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!

In the background section the authors wrote “Immediately after TBI, there is a rapid and pathophysiological increase in extracellular glutamate (Glu).” Where does Glu come from? (1 point)

What controls extracellular Glu? (1 point)

In the background section the authors wrote “Immediately after TBI, there is a rapid and pathophysiological increase in extracellular glutamate (Glu). This causes neuronal damage and leads to motor and cognitive functional deficits.” What kind of damage was done? Be specific. (1 point)

Quote something from the article as evidence that your answer to question 3 is correct? (1 point)

In the MRI and 1H-MRS acquisition section of the methods section the authors wrote “The NAA peak was referenced to 2.02 ppm, [10]. We detected and quantified the NAA peak at 2.02 ppm and 2.50 ppm, the Glu peak at 2.3 ppm, and the creatine peak at 3.03 ppm and 3.93 ppm in mouse brains.” Why didn’t the authors mention a NAAG peak? (1 point)

In the 1H-MRS examination section of the results section the authors wrote “The NAA/Cr ratio of the ipsilateral hippocampus in GCP II-KO mice was significantly lower than that of the contralateral side and the two sham CCI groups.” Why was the NAA/Cr ratio in GCP II-KO mice lower than the two sham CCI groups? (1 point)

In the brain water-content section of the results section the authors wrote “Moreover, the KO + CCI group had a significantly lower brain water-content than did the WT + CCI group. Therefore, the neuroprotective effect of GCP II-KO against CCI was verified in this study.” Why would the KO + CCI group have lower brain water? (1 point)

In the discussion section the authors wrote “At the mGluR3, the escape of abundant excitotoxic Glu is partially inhibited by NAAG, which acts as a potent agonist of the receptor.” How specifically does NAAG inhibit Glu? Be specific. (1 point)

Where does the inhibition mentioned in question 8 occur? You have to be more specific than saying “in the cell.” (1 point)

How do you know that your answer to question 9 is correct? (1 point)

In the discussion section the authors wrote “This requires energy consumption and changes in the transmembrane ion gradients, leading to neuronal depolarization, which induces an increased influx of Na+ and Ca2+ into the cell. The concomitant energy failure injures the Na+/K+ ATPase pump system, and the Na+ cannot be compensated. Consequently, water enters into the cell and the cell volume increases.” Why does water enter the cell? (1 point)