PG Pharma 2

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Jun 21, 2024

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Biopsychology Prep Guide: Pharma 2 Materials: Pinel Barnes, Ch.18 pages 473-481, Ch.4 Page 78 “The Lizard, a Case of Parkinson’s Disease", Ch.10 pages 252-253 (section 10.9) NOTE: I am drawing from different sections of the book to give you a more comprehensive picture of the role(s) of dopamine in disorders. I would suggest reading all of the material before answering the questions below! Be sure to draw on previous knowledge! 1. Briefly summarize each revision of the dopamine theory of schizophrenia in your own words, so that your grandmother can understand it. Originally, the dopamine theory suggested that schizophrenia is caused by the overproduction of dopamine in the brain because antipsychotic drugs were able to lower dopamine levels. Later research showed that effective antipsychotics bind tightly to dopamine receptors, especially D2, leading to a major revision made to focus on hyperactivity at D2 receptors rather than focusing on the ability for antipsychotic drugs to lower dopamine levels. a. Why do we have this theory? The dopamine theory suggests that schizophrenia is liked to problems with dopamine and is supported by medication effects and brain scans. b. What were the first two antipsychotics used to treat schizophrenic patients, and how do they differ in function? Reserpine and chlorpromazine both antagonize transmission at dopamine synapses; reserpine was used to decrease dopamine by breaking down the synaptic vesicles and chlorpromazine binds to dopamine receptors. c. How was haloperidol different from most (phenothiazine) antipsychotics, and what did learning this contribute to our understanding of the neural basis of schizophrenia? Haloperidol was one of the most potent antipsychotic drugs and had a low affinity for dopamine receptors leading to the understanding that schizophrenia is caused by hyperactivity at D2 receptors, rather than at dopamine receptors in general. 2. Suppose you are a psychiatrist and you suspect a client may be affected by Schizophrenia. a. What is the distinction between positive and negative symptoms of this disorder? Positive symptoms tend to represent an exaggerated typical function and negative symptoms tend to represent a reduction or loss of typical function. b. What are possible negative symptoms they might exhibit? Diminished emotional expression (affective flattening), reduction or absence of motivation (avolition), and tendency to remain motionless, often in awkward positions for long periods (catatonia). c. Why do these symptoms (positive OR negative) make schizophrenia a difficult disease to treat? The symptoms vary so greatly that it is difficult to make a treatment plan that works to mediate psychosocial, neurological, and bodily functioning issues. not everyone has the same symptoms. d. Can schizophrenia be entirely attributed genetics (provide at least one piece of evidence why/why not)? Schizophrenia cannot be entirely attributed to genetics because there is evidence of environmental factors like early birth complications, maternal stress, and childhood adversity playing a significant role in the development of the disease. e. How might epigenetics contribute to the development of schizophrenia? Epigenetics might modify gene expression in response to early developmental experiences which can alter neurological paths in individuals genetically susceptible to the disorder. 3. Pretend you are a doctor treating a patient suspected of having schizophrenia, and you order an fMRI of the patient. a. What differences would you look for in the brain that may lend support to the schizophrenia diagnosis? I might look for a significantly smaller than normal hippocampus, amygdala, thalamus, nucleus Accumbens; general reduction in brain size and continuous brain changes/alterations. b. How would your fMRI differ if your patient had Parkinson’s disease? I might look for continuous brain changes/alterations especially in the midbrain where the substantia nigra is going through degeneration.

Biopsychology Prep Guide: Pharma 2 c. You then prescribe a dopamine antagonist for treatment. Based off what you already know about the functions of dopamine, and disorders involving dopamine, what physical effects do you think would occur if you prescribed an overabundance of the dopamine antagonist? An overabundance of the dopamine antagonist could lead to motor disturbances similar to symptoms of Parkinson’s disease; muscle stiffness, tremors, chance of cognitive impairment. 4. What are the main symptoms of Parkinson’s disease? Tremors (pronounced during inactivity), muscular rigidity, slow and difficult movement, and a masklike face. pain and depression develop before the motor symptoms become more severe. a. Which dopaminergic pathway is being affected? nigrostriatal pathway (midbrain neurons to the striatum) b. What is happening to the substantia nigra? widespread degeneration of the neurons in this area c. Why is dopamine an ineffective treatment? Dopamine cannot effectively cross the bbb when administered orally and it administering pure dopamine does not directly aid in adjusting dopamine depletion. d. What are patients prescribed instead and how does this help avoid the problems of pure dopamine? Patients are prescribed L-Dopa which is a chemical that can pass through the bbb and helps the body synthesize dopamine. - but its temporary effects become less and less effective with continued use and eventually its side effects outweigh its benefits 5. Describe deep-brain stimulation and provide an explanation (based off what you have already learned in class) for why this treatment might help patients with Parkinson’s disease. Deep-brain stimulation is a treatment in which low-intensity electrical stimulation is continually applied to an area of the brain through a stereotaxically implanted electrode. This treatment might help patients with Parkinson’s disease because it can target specific brain regions to help regulate motor functioning and provide symptom relief. a. Why might it be considered controversial? The effectiveness of deep brain stimulation slowly declines over the course of a few months and once stimulation turns off, therapeutic improvements dissipate causing side effects like cognitive, speech, and mobility problems.

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