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Biochemistry (Cole) > Lecture 48 Neuromuscular Control > Flashcards

Lecture 48 Neuromuscular Control Flashcards

1
Q

what form of termination of transmitter would NT being returned to axon terminals or transported into glial cells?

A
  • reuptake
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2
Q

Enzymes inactivating neurotransmitters would be?

A
  • breakdown
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3
Q

Neurotransmitters diffusing out of synaptic cleft would be?

A
  • diffusion
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4
Q

Where are small molecule NT made?

A
  • nerve terminal
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5
Q

Where are peptide NTs made?

A
  • in the cell body at ER and golgi packages them
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6
Q

What is lidocaine a derivative of?

A
  • cocaine

- VGNA channel blocker

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7
Q

How does lidocaine block pain?

A
  • it prevents Na from producing AP to tell brain you have pain
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8
Q

Tetrodotoxin

A
  • VGNa channel blocker
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9
Q

Caffeine

A
  • increases cAMP which increases excitability of neuron
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10
Q

How do SSRIs work?

A
  • block reuptake of NTs like seratonin so you are increasing seratonin in blood and altering mood
  • reduce anxiety and depression
  • seratonin must remodel circuitry in blood bc it takes weeks
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11
Q

What does cocaine do?

A
  • block reuptake in DA and NE

-

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12
Q

What systems to ectasy and amphetamines do?

A
  • effect DA, NE, 5HT neurons
  • cause NT to leak out of vessicle and out of reuptake channels (wrong way)
  • increases dopamine, norepinerine, seratonin in blood
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13
Q

Where does long term potentiation occur?

A
  • hippocampus

learning and memory

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14
Q

What is long term potentiation?

A
  • strengthening synapse
  • increasing sensitivity ( adding more receptors to membrane)
  • can also increase the quanta
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15
Q

What are efferent signals?

A
  • motor neurons

- away from CNS

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16
Q

What is a motor unit?

A
  • motor neuron and all the fibers it innervates
17
Q

What type of receptor does ach bind to in a muscle contraction?

A
  • nicotinic which allows Na+ in the muscle
18
Q

What happens once Na+ travels into muscle?

A
  • opens voltage gated na channel which makes action potential to spread through muscle
19
Q

What type of potential does the ach cause?

A
  • it causes an end plate potential that reaches threshold and then an action potential occurs
  • unless a diseased state
20
Q

How does the AP translate into an increase in Ca and ultimately a muscle contraction?

A
  • Na travels down T tubule then interacts which DHPRs

- DHPRS changes conformation to touch RyR1 which will then release Ca for muscle contraction

21
Q

where does the calcium go from the RYR?

A
  • it goes to the actin and myosin for muscle shortening

- it also goes to other Ryodine receptors to release more calcium for muscle contraction

22
Q

How does Duchenne muscular dystrophy work?

A
  • mutation in DMD gene encoding dystrophin
  • dystrophin provides scaffolding for muscle
  • strength of muscle contraction way down bc no scaffolding
23
Q

What does ache do?

A
  • break down ACh to choline and acetic acid

- essential to make sure we aren’t in tetnus

24
Q

How do we get rid of calcium to terminate of contraction?

A
  • SERCA pump
  • pumping calcium against gradient into SR
  • also can pump CA through ATPase out of cell
25
Q

What is calsequestrin?

A
  • protein to bind Ca to get more and more into SR
26
Q

How do nerve gases work?

A
  • inhibit ACHE so you have so much ACH that you go into spastic contraction in diaphragm and you die
27
Q

What is physostigmine?

A
  • also an ACHE inhibitor but it is not permanent and only inhibits ACHE a little to increase muscle contraction
  • also reversible
28
Q

Nicotine and acetylcholine do what to muscle contraction?

A
  • increase
29
Q

What does curare do to muscle contraction?

A
  • blocks it so you cant breathe
30
Q

What happens in myasthenia gravis?

A
  • antiobody production to Ach nicotinic receptors
  • lowers epp because you dont have as many receptors
  • cant form AP bc epp is lower
  • muscles keep getting weaker and weaker

Biochemistry (Cole) (25 decks)

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