Shown are different derivatives of acetylcholine. N' A H2N H2N 1. Which one is expected to lose its ability to bind to the receptor but could elicit CNS side effects? Explain. 2. Which is/are expected to resist metabolism by choline esterase? 3. Which one is not expected to bind and yet prone to metabolism? Explain ZI
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- 1a.Arrange these ligands in their order of potencies(high to low) 1b. Choose an appropriate concentration of Propranolol needed to block 50% of epinephrine or isoproterenol induced cAMP production via adrenergic receptors expressed in a cell culture model system. 1c. Which of the following has more affinity to bind to adrenergic receptors? And why?I. EpinephrineII. IsoproterenolIII. PropranololBriefly explain....Represent the reactions when Phosphatidylethanolamine was treated with; (I) Phospholipase C (ii) Phospholipase DUsing the cultured cells used in this experiment and described in the introduction, how would you approach determining the potency of an agonist to the D2 receptor?
- The EC50 of an agonist for a GPCR is almost always (greater than, equal to, or less than) the KD of the same agonist at the same GPCR. Why?explain in detail ephrin receptor EPHB2 receptor interaction with PDZ ligand. give full step by step explanantion.Atropine (I) and Ipratropium bromide (II) are both muscarinic acetylcholine receptor antagonists. Common side effects of atropine (1) include dizziness, blurred vision, and sedation. With Ipratropium bromide (II) these side effects are much less common. Given the two structures below, what might be the reason for the different side-effect profile of the two drugs? Br HO HO
- Depending on the size and complexity of the molecule, small chemical alterations can impart significant activity differences, especially if a certain part of the molecule is critical for binding. Considering this, select structure(s) below that are expected to have high cholinergic agonist activity based on what we leamed about acetylcholine's SAR.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)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.
- Ethanol is unusual in that it is freely soluble in both water and lipids. Thus, it has access to all regions of the highly vascularized brain. Although the molecular basis of ethanol action in the brain is not clear, ethanol evidently influences a number of neurotransmitter receptors and ion channels. Suggest a biochemical explanation for the diverse effects of ethanol.To maximize the activity of an α4β2 nicotinic Achtylchcholine Receptor (nAChR), how many agonist binding sitea should be occupied?A series of novel phenadoxone derivatives without mu2 receptor activity (mu2 activity is responsible for physical dependence) proposed to be developed as analgesics is shown below. Addition of which heterocyclic substituent R to phenadoxone is LIKELY to cause the MOST binding of the corresponding derivative to plasma proteins? Use the additivity of approximate estimates of logP to answer this question. phenadoxone derivatives A. Azetidine B. Thiophene C. Oxetane D. Furan E. Pyrrole ترف لي تي في R= -NH