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Homework answers / question archive / 1) A)Why are glycine modulatory site agonists, glycine transporter inhibitors, and serine racemase enhancers considered potential therapeutic adjuncts to antipsychotic drugs? How do they work?B)Describe the therapeutic potential of antiinflammatory drugs

1) A)Why are glycine modulatory site agonists, glycine transporter inhibitors, and serine racemase enhancers considered potential therapeutic adjuncts to antipsychotic drugs? How do they work?B)Describe the therapeutic potential of antiinflammatory drugs

Psychology

1) A)Why are glycine modulatory site agonists, glycine transporter inhibitors, and serine racemase enhancers considered potential therapeutic adjuncts to antipsychotic drugs? How do they work?B)Describe the therapeutic potential of antiinflammatory drugs. C)What is the treatment approach called NAVIGATE, and what are its benefits?

2) A)Why are “real-world” clinical trials important, and how do they differ from the usual well-controlled drug development trials? What did the CATIE study demonstrate? B)In what three ways have researchers attempted to enhance cholinergic function to treat cognitive symptoms of schizophrenia? C)Describe the two approaches for enhancing PFC DA function.

3) A)What are the benefits and risks of the broad-spectrum antipsychotic clozapine? B)Discuss the metabolic side effects and cardiac arrhythmias caused by some of the broadspectrum antipsychotics. C)What are the possible neurochemical explanations for the atypical effects of clozapine?

4) A)List side effects of antipsychotics and their neurochemical basis. B)All the antipsychotics block D2 receptors except aripiprazole. Describe its mechanism of action. C)What is the principal benefit of the “atypical” antipsychotics? Describe the three general approaches used to develop those drugs.

5) A)Summarize the dopamine hypothesis of schizophrenia, and provide several pieces of evidence. B)How does the neurodevelopmental model attempt to explain the positive and negative symptoms? C)How does glutamate regulate mesocortical and mesolimbic neurons? What seems to be responsible for the hypoglutamate function?

6) A)How can galanin cause depression and also have antidepressant effects? What is its relationship to other antidepressant agents? B)Provide evidence to suggest that exercise has antidepressant effects. C)Describe the effectiveness of lithium for bipolar disorder, as well as its side effects. Describe one signaling cascade that may be responsible for the drug’s ability to modify both the highs and the lows of mood.

7) A)What role does NE play in antidepressant action? What is the role of NE/5-HT interaction? B)How do the structural and functional abnormalities in the brains of depressed individuals prompt the formulation of the glucocorticoid hypothesis? The neurotrophic hypothesis? C)Describe the mechanism of action of MAOIs. How does their mechanism of action explain the occurrence of their major side effects?

8) A)Summarize the central characteristics of major depressive disorder and bipolar disorder. B)Provide evidence for a genetic contribution to affective disorders. C)Describe the HPA axis, including its negative feedback mechanism. What are the three most consistent neuroendocrine abnormalities found in clinically depressed patients?

9) A)What are the principal therapeutic uses of BDZs? B)What are the advantages of BDZs compared with other sedative–hypnotics? What are the drugs’ side effects? C)How do GABAA receptor subunit–selective drugs target specific symptoms such as insomnia? Anxiety? Reinforcement?

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