IDM - Ligand Gated Ion Channels

1. What are receptors? Molecular structures that bind specific substances. 2. What are the four main types Ligand gated ion channels, G protein couof receptors? pled receptors, kinase receptors, nuclear/intracellular receptors. 3. What are ligand gated ion channels? Ionotropic receptors directly coupled to ion channels. 4. What are examples of ligand gated ion channels? Nicotinic, GABAA, GABAC, and glutamate receptors. 5. What is the endogenous ago- Acetylcholine (ACh). nist for the nicotinic receptor? 6. Where are nicotinic receptors On the plasma membranes of cells in the found? neuromuscular junction (NMJ), in autonomic ganglia, and in the central nervous system (CNS). 7. What is the structure of the nicotinic receptor? A pentamer of four different subunits: 2 x ± (40KD), ² (49KD), µ (57KD), ´ (65KD). 8. What are nicotinic receptors? Ionotropic receptors that bind ACh. 9. What are the variants of nico- ±-, ²-, and ´-subunits. tinic receptor subunits? 10. What is the role of ±subunits in They trigger the receptor. nicotinic receptors? 11. How are agonists distinguished pharmacologically? Little selectivity between receptors. 12. What is the exception to the rule of agonist selectivity? Decamethonium. 13. How are antagonists distinguished pharmacologically? Strong selectivity between receptors. 1/5 14. What is an example of an an- ²-bungarotoxin. tagonist that blocks NMJ nicotinic receptors? 15. What is an example of an an- Mecamylamine. tagonist that has no effect on the NMJ? 16. What happens when ACh Ion channel opens quickly. binds to a nicotinic receptor? 17. What happens when the ion Increases Na+ and K+ permeability. channel of a nicotinic receptor opens? 18. What is the result of increased Depolarization of the cell. Na+ and K+ permeability? 19. What is responsible for the de- Inward rush of Na+ ions. polarization of the cell? 20. What is the charge difference Negative on intracellular side. between the intracellular and extracellular surface of a plasma membrane? 21. What is the rate of ion influx 1x107 ions. per second per channel in motor endplate nicotinic receptors? 22. How long are motor end1-2 milliseconds. plate nicotinic receptor channels open for? 23. What is the role of the Na/K AT- Sets up uneven distribution of Na+ and K+ Pase pump in the distribution ions. of ions? 2/5 24. What is the effect of an inward Reduces negative membrane potential. rush of positively charged Na+ ions on the membrane potential? 25. What is the function of the NMJ? To transmit action potentials across the synaptic clefts in motor endplates. 26. What is the postsynaptic membrane in the NMJ? The sarcolemma of a skeletal muscle fibre. 27. What is the role of choline acetyltransferase (C.A.T.) in the NMJ? To catalyze ACh synthesis in the motor neurone terminal. 28. What is the source of acetyl groups in ACh synthesis? Acetylcoenzyme A (acetyl CoA). 29. What is the role of ACh in the To increase membrane permeability to Na+ NMJ? and K+ ions. 30. What triggers ACh release into Influx of Ca2+ ions. the synaptic cleft? 31. What happens to the ion chan- It opens. nel in the nicotinic receptor when ACh binds? 32. What ions does the ion chan- Na+ and K+ ions. nel in the nicotinic receptor allow to pass through? 33. What is the effect of ACh bind- It increases membrane permeability to Na+ ing to the nicotinic receptor? and K+ ions. 34. What is the conformation It opens the ion channel. change in the nicotinic receptor when ACh binds? 35. Closed. 3/5 What is the state of the ion channel in the nicotinic receptor when it is unbound? 36. What is the state of the ion Open. channel in the nicotinic receptor when it is bound to ACh? 37. Is each transition state in the Yes. nicotinic receptor reversible? 38. What is the role of vesicles in To store ACh for release. the NMJ? 39. What is the endplate potential? Depolarization caused by ACh binding to nicotinic receptors. 40. What is acetylcholinesterase? Enzyme that hydrolyses ACh to choline and acetic acid. 41. What happens when no more Acetylcholinesterase reduces the synaptic ACh is being released? concentration of ACh. 42. What happens to the choline produced? Approximately 50% is recaptured by the nerve terminal. 43. What are some nicotinic agonists at the neuromuscular junction? ACh, nicotine, suxamethonium, decamethonium. 44. What are some nicotinic agonists at the autonomic ganglia? ACh, nicotine, lobeline, epibatidine. 45. What are some nicotinic an- Tubocurarine, pancuronium, atracurium, vetagonists at the neuromuscu- curonium. lar junction? 46. Trimetaphan, hexamethonium, alpha-bungarotoxin. 4/5 What are some nicotinic antagonists at the autonomic ganglia? 47. What are some agents that re- Hemicholinium, botulinum toxin, Mg2+, duce ACh release? Mn2+ and Co2+ ions, aminoglycoside antibiotics. 48. What are some transmission potentiating agents? Anticholinesterases such as pyridostigmine, neostigmine, edrophonium, distigmine, ambenonium, physostigmine (eserine), and Dyflos. 49. What are some competitive neuromuscular blocking agents? Tubocurarine, gallamine, pancuronium, alcuronium, atracurium, vecuronium. 50. What is the choline carrier in- Hemicholinium, which inhibits the synthesis hibiting agent? of ACh. 51. What is the ACh release enhancing agent? 4-aminopyridine. 52. What are some depolarizing neuromuscular blocking agents? Suxamethonium and decamethonium. 53. What is Tubocurarine? Alkaloid mixture extracted from Chondrodendron tomentosum plant. 54. What is Curare? Mixture of alkaloid substances found in Tubocurarine. 55. What is the source of Tubocu- Chondrodendron tomentosum plant in rarine? South America. 5/5