Neuroscience Annotated Bibliography Example

Annotated Bibliography

1. American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (DSM-5®). American Psychiatric Pub.

The Diagnostic and statistical manual of mental disorders (5th ed.) is used by psychologists to diagnose mental disorders and there this manual will be used to reference diagnostic criteria for bipolar disorder. This manual also could shed some light on any known etiologies of the disorder.

Main take away: Will be used in paragraph 1 when describing Bipolar disorder and the difference between Bipolar I and Bipolar II.

2. Bechtholt-Gompf, A. J., Walther, H. V., Adams, M. A., Carlezon, W. A., Öngür, D., & Cohen, B. M. (2010). Blockade of astrocytic glutamate uptake in rats induces signs of anhedonia and impaired spatial memory. Neuropsychopharmacology, 35(10), 2049-2059.

In this paper, Berchtholt-Gompf and colleagues (2010) investigated the behavioral expressions of glutamate by blocking the central astrocytic glutamate uptake with the astrocytic glutamate transporter (GLT-1) inhibitor dihydrokainic acid (DHK) in rat models. DHK elevated ICSS thresholds, a depressive-like effect that could reflect reduced sensitivity to reward (anhedonia) or increased aversion (dysphoria). DHK treatment did not establish conditioned place aversions, suggesting that this treatment does not induce dysphoria. DHK robustly increased c-Fos expression in the dentate gyrus and hippocampus and also was shown to impair spatial memory in the Morris Water Maze.

Main take away: Decreasing glutamate increases anhedonia and impairs spatial memory in rat models and also suggests a causal direction for the relationship between glutamate and depressive symptoms.

3. Song, D., Li, B., Yan, E., Man, Y., Wolfson, M., Chen, Y., & Peng, L. (2012). Chronic treatment with anti-bipolar drugs causes intracellular alkalinization in astrocytes, altering their functions. Neurochemical research, 37(11), 2524-2540.

Song and colleagues (2012) have a paragraph in this review paper discussing the role of glutamate signalling in bipolar disorder and this has a lot of background information about how astrocytes are involved in regulating glutamate homeostasis. This review paper also references other papers that have investigated the role of glutamate in bipolar disorders, and therefore this could be a good paper to use to find more references. This paper also suggests that glutamatergic signaling is increased during manic phases and decreased during depressive phases of bipolar disorder which could be useful for guiding my hypothesis.

Main take away: This paper will be really useful for the background information for the second paragraph about astrocytes and glutamate in general. This paper could also be useful in my conclusion (paragraph 5) to show that other researchers have proposed similar hypotheses.

4. Connolly, K. R., & Thase, M. E. (2011). The clinical management of bipolar disorder: a review of evidence-based guidelines. The primary care companion for CNS disorders, 13(4).

In this paper, Conolly and colleagues (2011) discuss the different episodes present in bipolar disorder and review the most effective treatments for each of these episodes. Traditional anti-bipolar drugs such as Lithium salts and Carbamazepine are FDA approved for treatment of acute manic episodes, whereas quetiapine and olanzapine/fluoxetine combination are FDA approved treatments for acute depression.

Main take away: Different drugs for different episodes suggests that there are differing mechanisms for each type of episode, and therefore any papers investigating the effects of traditional anti-bipolar drugs are really only related to manic symptoms. This will be useful in both paragraph 3 and 4.

5. Peng, L., Li, B., Du, T., Wang, F., & Hertz, L. (2012). Does conventional anti-bipolar and antidepressant drug therapy reduce NMDA-mediated neuronal excitation by downregulating astrocytic GluK2 function?. Pharmacology Biochemistry and Behavior, 100(4), 712-725.

This paper provides a lot of background on how glucose is involved in the production of glutamate, and therefore may be helpful in explaining why Jia et al. (2018) research on the role of glycogen in BD is relevant. Peng and colleagues (2012) review research that shows chronic anti-bipolar drug treatment reduces expression of GluK2 in astrocytes. This suggests that antibipolar drugs inhibit glutamate signalling by inhibiting increase in [Ca2+]i by glutamate, and there indicates that there is increased glutamate signalling in BD. In contrast antidepressant drugs are associated with increases in expression of GluK2 in astrocytes.

Main take away: If anti-bipolar drugs are primarily used to treat the manic episodes, this supports the hypothesis that there is an increase in glutamate signalling during manic episodes and decreases in glutamate signalling during depressive episodes. This could be used in either paragraph 3 or 4, but most likely will be used in the conclusion paragraph.

6. Brennan, B. P., Hudson, J. I., Jensen, J. E., McCarthy, J., Roberts, J. L., Prescot, A. P., ... & Öngür, D. (2010). Rapid enhancement of glutamatergic neurotransmission in bipolar depression following treatment with riluzole. Neuropsychopharmacology, 35(3), 834-846.

Brennan and colleagues (2010) were able to show that the drug riluzole (a glutamate release inhibitor) rapidly increases Gln/Glu ratios (as early as day 2) in human participants —suggesting increased glutamate–glutamine cycling. This drug was also associated with decreasing depressive symptoms, and therefore this shows that increasing glutamate early on (even if Gln/Glu ratios decrease by 6 week) is related to later decreases in depressive symptoms.

Main take away: Rapid increases in glutamate may be involved in treatment of acute depressive episodes in bipolar disorder, and will be used in paragraph 4.

7. Shen, Y. C. (2018). Treatment of acute bipolar depression. Tzu-Chi Medical Journal, 30(3), 141.

As many typical antidepressants such as SSRIs can trigger manic episodes, psychiatrists use alternate treatments for acute depressive episodes in bipolar disorder. This paper review approved treatments for acute bipolar depression (olanzapine/fluoxetine combination, quetiapine, and lurasidone) and nonapproved agents and nonpharmacologic treatment (lamotrigine, antidepressants, modafinil, pramipexole, ketamine, and electroconvulsive therapy) used to treat these acute depressive episodes.

Main take away: Treatments for depressive and manic episodes differ, and so investigate these drugs for paragraph 4. This will be useful in the first paragraph on background for bipolar disorder.

8. Yüksel, C., & Öngür, D. (2010). Magnetic resonance spectroscopy studies of glutamate-related abnormalities in mood disorders. Biological psychiatry, 68(9), 785-794.

This study provides contradictory evidence for the hypothesis that glutamate is dependent on the disease state of the patient, as 6 of the 12 studies reviewed found elevated Glx levels in BD patients regardless of disease state. It does however suggests that elevations in glutamate may be dependent on the brain region.

Main take away: Glutamate functioning in specific brain regions could be important in determining which symptoms manifest.

9. Gigante, A. D., Bond, D. J., Lafer, B., Lam, R. W., Young, L. T., & Yatham, L. N. (2012). Brain glutamate levels measured by magnetic resonance spectroscopy in patients with bipolar disorder: a meta‐analysis. Bipolar disorders, 14(5), 478-487.

Like Yüksel & Öngür (2010), this meta-analysis found elevated Glx levels in BD compared to healthy subjects when all brain areas were combined, and this remained true in medicated and non‐medicated patients, and in frontal brain areas in adults. The researchers however could not rule out disease state.

Main take away: Increase in glutamate functioning in manic episodes could be greater than the decrease in glutamate functioning during depressive episodes. Emphasizes that glutamate however does play an important role in the pathophysiology of BD and could be a potential treatment target.

10. Öngür, D., Jensen, J. E., Prescot, A. P., Stork, C., Lundy, M., Cohen, B. M., & Renshaw, P. F. (2008). Abnormal glutamatergic neurotransmission and neuronal-glial interactions in acute mania. Biological psychiatry, 64(8), 718-726.

In this study, the researchers found increased Gln/Glu ratios during mania. This paper also provides some background for how cerebral metabolic rate is related to specific symptoms of mania including insomnia and racing thoughts.

Main take away: Increase in glutamate functioning in manic episodes - useful for paragraph 3 on glutamate and manic symptoms.

11. Dager, S. R., Friedman, S. D., Parow, A., Demopulos, C., Stoll, A. L., Lyoo, I. K., ... & Renshaw, P. F. (2004). Brain metabolic alterations in medication-free patients with bipolar disorder. Archives of general psychiatry, 61(5), 450-458.

In this paper, the researchers found elevated levels of GLx and gray matter lactate in patients with BD when compared to control participants. The authors hypothesized that disturbance in the brain energy metabolism, in particular the change in the energy redox state from oxidative phosphorylation to glycolysis, might explain the changed Glx level.

Main take away: This could be useful in the discussion paragraph or in the manic symptoms paragraph (paragraph 3) to describe what causes the change in glutamate functioning.

12. Ogden, C. A., Rich, M. E., Schork, N. J., Paulus, M. P., Geyer, M. A., Lohr, J. B., ... & Niculescu, A. B. (2004). Candidate genes, pathways and mechanisms for bipolar (manic–depressive) and related disorders: an expanded convergent functional genomics approach. Molecular psychiatry, 9(11), 1007-1029.

Ogden and colleagues (2004) investigated candidate genes that underlie bipolar disorder and one of the key candidate generes was DARPP-32. The researchers explain that GLUL (glutamine synthase) directly regulates DARPP-32 activity by regulating glutamate metabolism. They also found a number of glutamate-related candidate genes and therefore this suggests that glutamate could play a vital role in the pathophysiology of BD.

Main take away: Glutamate is important in the pathophysiology of the disease and therefore this paper could be used in the conclusion. Also glutamate could play other roles in the pathophysiology of the disease e.g. by regulating the gene expression of candidate genes that increase risk for the disorder.

13. Liu, Z., Song, D., Yan, E., Verkhratsky, A., & Peng, L. (2015). Chronic treatment with anti-bipolar drugs suppresses glutamate release from astroglial cultures. Amino Acids, 47(5), 1045-1051.

The researchers found that exposure of astroglial cultures to Li+, CBZ and VPA (antipsychotic drugs) for 2 weeks led to a significant (more than 2 times) inhibition of glutamate release but it did not affect intracellular glutamate content in astrocytes, indicating that the release mechanisms were the primary targets. Inhibition of glutamate release may alleviate the hyperactivity of the glutamatergic transmission in the brain of patients with bipolar disorders.

Main take away: This could be used for paragraph 3 to show that antipsychotic drugs decrease glutamate release, therefore suggesting that there is a therapeutic effect of decreasing glutamate during manic episodes.

14. Bélanger, M., Allaman, I., & Magistretti, P. J. (2011). Brain energy metabolism: focus on astrocyte-neuron metabolic cooperation. Cell metabolism, 14(6), 724-738.

Astrocytes are responsible for the replenishment of brain glutamate, as they are the only neural cell type expressing pyruvate carboxylase, a key enzyme in the main anaplerotic pathway in the brain. This there means that they can synthesize glutamate from glucose.

Main take away: This could be used for paragraph 2 to describe astrocytes' role in glutamate neurotransmission, and also supports information about why glycogen, glucose and cellular metabolism are impacted in BD.

15. Weis, S., Llenos, I. C., Dulay, J. R., Verma, N., Sabunciyan, S., & Yolken, R. H. (2007). Changes in region-and cell type-specific expression patterns of neutral amino acid transporter 1 (ASCT-1) in the anterior cingulate cortex and hippocampus in schizophrenia, bipolar disorder and major depression. Journal of neural transmission, 114(2), 261-271.

The researchers found there was a significant decrease in the intensity and the density of ASCT1-ir neurons, a transporter that mediates glutamate efflux, in the ACC. They also found reduced neuronal immunoreactivity in the hippocampus.

Main take away: This could be used for paragraph 5 to give further evidence that glutamate is implicated in bipolar disorder.