Synaptic Transmission

  1. What is an example of electrical synapse?
    Gap junction
  2. What is the speed of an electrical synapse?
    Fast (no delay)
  3. Where can electrical synapses be found?
    • Cardiac muscle
    • Smooth muscle
  4. What is a characteristic of the electrical synapses that distinguish them from chemical synapses?
    Electrical synapses connect a large group of neurons together, so signals can e passed in a very fast manner
  5. Where are peptide neurotransmitters made and where are they released?
    In the cell, released from Golgi
  6. Where are non-peptide neurotransmitters made?
    In the nerve terminal
  7. Where are vesicles released from?
  8. What is the role of calcium in vesicle release?
    Voltage gated calcium channels in the presynaptic membrane opens when AP reaches in the terminal, this allows calcium to flow down the electrochemical gradient and Ca2+ controls the fusion of vesicle and mobilization of the vesicles
  9. What is the role of synapsins in vesicle release?
    Synapsins in resting state, bind vesicles to actin filament
  10. When do synapsins release vesicles from binding to actin?
    When Ca2+ enter the neuron
  11. What is the role of Rab protein in vesicle release?
    Binds GTP and guides the freedup vesicle to move to the active zone
  12. What is the SNARE complex?
    Formed by protein on the vesicle – snaptobrevin (VAMP) and membrane proteins (SNAP 25 and Syntaxin)
  13. What is the role of SNARE Complex?
    Docks the vesicle to the presynaptic membrane
  14. What is the role of Munc18?
    Protein in the presynaptic membrane that is required for exocytosis of the synaptic vesicles
  15. What happens if Munc18 is not present?
    Vesicle would not be able to fuse to membrane
  16. What is the role of synaptotagmin?
    It is a protein on the vesicle that sense calcium and binds to calcium which triggers the fusion of vesicle, pore formation and NT release
  17. What is the role of NSF?
    To recycle vesicles and disassemble the SNARE complex
  18. How do clostridial toxins disrupt vesicle release?
    They target and cleave VAMP, therefore inhibit the release of Ach at NMJ resulting in paralysis
  19. What are some examples of clostridial neurotoxins?
    Tetanus and botulinum toxins
  20. How do alpha-latrotoxins disrupt vesicle release?
    This is a spider toxin that binds to neurexin which results in massive calcium influx inside the neuron and consequently lead to a massive release of vesicle depletion and Ach release.
  21. What are some symptoms as a result of the alph-latrotoxin (spider toxin)
    Acetylcholine related sxs such as pain, muscle rigidity, vomiting and sweating
  22. What are some methods to terminate neurotransmission?
    • Diffusion
    • Enzymatic degradation
    • Reuptake
  23. What is the transporter that is used for glutamate reuptake?
    • Na+/K+ exchange, no chloride dependence
    • Na+ and glutamate into cell, K+ out
  24. What is the transporter for other neurotransmitters reuptake?
    • Na+ and Cl- cotransport
    • Na+, Cl- and NT all into cell
  25. What are the vesicular uptake transporters used for monoamines?
    VMAT 1 and VMAT 2
  26. What is the vesicular uptake transporter used for GABA?
  27. What is the vesicular uptake transporter used for Acetylcholine?
  28. Which ion gradient do plasma membrane transporters utilize for reuptake of neurotransmitters?
    Na+ gradient
  29. Which ion gradient do vesicular transporters use for reuptake of neurotransmitters?
    H+ gradient
  30. What does Acetylcholine breaks down into?
    Acetate and choline
  31. What enzyme is involved in the breakdown of acetylcholine?
  32. Serotonin reuptake utilize which ion gradient?
    Na+ gradient
  33. What is the enzyme responsible for degrading serotonin inside the presynaptic terminal?
  34. What does serotonin break down into?
    5-HIAA (5-hydroxyindoleacetic acid)
  35. What is the role of astrocyte in synaptic transmission?
    It wraps around the synapse and has NT receptors, and when bound to NT, Ca2+ increases intracellularly and release transmitters of their own that can either enhance or inhibit synaptic activity
  36. What is the cause of Lambert-Eaton Myasthenic Syndrome (LEMS)?
    An autoimmune disorder in which antibodies against voltage0gated Ca2+ channels in the presynaptic terminals is affected. Preventing motor neurons from sending Ach to muscles
  37. What part of body is affected by LEMS?
    Skeletal muscles weakness
  38. What receptors are found on postsynaptic membrane in neuromuscular junction?
    Nicotinic ionotropic receptors
  39. What is an ionotropic receptor and how does it differ from metabotropic receptor?
    Ionotropic is ligand-gated, once a ligand binds, the channel is activated. Metabotropic requires a second messenger and thus it is slower in nature
  40. What ion enters the postsynaptic neuron once the nicotinic receptor is activated by Ach binding?
    Na+ ion enters and leads to depolarization of the muscle end plate
  41. Which neurotransmitters have receptors in the same ligand-gated receptor family and what is the characteristic of said receptor?
    • GABA, Acetylcholine and glycine
    • 5 subunits each with 4 transmembrane alpha helices
  42. What is the characteristic of the glutamate receptor?
    Ligand-gated receptor that has just 4 subunits each with 3 trans membrane alpha helices
  43. What is the characteristic of gap junctions?
    Formed by hemichannels with 6 subunits each with 4 transmembrane regions
  44. What is the characteristic of voltage gated channels?
    4 subunits each with 6 transmembrane domains
  45. What are some of the groups of metabotropic receptors?
    • G-protein coupled
    • Receptor tyrosine kinases (RTKs)
  46. What is the characteristic of Transient Receptor potential (TRP) channels?
    Similar to voltage-gated in that each subunit has 6 transmembrane domains but these are not voltage-gated. Sensitive to nociceptive stimuli, some are G protein coupled
  47. How many transmembrane domains are in G protein coupled receptors?
  48. What are the ligands for receptor tyrosine kinases?
    Peptide hormones (EFG, GFG, NGF, BDNF) and insulin
  49. What type of receptor (metabotropic or ionotropic) is nicotinic receptor?
  50. What type of receptor (metabotropic or ionotropic) is muscarinic receptor?
  51. What happens to muscarinic receptor when Acetylcholine binds?
    • Slow EPSP, leading to decrease outward of K+ current by closing K+ leak channel thus encouraging depolarization
    • Closes M-type K+ Channel
  52. What happens to nicotinic receptor when acetylcholine binds?
    Results in FAST EPSP; leading to decrease outward of K+ current by closing K+ leak channel thus encouraging depolarization
  53. What happens when GIRK is activated by acetylcholine binding to muscarinic receptors on cardiomyocytes?
    K+ leaves the cell leading to hyperpolarization thereby slows down heart rate
  54. Is 5-HT1 G-protein coupled channel inhibitory or excitatory?
    Inhibitory; effects K+
  55. Is 5-HT2 G-protein coupled channel inhibitory or excitatory?
    Excitatory; effects K+
  56. What kind of channel is 5-HT3 and what is its effect?
    Ligand-gated channel permeable to Na+, K+ and Ca2+; excitatory
  57. True/False: Neostigmine is used to treat myasthenia gravis because it is an acetylcholinesterase inhibitor.
  58. What is the difference between myasthenia gravis and Lambert-Eaton myasthenic syndrome?
    • In MG, there are antibodies that are against nicotinic acetylcholine receptors binding on the POSTsynaptic membrane, preventing depolarization
    • In LEMS: antibodies are against Ca2+ voltage gated receptors in the PREsynaptic membrane
Card Set
Synaptic Transmission
Zawada NMSK exam 1 Synaptic transmission