Other : EXAM 3 This exam has a total of 11 points. Each point corresponds to a numbered question. The numbered question is to be answered.



This exam has a total of 11 points. Each point corresponds to a numbered question. The numbered question is to be answered. The correct answer to a numbered question will give you one point. If the answer is partially correct, partial credit will be given as a decimal value. If the answer is incorrect, no credit will be given. If the question is unanswered, no credit will be given so it is better to guess than to leave a question blank. The number of points earned will be divided by the total number of points on the exam and multiplied by 100 to get your grade. Good luck!


  1. In the background section the authors wrote “High permeability of NMDARs to Ca 2+ makes them involved in synaptic plasticity, while their hyperactivation during ischemia or stroke causes neuronal Ca 2+ overload and apoptosis.” Is this high permeability pre or post the synaptic cleft? (1 point)


  1. How do you know that your answer to question 1 is correct? (1 point)


  1. In the background section the authors wrote “Ca 2+ -dependent desensitization of NMDARs represents a feedback regulation of the NMDAR open probability by the Ca 2+ entry into neurons.” What kind of feedback regulation is this? Positive or negative? (1 point)


  1. What one word in the quote of question 3 is evidence that your answer to question 3 is correct? (1 point)


  1. How do you know, or why is your answer to question 4 correct? (1 point)


  1. In the lithium inhibition of NMDA-elicited currents section of the results section the authors wrote “Previously, we demonstrated that the inhibition of NMDA-activated currents by Li + is Ca 2+ -dependent, because it could not be observed in the nominal absence of Ca 2+ in the external solution.” Why can’t inhibition of NMDA activated currents by Li not be observed in the absence of Ca 2+ ? (1 point)


  1. In the lithium inhibition of NMDA-elicited currents section of the results section the authors wrote “This requires some functional interaction between NCX and NMDARs that could occur if these molecules are located closely and interact within lipid nanoclusters or rafts.” Do interactions between NCX and NMDARs occur? (1 point)


  1. Quote something from the article as evidence that your answer to question 7 is correct. (1 point)


  1. In the lithium inhibition of NMDA-elicited currents section of the results section the authors wrote “This could be the case, if NCXs maintain low intracellular free Ca 2+ concentration in the close proximity of NMDARs, which prevents the development of Ca 2+ -dependent inactivation of NMDARs.” Quote something from the article that explains why low intracellular free Ca 2+ concentrations in close proximity of NMDARs would prevent the development of Ca 2+ -dependent inactivation of NMDARs. (1 point)


  1. In the calcium-dependent and –independent effects of cholesterol extraction on NMDARs section of the results section the authors wrote “In the absence of Ca 2+ in the external solution the ratio of amplitudes of NMDA-activated steady-state currents, recorded after and before 5 min MβCD treatment was 47 ± 6% (n = 6). The decrease of the steady-state amplitudes of NMDAR currents after the treatment is caused by the direct effect of the cholesterol extraction by NMDARs, because under these particular conditions the Ca 2+ -dependent desensitization was not observed.” Why was Ca 2+ -dependent desensitization not observed? (1 point)


  1. Why is Ca 2+ -dependent desensitization of NMDARs significantly greater when cholesterol was extracted? (1 point)

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