LG 1.4 - Physiology of Neuromusular Junction Flashcards

1
Q

What are motoneurons? What are motor units?

A
  • Motoneurons: nerves that innervate muscle fibers.

- Motor units: comprises a single motoneuron and the muscle fibers it innervates.

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2
Q

(2) Excitation-contraction coupling of muscles requires energy from axons to go from Electrical, to Chemical, to Mechanical. Explain each of these individually, aka how does the energy go from electrical -> chemical -> mechanical.

A
  • Electrical: An action potential depolarizes the presynaptic terminal.
  • Chemical: Presynaptic terminal releases a neurotransmitter that will create a change in postsynaptic membrane.
  • Mechanical: These ultimately result in development of tension in the muscle fiber.
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3
Q

(4) Where is ACh synthesized and where is it placed prior to release into synaptic cleft?

A
  • Synthesized in cytosol of terminal.

- Transported into vesicles.

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4
Q

(4) Roughly how many ACh molecules per vesicle?

A
  • 10,000
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5
Q

(4) What happens to choline after ACh is broken down?

A
  • Choline is reabsorbed by presynaptic terminal to be recycled into more ACh.
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6
Q

(4) Regarding the small vesicles, where are these synthesized and where do they then get transported?

A
  • Golgi apparatus in cell body.

- Transported down to the synapse.

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7
Q

(4) Due to the finite number of vesicles that accumulate at the terminal, what is the process of these becoming regenerated? (from what are they regenerated and how).

A
  • Presynaptic membrane regenerates these vesicles.

- Clathrin proteins contract causing membrane to break away and form new vesicles.

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8
Q

(6) What is the role of Ca2+ in synaptic transmission?

A
  • Ca2+ is involved in the mobilizing and docking of synaptic vesicles.
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9
Q

(7) What is the difference between Endplate Potential and Action Potential?

A
  • Endplate potential: local depolarization of the specialized motor end plate.
  • 1 synaptic vesicle creates a miniature endplate potential.
  • These endplate potentials add up to reach threshold for an action potential to develop in postsynaptic terminal.
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10
Q

(7) Name the 5 ways that you can disrupt the NMJ?

A
  • Mimicking ACh
  • Blocking choline uptake
  • Stopping ACh release
  • Inactivating ACh esterase
  • Blocking the ACh receptor.
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11
Q

(7) Name 3 drugs that mimick ACh and why they can effectively act as ACh?

A
  • Methacholine, carbachol, nicotine.

- Drugs are not destroyed by acetylcholinesterase so they persist in synaptic cleft for many minutes to several hours.

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12
Q

(7) Name a drug which blocks choline uptake, and what would this result in?

A
  • Hemicholinium.
  • Blocks choline reuptake into presynaptic terminals -> depleting choline stores from motoneuron terminal and decreasing the synthesis of ACh.
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13
Q

(7) What is the main method of blocking ACh release? What bacterial toxin is used to do this, how? How does black widow venom block ACh release?

A
  • Stop depolarization of presynaptic terminal. Block arrival of action potential.
  • Botulinum toxin: prevents docking of the synaptic vesicles.
  • Black widow venom: depletes terminal of ACh by binding the synaptic vesicle too good.
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14
Q

(7) What 3 drugs can be used to inactivate acetylcholinesterase? How long do each last?

A
  • Neostigmine, physostigmine, diisopropyl fluorophospate.

- Neostigmine and physostigmine work for hours, diisopropyl fluorophosphate (a nerve gas poison) can last for weeks!

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15
Q

(7) What drugs are used to block the ACh receptor, how do they do this?

A
  • Curariform drugs: bind nicotinic ACh receptor on postsynaptic membrane.
  • Succinylcholine is used as muscle relaxant and does this.
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16
Q

(7) What is Myasthenia Gravis, what is the pathology, how is it treated?

A
  • Autoimmune disease in which antibodies are developed that block or destroy their own ACh receptors.
  • Endplate potentials are not strong enough to open the voltage-gated Na+ channels so that the muscle fiber does not depolarize. Paralysis of respiratory muscles would be fatal.
  • Treat with neostigmine, an acetylcholinesterase inhibitor.
  • Read clinical vignette on pg. 28 of Costanzo.