Exam 11: Brain Disorders

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In patients with Parkinson's disease, neurons in the SNc die. Based on the basic circuitry in Figure Q11-13, why does the absence of these neurons result in excessive activation of the inhibitory output neurons in the GPi/SNr? In patients with Parkinson's disease, neurons in the SNc die. Based on the basic circuitry in Figure Q11-13, why does the absence of these neurons result in excessive activation of the inhibitory output neurons in the GPi/SNr?   Figure Q11-13 Figure Q11-13

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Patients taking reserpine also experience symptoms of which disease?

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Mecp2 was knocked out only in GABAergic neurons. What do the results shown in Figure suggest about the actions of MeCP2? Mecp2 was knocked out only in GABAergic neurons. What do the results shown in Figure  suggest about the actions of MeCP2?   Figure Q11-37 Figure Q11-37

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An experiment discussed in Chapter 10 and shown in Figure shows in vivo single unit recordings from VTA dopaminergic neurons in a monkey trained to associate a light with a reward, juice. How does the enhancement of dopamine action of VTA neurons lead to addiction if the dopamine VTA pathway normally signals reward prediction errors? What is the pathway involved and what happens in addiction? An experiment discussed in Chapter 10 and shown in Figure shows in vivo single unit recordings from VTA dopaminergic neurons in a monkey trained to associate a light with a reward, juice. How does the enhancement of dopamine action of VTA neurons lead to addiction if the dopamine VTA pathway normally signals reward prediction errors? What is the pathway involved and what happens in addiction?   Figure Q11-31 Figure Q11-31

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Reserpine is used to treat schizophrenia and it acts by blocking vesicular monoamine transporters (VMATs). Which neurotransmitter systems are influenced by reserpine? Select all that apply.

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Rett syndrome is caused by mutation in an X-linked gene called MeCP2. Why does mutation of this one gene cause so many neurological defects?

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It has been difficult to develop drugs for brain disorders including AD. For example, many groups have tried to target γ-secretase. A. Why is γ-secretase a good target for Alzheimer's treatment? B. What is one reason, so far, that drugs targeting γ-secretase have not been successful?

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Most current anti-depressants are SSRIs. What is the result of SSRI action? Select all that apply.

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What evidence is there for systems other than dopaminergic systems that are altered in schizophrenia?

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What is the main pathological feature of prion diseases?

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How does Figure contribute to the evidence that the Aβ oligomer interferes with loss of memory in Alzheimer's disease? How does Figure  contribute to the evidence that the Aβ oligomer interferes with loss of memory in Alzheimer's disease?   Figure Q11-2 Figure Q11-2

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List three pieces of evidence that Aβ production contributes to Alzheimer's disease?

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You have discovered a potential new drug to treat schizophrenia that binds competitively to the dopamine D2 receptor. You perform a competitive binding assay to test the effectiveness of the drug action. What is the idea behind the assay and what result would give you a high affinity drug-receptor binding?

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Many neurodevelopmental disorders are associated with alternations in synaptic function. Why would alterations in synaptic function during development result in long-term changes in synaptic circuitry and behavioral deficiencies??

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In thinking about finding a treatment for ID, Rho-GTPases might be a target for therapeutic drugs. In general, why is this problematic?

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In Figure , if you were to conditionally restore MeCP2 protein to a MeCP2 knockout mouse at week 10, through removing a lox-stop allele with an inducible excision, how do you predict that would change the percent surviving animals? Justify your answer. In Figure , if you were to conditionally restore MeCP2 protein to a MeCP2 knockout mouse at week 10, through removing a lox-stop allele with an inducible excision, how do you predict that would change the percent surviving animals? Justify your answer.   Figure Q11-39 Figure Q11-39

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Reserpine is used to treat schizophrenia and it acts by blocking vesicular monoamine transporters (VMATs). Where does reserpine act in neurons and what happens to these neurotransmitters when the neurons are exposed to reserpine?

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What is one cellular/molecular basis for dopamine action on VTA leading to addiction?

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What are two pathological features of patients with Alzheimer's disease?

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There are many neurodegenerative diseases with many symptoms. List two common themes with these different diseases and two properties that make each disease unique. Psychiatric Disorders

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