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Explain how inhibition can be produced by (a) muscarinic ACh receptors in the heart; and (b) GABA
receptors in neurons of the CNS.
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- Discuss the concept of termination of neurotransmitter action by comparing the mechanisms by which acetylcholine and nitric oxide's actions are terminated. (a) Name the three primary mediators of purinergic receptors. (b) Which one of these mediators is sometimes used to treat supraventricular tachycardia? (c) Explain why the drug in (b) is considered safer than verapamil in the treatment of supraventricular tachycardia?A patient has been exposed to the organophosphate pesticide malathion,which inactivates acetylcholinesterase. Which of the following symptoms would you predict: blurring of vision, excess tear formation, frequent or involuntary urination, pallor (pale skin), muscle twitching, orcramps? Would atropine be an effective drug to treat the symptoms?(See Clinical Impact 16.2 for the action of atropine.) Explain.Both rhodopsin in vision and the muscarinic acetylcholine receptor in cardiac muscle are coupled to ion channels via G proteins. Describe the similarities and differences between these two systems.
- What is the muscarininc acetylcholine receptor? Where is it expressed?Calcium entry through NNDA receptor can potentiate synaptic transmission through the following mechanisms EXCEPT: a.) Insertion of AMPA receptors to postsynaptic membrane b.) Synthesis of NO to increase presynaptic transmitter release c.) Phosphorylation of AMPA receptors d.) Slowing down glutamate reupdate, so it remains longer in the synapseUnder anesthesia, acetylcholinesterase inhibitors can be given in combination with blockade of muscarinic receptors. Explain the purpose of the two treatments.
- Clostridium tetani toxin blocks the exocytosis of GABA. A. What anatomical part of a pre-synaptic neuron would be affected by this? B. How would a post-synaptic neuron’s likelihood of experiencing an action potential be affected by this toxin? C. Explain, using at least TWO of the following terms: threshold, depolarization, repolarization, hyperpolarization, summation, IPSP, EPSP, exocytosisWhat type of synaptic potential (if any; be sure to indicate if any modification is occurring as well) would occur if: a.) An MAO inhibitor type of antidepressant is functioning at an active dopaminergic synapse that increases the rate of sodium flowing into the cell. b.) Prozac is present at an active serotonin synapse where receptor activation increases the flow of potassium out of the cell.Local anesthetics "block" the action potential and therefore do not allow "pain" information to proceed to the brain and spinal cord. In the presence of these molecules (local anesthetics) 'threshold' is essentially "ignored". The molecules most logically work by: 23. a. Decreasing the intracellular [potassium] b. Blocking the opening of the voltage-gated potassium channels c. Decreasing the extracellular [sodium] d. Blocking the opening of the voltage-gated sodium channels
- 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 HOWhat do you think is the muscarinic receptor subtype that has a greater role in generating contractions in human detrusor smooth muscle (M2 or M3)?Describe how nitric oxide and endocannabinoids function as neuromodulators.