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1) A)Discuss the mechanism of action underlying caffeine’s effects on behavior

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1) A)Discuss the mechanism of action underlying caffeine’s effects on behavior. Include in your answer a description of the adenosine signaling system, including the source of neurotransmitter-related adenosine, the principal receptors for this substance, and interactions between adenosine and dopamine signaling. B)What is the difference between phytocannabinoids and endocannabinoids? List two examples from each category.

2) A)What is meant by the term gliotransmission? Which kind of glial cell has been implicated in this process?

B)Discuss (a) the function and cellular expression of excitatory amino acid transporters and (b) the interplay between neurons and glial cells in the regulation of glutamate metabolism and signaling.

3) A)Show the reactions for glutamate interconversion with glutamine, including the name of the enzyme catalyzing each reaction. B)Describe the function of vesicular glutamate transporters, including which ones are most widely expressed in the brain. Provide an example of co-expression of a VGLUT with a vesicular transporter for a different transmitter or group of transmitters. What is the functional significance of such co-expression?

4) A)Discuss the underlying rationale for the idea of using nicotinic or muscarinic allosteric modulators in the treatment of Alzheimer’s disease or other neuropsychiatric disorders involving deficits in cognitive functioning. B)What is meant by the terms parasympathomimetic and parasympatholytic agents? List examples of drugs belonging to these categories along with their physiological effects and medicinal or other uses.

5) A)Describe the locations and functional roles of muscarinic receptors expressed by peripheral organs and glands. Include in your answer a discussion of the so-called dry mouth effect. B)Discuss the role of pancreatic M3 muscarinic receptors in the control of insulin secretion and the involvement of this receptor subtype in the development of insulin resistance that accompanies the administration of certain antipsychotic drugs.

6) A)Discuss the molecular structure, signaling mechanisms, and localization of muscarinic cholinergic receptors in the brain. B)Discuss the role of M5 muscarinic receptors in the control of dopaminergic cell firing and the rewarding and reinforcing effects of abused drugs. Include relevant experimental findings in your answer.

7) A)A nicotinic receptor complex can be in one of three different states: open, closed, and desensitized. Describe the properties of each state, including whether agonist is bound or not as well as the state of the receptor channel. B)The text discusses three different drugs that act on nicotinic receptors: succinylcholine, mecamylamine, and d-tubocurarine. For each compound, indicate whether it is an agonist or an antagonist, and briefly discuss the effects of administering the drug (including any current medical use).

8) A)Describe the localization and functions of ACh in the peripheral nervous system. B)Name and indicate the location of the principle cholinergic cell groups in the brain. Discuss the role of the BFCS in cognitive function, including relevant experimental findings. C)Describe the molecular structure and signaling mechanism of nicotinic cholinergic receptors.

9) A)By what mechanism is ACh taken up and stored in synaptic vesicles? Name a drug that interferes with vesicular ACh uptake, and describe the effects of this drug on cholinergic transmission. B)List and discuss the effects of toxins that either stimulate or inhibit ACh release. Include in your answer the therapeutic applications of toxins that inhibit the release of this neurotransmitter.

10) A)What are the chemical reactions involved in ACh synthesis and breakdown? Include the names of the enzymes catalyzing each reaction. Which of these enzymes is used as a biochemical marker for cholinergic neurons? B)Briefly discuss the factors that regulate the rate of ACh synthesis. Are there any current therapeutic interventions targeting the process of ACh synthesis?

11) What is meant by the “serotonin deficiency” hypothesis of aggression? Discuss experimental evidence that either supports or contradicts this hypothesis. Which kinds of aggressive behavior appear to be most clearly related to the serotonergic system?