neurosci 3.2

Receptors, Reuptake Proteins, and the Termination of NT Action
12. Describe the “life cycle” of the neurotransmitter and be able to identify and describe the function of all the
proteins that affect it (i.e., reuptake protein, postsynaptic receptor, degradative enzyme, and autoreceptor
proteins) on a drawing of the synapse. Do similar mechanisms exist for neuropeptides?
13. What are the three functions of autoreceptors and how does the location of autoreceptors on the neuron
determine their functions?
14. List the ways in which a neurotransmitter’s (NT) or a neuropeptide’s action can be terminated.
15. Why is it important to have active mechanisms that terminate NT and neuropeptide action?
16. Which four requirements have to be met by a neurochemical for it to be considered a NT/neuropeptide?
Techniques
17. How do detection techniques (i.e., microdialysis, FSCV, fiber photometry) measure the levels of
NT/neuropeptides?
18. How do receptor imaging texhniques (i.e., PET, photoactivated receptor visualization) work?
19. What are the advantages and disadvantages of each of the above technique?
20. What exactly is measured in receptor binding assays, in situ hybridization, RNAScope, Western blot and
hat are the advantages and disadvantages of each?
21. Know and understand the terms indicated in color font on the slides (e.g., total, specific, nonspecific,
receptor affinity, Scatchard plot, titration plot, Bmax, Kd) and be able to use the plots to deduce information
about affinity and receptor number?
22. What are full and partial direct agonists, indirect agonist, direct/competitive and indirect/non-competitive
antagonist, inverse agonists, and positive/negative allosteric modulators? Be able to categorize drugs
based on a description of where they bind and what they do there.
23. What does drug selectivity, efficacy, potency, refer to and how can you determine which of two drugs has
greater selectivity, efficacy, potency, or safety on a dose response curve? Know and understand the
terms indicated in color on the slides (ED50, TD50, EC50, and TI, LD50).
24. What is the deference between receptor knock-out versus knock-down and which techniques can
produce these changes in receptor expression?
25. Which techniques provide causal information about the function of NTs/receptors (i.e., pharmacology,
gene manipulations, optogenetics, and chemogenetics), how do they work and what are their advantages
and disadvantages?
26. What is the difference between an opsin vs a DREADD and what makes them inhibitory or excitatory?
27. What is behavioral pharmacology? How does can the drug discrimination paradigm permit the
characterization and categorization of novel drugs and the study of normal and pathological brain
function?