235) mGluRs are metabotropic receptors that are activated by the binding of the neurotransmitter glutamate. Based on this information, which of the following statements about mGluRs is correct? a. mGluRs open for Cl- ions to flow through in response to activation by glutamate. b. Activation of mGluRs does not result in graded potentials. C. mGluRs activate signaling pathways that act through a second messenger cascade. d. Signal transduction pathways close mGluRs to elicit depolarizations. e. mGluRs are embedded in the membrane of the presynaptic cell.
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- Identify which of the following statements is a lie? Select one: a.Diacylglycerol (DAG) and inositol triphosphate (IP3) are byproducts of enzymatic cleaving of PIP2 using phospholipase C while PIP2 formed via enzymatic activity of kinases. b.cAMP is an important second messenger because it serves to activate or inactivate proteins within the cells, especially those cells which their metabolic pathways are regulated by cAMP-dependent kinase (A-kinase). c.Second messengers are molecules that act alternative to signaling molecules to bind to the receptors by altering the structure of cellular proteins.All the B - adrenergic receptors are linked with Gs G-protein. Physiological processes mediated by the intracellular second messenger cyclic AMP include: YOU CAN CHOOSE MORE THAN ONE A.carbohydrate breakdown by the liver (glycogenolysis) B.increased contractility (e.g. increased cardiac contractility) C.smooth muscle relaxation (e.g. bronchodilation or vasodilation) D.Triglyceride breakdown (lipolysis)In relation to Cushing’s Syndrome, a method that some scientists have used to treat the disease is to use small molecules that bind to, but do not activate, MC2R. This type of molecule is considered an antagonist. How can an antagonist bind to the same receptor as ACTH but not activate it ? a. The antagonist binds covalently while ACTH binds non covalently b. The antagonist is only partially complimentary to the binding pocket of MC2R c. The antagonist binds to ACTH and blocks it from binding to the receptor properly d. The antagonist is the exact same structure as ACTH but since it is synthetic it doesn’t work
- Explain the role, using diagrams wherever possible, of G protein coupled receptors mediating the following physiological effects. a. Positive inotropic and positive chronotropic effects in the heart b. Vasoconstriction in vascular smooth muscle cells.Represent the reactions when Phosphatidylethanolamine was treated with; (i) Phospholipase C (ii)Phospholipase DWhich statement(s) is/are true regarding the release of glutamate? (Select all that apply) Question 4 options: A) It acts by opening up Cl channels B) It can cause an EPSP in the postsynaptic membrane of a typical cortical neuron C) It can cause an EPSP in the postsynaptic membrane of a retinal neuron D) It can cause an IPSP in the postsynaptic membrane of a retinal neuron
- The NMDA receptor I/V curve is nonlinear, why? What about the GluA2-containing AMPA receptor I/V curve? Draw both under normal physiological conditions. In addition, explain what happens for the NMDA receptor I/V curve when you lower the magnesium concentration.One such neurotoxin, Sarin (chemical name: propan-2-yl methylphosphonofluoridate) is considered a weapon of mass destruction by the United Nations by virtue of its ability to kill with great efficiency in very low concentrations. a. Where does Sarin have its effect (what is/are its target) and describe the mechanism of action of Sarin (how does it kill)? b. Describe the physical symptoms observed in those stricken with Sarin that are consistent with this mechanism of action. Include flaccid/tonic paralysis, as applicable.The synthesis of phosphatidylcholine from phosphatidylethanolamine requires: a. Tetrahydrofolate b. Glycine c. Choline d. S-Adenosylmethionine
- The catechol system is important for the binding of adrenergic agonists, yet is not required for adrenergic antagonists. Why should this be the case? The active enantiomer of arylpropanolamines is S, yet for the arylethanolamines it is R. What do you think is going on in the binding site? Summarize what a selective noradrenaline reuptake inhibitor does and how it would affect depression.A hormone signals through a G protein-coupled receptor as shown in the diagram. After the production of IP3, which of these events will MOST quickly stop the transduction of the signal? A. the hydrolysis of IP3 B. the hydrolysis of GTP C. the hydrolysis of PIP2 D. the hydrolysis of the hormone I believe the answer is (B) the hydrolysisof GTP, because the G protein becomes inactive after GTP is hydrolyzed to GDP. However, the solution provided by Bartleby is (C). Please explain. ThanksThe drug Buckeyium binds to the NMDA receptor at the orthosteric binding site (were glutamate would normally bind). Assume that glycine is already bound, and that magnesium is not blocking the NMDAR ion channel. If the channel does not open as a result of Buckeyium binding than Buckeyium would be considered a