Exam 12: Indirect Mechanisms of Synaptic Transmission

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In a cell with β-adrenergic receptors coupled to the cAMP second messenger system, what would happen to that signaling pathway if you blocked phosphodiesterases?

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B

In a cell with β-adrenergic receptors coupled to the cAMP second messenger system, what would happen to that signaling pathway if you added forskolin?

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E

Which experimental approach could provide evidence that norepinephrine uses the cAMP second messenger system to modulate calcium channels?

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A

An example of convergent signaling mediated by indirectly coupled receptors is…

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How are endocannabinoids synthesized, released, and used to modulate synapses?

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How many transmembrane domains do all G protein-coupled metabotropic receptors have?

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When comparing ionotropic and metabotropic receptors which of the following is true?

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Which protein is most commonly used by cells to bind cytoplasmic calcium and trigger biochemical events within the cell?

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How is the lifetime of activated G proteins controlled?

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How is nitric oxide synthesized?

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G proteins are activated when GDP is

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How many different types of G protein-coupled metabotropic receptors are present in the nervous system? Include five different examples of G protein-couple metabotropic receptors and how each can maintain transmitter specificity, but all be coupled to G proteins.

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What does it mean that inhibition of calcium channels by norepinephrine is "voltage-dependent"?

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What would happen in muscle cells dissociated from the atrium of the heart if you added acetylcholine in the presence of an inhibitor of RGS proteins?

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What would happen to G protein-coupled metabotropic signaling in a cell if you removed GTP from the cell cytoplasm?

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How is Nitric oxide generated as a result of acetylcholine acting on vascular smooth muscle cells?

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What is a "calcium microdomain"?

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Why are the physiological effects of Nitric oxide (NO) affected by phosphodiesterase inhibitors?

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How is G protein-mediated signaling terminated?

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Explain how norepinephrine causes an increase in the rate and force of contraction of the heart.

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