is depolarized past its threshold potential. Distinguish between hyperpolarization and depolarization. Hyperpolarization is the influx of negative charge, making the membrane potential more negative. Ex. Is the efflux of K+ Depolarization is the influx of positive charge, making the membrane potential more positive. Ex. The influx of Na+ Suppose you are recording action potentials from a neuron. How would the action potential be affected if you remove Na+ from the external medium? What if you remove external K+ instead? . If you remove Na+ you probably wont have an action potential because they occur when sodium ions rush into the membrane causing depolarization. Youre early current will be Na+ rushing out of the cell with the gradient. . If you remove external K+, it will make the membrane resting more negative making it have a higher threshold. Also, you will have more K+ efflux during the second current. How does the voltage sensitivity of K+ conductance contribute to the action potential? K+ voltage gated channels only open after significant depolarization, and this opening of K+ channels causes the second current we see with an efflux of K+ returning the nerve cell back to its resting potential. Do unmyelinated axons carry action potentials? Draw a diagram to help explain the regenerative property of the action potential, using the concepts of active and passive current flow. . yes they do but it is much slower and much more inefficient because channels need to open and close at every section of the axon. What is the purpose of myelin? Explain how myelin speeds the conduction of the action potential. . It speeds up and insulates the axon and prevents leakage of axons. Why don’t action potentials turn around and go back up the axon? . Na+ channel inactivation Why did Hodgkin and Huxley surmise that neuronal membranes must have ion channels? What properties did they think ion channels would have? What properties did they not anticipate? . they knew ion channels had to be voltage dependent, allow a large influx of ions, be selective to ions, pass them through the gradient What are the voltage and patch clamping techniques useful for? . They are very good for determining the cellular milleu of the neuron. You can measure the activity of the neuronal membrane as a whole (voltage clamp) or individual ion channels (patch clamp). You can introduce different chemical environments and measure how the cell reacts to it, etc. What criteria define a neurotransmitter? . 1. NTs need to be stored in a sequestered form (i.e. small clear-core or large dense- core vesicles) in the presynaptic terminal. Release of the NT must be Ca2+ dependent. . 2. Applying a mimicked form of the transmitter should elicit the same effect at the postsynaptic effect as a natural release. . 3. Precursor and enzymes that can synthesize the NT must be present at the synaptic terminal. Enzymes needed to synthesize NTs are produced in cell body and slowly transported to nerve terminal (via slow axonal transport). NT is synthesized in cytoplasm of presynaptic terminal. Neuropeptides are manufactured in cell body of neuron and therefore travel in their large dense-core vesicles via fast axonal transport. . 4. Mechanism to inactivate the transmitter, i.e. a catabolic enzyme system or active reuptake system, must be present in the presynaptic terminal or adjacent. This leads to consistent release and reuptake of the NT. . 5. Drugs that alter the transmitter’s synthesis, release, action, reuptake, or degradation should have the same effect in vivo. . What is the significance of the quantal nature of MEPPs? What is the evidence that EPPs are composed of MEPPS? . MEPP’s (miniature end plate potentials) – discovered by Katz, he noticed that there were spontaneous release of NT into the cleft, that were much smaller than regular EPP’s. He said that this was due to the spontaneous binding of single vesicles to the membrane. . Quantized because each MEPP can only cause a certain potential depending on how much NT is stored inside of it. . Evidence, when stimulated, the muscle cell showed a large EPP which was the summation of many vesicles releasing NT at the same time, or the summation of many MEPPs. Summarize the experimental evidence that synaptic vesicles are recycled in the axon terminal. . Molecules like clathrin bind to the bound vesicle and enwrap it causing it to reform and close, and go back into the endosome to be reprocessed and filled with NT again. It has been demonstrated that a rise in presynaptic Ca2+ is necessary and sufficient for neurotransmitter release. What experimental evidence supports the claim that Ca2+ is necessary and sufficient? . Kats showed that blocking of Ca2+ past a certain threshold level or the sequestering of extracellular level of a neurotransmitter, “putative” neurotransmitter, “the dose makes the drug”. True or False: All told, there appear to be more than 100 different neurotransmitters in the brain. Two major second messenger systems linked to metabotropic neurotransmitter receptors are the cAMP system and the phosphoinositide system. Please compare the main steps in these second messenger systems. 2+ . Why is it so important to keep Ca levels low inside the cell, and how is this accomplished? . Ca2+ is used as a 2nd messenger and could also cause unessary release of NT. Use Ca2+ pump plus Ca/Na exchanger Protein kinases and phosphatases are major targets of second messenger systems. Why is it so important to regulate protein phosphorylation? . 2nd messenger system. Kinases tend to activate proteins and channels and cause effects while phosphatases tend to deactivate proteins and other molecules Define the following terms and give examples of each: amplification of neurotransmission cell signaling moleculesreceptorseffector proteins second messengers later effectors heterotrimeric G-proteins transcription factors immediate early genes The nervous system is known for its plasticity (modifiability), or ability to show enduring changes in response to environmental changes. This typically involves changes in gene expression. Please describe how neurotransmission can lead to changes in gene expression. Other terms: signal transduction; chemical signaling; paracrine; endocrine; synaptic transmission; cyclic nucleotides; cAMP; cGMP; adenylyl cyclase; guanylyl cyclase; CRE; c-fos What are the relative merits of phasic (rapidly adapting) versus tonic (slowly adapting) receptors? . Rapidly adapting is good when your environment is changing rapidly and you need to adapt to it. . Tonic (slowly adapting) is better when your environment is constant and you don’t need to quickly adapt. Better for determining things like size, etc. What is proprioception? Name five kinds of proprioceptors/mechanorceptors and their properties. Determining the orientation of your body in space. Merkels – less sensitive but more spatial resolution than merkels – slow acting Meisnerrs – more sensitive than merkels but less spatial resolution – fast acting Pacinian – deep mechanosensation, vibrations Free Nerve Endings – pain + temperature Ruffini – stretch representation of the actual physical stimulus. Do you agree? Please explain in terms of phantom limb and referred pain. Yes, in terms of phantom limb, even children born without limbs at birth still experience this syndrome and pain in their phantom limbs meaning that it is instilled in the brain without experience needed, distorted from actual physical stimuli. Referred Pain – ex. Heart damage can cause chest pain (angina) – this is because there may be convergent neurons with a pain signal that makes it seem like the pain is coming from one area. Due to a spinal injury, a patient lost pain and temperature sensation on the left half of his body from the waist down. Where was his injury? Where would you expect loss of tactile sensation in this patient? Tactile sensation loss would be on the right side of the body because it is crossed. Injury occurred on the Right half of his body. Mechanosensation – dorsal root column crosses at THALMUS – therefore ipsilateral sensory lost to spinal chord lesion Why do you have both rods and cones instead of just one type of photoreceptor? Rods – slow adapting, detect changes in light levels Cones – fast adapting, detect changes in colors Do you have more rods or cones in your retina? In your fovea? What accounts for the fact that your rods do not contribute to vision in daylight? Retina has more rods than cones Fovea has only cones and no rods Rods are very slow adapting and only are sensitive to changes in light levels Please be familiar with the five types of retinal neurons. Which layer is the outer nuclear layer? . Photoreceptors (Rods + Cones) – hyperpolarize to light (less glutamate), depolarize to
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