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- 3. What effect would pre-synaptic injection of the Ca²+ chelator EGTA have on a nanodomain vs. a microdomain synapse, respectively?1.A poison causes a drastic rise inE value with stimulation of the membrane.Thereafter membrane is slow to return towards resting membrane potential and levels off several millivolts above the threshold potential. This poison has likely affect which feature of the membrane? a) voltage gated na+ channels. b) voltage gated K+ channels. c) Na+/K+ Atp pump 2. All cell membrane demonstrate action potential if stimulated enough? True/False. 3. how many peaks are there in a compound action potential? a)2. b)4 c)6 d)8 4. Increasing the ionic concentration in the salt bridge results in E value increase to a point after which it plateeus. This is evidence brownian movement at work in the ionic solution that is keeping from energy flowing through the bridge with the fidelity that is seen in the metal bridge? True/ False 5. All cell membrane demonstrate action potential if stimulated enough? True or False.Clostridium tetani toxin blocks the exocytosis of GABA. A. What anatomical part of a pre-synaptic neuron would be affected by this? B. How would a post-synaptic neuron’s likelihood of experiencing an action potential be affected by this toxin? C. Explain, using at least TWO of the following terms: threshold, depolarization, repolarization, hyperpolarization, summation, IPSP, EPSP, exocytosis
- 5.Myasthenia (muscle weakness)is characterized by damage in the transmission of neurotic impuise and decreased amount of acetylcholine due to autoimmune mechanisms. Prozerine is used for treatment of this disease.Specify the mechanism of this drug action. For this: 1)Write the reaction of acetylcholine degradation at neuromuscular junction. 2)What enzyme will be inhibited with prozerine? Name the class of this enzyme. 3)What is the mechanism of this enzyme inhibition?3) Acetylcholine binds to a GPCR on heart muscle, making the heart beat more slowly. The activated receptor stimulates a G protein, which opens a K+ channel in the plasma membrane, as shown in Figure 1. Which of the following would enhance this effect of the acetylcholine? (a) (b) (c) (d) Figure 1 addition of a high concentration of a non-hydrolyzable analog of GTP addition of a drug that prevents the a subunit from exchanging GDP for GTP mutations in the acetylcholine receptor that weaken the interaction between the receptor and acetylcholine mutations in the acetylcholine receptor that weaken the interaction between the receptor and the G protein11. Sodium, chloride, and potassium ions are involved in setting up voltages across neuronal membranes. a. Describe the equilibrium potential and resting membrane potential in your own words. How would you find the equilibrium potential of sodium? What else would you have to consider to find the resting membrane potential? b. How does the membrane potential change in response to opening selectively permeable chloride channels (assuming Ec is more negative than Vrest)? C. How does the membrane potential change in response to opening selectively permeable sodium channels instead (assuming Ena is more positive than Vrest)? d. Describe a situation in which chloride ions can result in the same change in membrane potential as the sodium ions in the question above.
- Which of the following does not contribute to propagation of action potentials? a. As the area outside the membrane becomes negative, itattracts ions from adjacent regions; as the inside of the membrane becomes positive, it attracts negative ions from nearby in the cytoplasm. These events depolarize nearby regions of the axon membrane. b. The refractory period allows the impulse to travel in only one direction. c. Each segment of the axon prevents the adjacent segments from firing. d. The magnitude of the action potential stays the same as it travels down the axon. e. Up to a limit, increasing the intensity of the stimulus increases the number of action potentials.Describe the contribution of each of the following to establishing and maintaining membrane potential: (a) the Na+K+ pump, (b) passive movement of K+ across the membrane, (c) passive movement of Na+ across the membrane, and (d) the large intracellular anions.3.) Signals are passed from axon to axon when neurotransmitter molecules are released from the presynaptic axon and diffuses across a small distance, called the synaptic cleft, to reach the post synaptic axon. If the neurotransmitter released by the presynaptic axon is dopamine and the diffusion distance across the synaptic cleft is 20 nm then how long will it take to pass the signal? The viscosity of the interstitial fluid in the synapse is 0.012 Pa*s. (You must look up dopamine properties to solve) Synapse Suiknce Facts aut Synaptic vesicle Voltage-gated Ca? /channel Presynaptic neuron Neurotransmitter molecules Synaptic cleft lon channel receptor Postsynaptic- neuron
- 4. Illustrate (draw) what an action potential might look like with the following voltage-gated channels present. Briefly explain why these changes may occur. a. Normal sodium voltage-gated channel and a potassium voltage-gated channel (delayed rectifier); classic action potential as seen with the squid giant axon Normal sodium voltage-gated channel and an A channel (KA voltage-gated channel) b. C. Mutant sodium voltage-gated channel ONLY, where the N-terminal inactivation particle is missing d. Mutant sodium voltage-gated channel, where the N-terminal inactivation particle is missing, plus a potassium voltage-gated channel (delayed rectifier)1. (a) In class thus far, we have focused our membrane transport energetics discussions on the transfer of K+ ions. Of course, in the cell there are other ions that contribute to the overall resting membrane potential (Autotal). To estimate the overall resting membrane potential for the predominant ions present in the cell, we must first calculate the individual resting membrane potential. Using the Nernst equation discussed in class, and the values provided below, calculate A for each ion. lon K+ Na+ Ca²+ CI- [ion] outside cell 6 mM 145 mM 4 mM 90 mM [ion] inside cell 145mM 8 mM 0.001 mM 6 mM1. Ionotropic GABA receptors are ligand-gated Cl channels which open during GABA-ergic signaling. a) Describe how under normal circumstances the opening of these channels leads to an IPSP. Do this in the context of Eci. b) Some cells in the body express a Na*/K+/2Cl cotransporter which pumps Cl- into the ICF. Where these pumps are present, the same GABA receptor is actually excitatory. Again, in the context of Ea describe how the same receptor would be excitatory in cells which actively pump Cl- into the ICF. You do not need to repeat information you provided in part (a)
