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UM - Neuro Science > Neuropain and histology and Degeneration and Recovery of Function FINISH- E2 > Flashcards

Neuropain and histology and Degeneration and Recovery of Function FINISH- E2 Flashcards

1
Q

What are the steps of an AP release at a synapse

A
  1. AP arrives @ presynaptic terminal
  2. Mem depol, opens VGCa++C
  3. Influx Ca++ causes mvmt synaptic vesicles containing NT toward release site
  4. Synaptic vesicles fuse w/mem and release NT
  5. NT diffuses across cleft
  6. NT binds to postsynaptic receptors
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2
Q

List the 3 types of synapses

A

Axodendritic
Axosomatic
Axoasonic

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3
Q

What is an axodendritic synapse

A

b/t axon pre and dendrite of post synaptic

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4
Q

What is an axosomatic synapse

A

b/t axon pre and cell body post synaptic

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5
Q

What is an axoaxonic synapse

A

b/t axon pre and axon post synaptic

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6
Q

Which synapses generate a local postsynaptic potential?

A

Neuromuscular
Axosomatic
Axodendritic

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7
Q

Which synapses modulate the membrane potential of a postsynaptic cell

A

Axoaxonic

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8
Q

How do axoaxonic neurons regulate NT release?

A

They change the amount of Ca++ influx to the presynaptic neurons

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9
Q

What are the steps of presynaptic inhibition

A
  • IN release NT
  • NT bind to presynaptic neuron, reduce Ca++ influx
  • Presynaptic neuron releases less NT when an AP arrives at its terminal
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10
Q

What are the steps of presynaptic facilitation

A
  • IN releases NT
  • NT bind to presynaptic neuron, increase Ca++ influx
  • Presynaptic neuron releases more NT when an AP potential arrives
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11
Q

Define nociception

A

the neural process of encoding noxious stimuli

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12
Q

What are nociceptors?

A

“free” peripheral nerve endings consisting of a series of spindle-shaped, thick segments linked by thin segments, creating a “string-of-beads” appearance

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13
Q

Where can you find nociceptors?

A
  • skin
  • muscles
  • joints
  • viscera
  • mouth, dental
  • almost all types of tissues
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14
Q

How do you activate a nociceptor

A
  • Intense thermal, mechanical, or chemical stimuli from exogenous or endogenous sources
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15
Q

T or F: Nociceptors are unimodal

A

False - polymodal

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16
Q

What nerve cells are part of the double pain sensation

A

A delta neurons and C fiber neurons

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17
Q

What kind of pain with…
a) A delta
B) C fiber

A

A) Initial, sharp, localized pain

B) Diffuse, prolonged, aching, dull pain

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18
Q

What % of pain-transmitting fibers are….

a) A delta
b) C fiber

A

a) 80

b) 20

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19
Q

What kind of neurons are A delta and C fibers?

A

Unipolar neurons w/cell bodies in DRG

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20
Q

Which has a faster nerve conduction velocity? (A delta or C fibers)

A

A delta (30m/s) not C fibers (1-4 m/s)

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21
Q

Which fiber type (nerve) has associated autonomic responses

A

C fibers

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22
Q

Which lamina of the SC do you find A delta and C fibers

A

Lamina I, II and V

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23
Q

What do C and A delta neurons synapse on?

A

Transmission cells (T cells) in the substantia gelatinosa of the SC

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24
Q

How does the gate control mechanism of pain work

A

A-beta fibers synapse on the inhibitory interneuron to block out the synapse of the a-delta and c fibers

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25
Q

What is the severity of pain sensation determined by

A

The balance of excitatory and inhibitory inputs to the T cells

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26
Q

What do the T cells synapse on

A

Efferent alpha motor neurons to cause mm contractions

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27
Q

What is responsible for the “pain-spasm-pain” cycle?

A

The C & A delta neurons synapsing on T cells that in turn synapse on efferent alpha motor neurons

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28
Q

What else do C & A delta neurons synapse on?

A

2nd order neurons

  • Autonomic neurons
  • Ascending sensory spinal cord tracts (to thal to sensory cortex)
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29
Q

Where does the lateral spinothalamic tract go to?

What does it transmit?

A

Medial thalamus

Sharp, localized pain

30
Q

Where does the antero- spinothalamic tract go to?

What does it transmit?

A

Reticular formation, hypothalamus, and limbic system, all of which synapse on the lateral, ventral, and caudal thalamus

Prolonged, aching pain

31
Q

What does the thalamus do

A

Processes and relays pain afferent sensations to various brain structures

32
Q

Pain interpretation in:

Sensory cortex

A

Conscious pain perception including location and quality of pain

33
Q

Pain interpretation in:

Anterior and posterior cingulate gyri

A

Pain interpretation plus focus attn towards the cause of the pain and evaluates its significance

34
Q

Pain interpretation in:

Temporal lobes

A

May start processes of storing memories associated w/pain

35
Q

Pain interpretation in:

Hypothalamus

A

Autonomic responses to pain

36
Q

Where is a NT synthesized

A

In the neuron cell body and then is transported to the presynaptic terminal

37
Q

How are NT removed from the synaptic cleft?

A

Synaptic vesicle recycling

38
Q

T or F: NT only excite the postsynaptic neuron

A

False! They excite or inhibit depending on the molecule released and the receptors present on the postsynaptic membrane

39
Q

Which are fast- acting and why?
A) NT that act directly
B) NT that act indirectly

A

A) NT that act directly bc their effects are extremely short lived

40
Q

Which are slow-acting and why?
A) NT that act directly
B) NT that act indirectly

A

B) NT that act indirectly bc their transmission requires 100ms to minutes

41
Q

How do ligand gated channels and NT work together?

A

Like a lock and key w/NT as the key

42
Q

How do indirect NT activate the ion channels?

A

By binding to a separate G-protein that will then activate the ion channel

43
Q

What are the steps for signal transmission at the G-protein

A
  1. Non-stim state, G prot complex assoc w/mem receptor
  2. NT binds to mem receptor, causing a conform change and activation of G protein
  3. GTP binds to G prot and conform change in the protein channel causes the channel to open, and ions (Na+) flow in
  4. GDP released and channel closes
44
Q

T or F: The G-protein can cause persistent opening of membrane channels

45
Q

What is a neuromodulator

A

It acts at a distance from the synapse and modulates the activity of many neurons at the same time, lasting minutes or days

46
Q

What is an example of a NT and Neuromodulator duo?

A

NT: Glutamate
NM: Substance P

47
Q

List 2 types of AA

A

Glutamate

GABA

48
Q

What are the most prevalent fast-acting neurotransmitters? What category are they?

A

GABA and Glutamate which are Amino Acids

49
Q

Glutamate:

a) Slow or fast
b) Excitatory or Inhibitory
c) What is it involved in
d) What does overactivity cause

A

a) Fast
b) Excitatory
c) Learning and memory
d) Seizures and too much may cause neuronal damage

50
Q

GABA

a) Slow or fast
b) Excitatory or Inhibitory
c) What is it involved in

A

a) Fast
b) Inhibitory
c) Preventing excessive neuronal activity

51
Q

What do bartiburates mimic?

What are they used for?

A

GABA

Sedation and anticonvulsants

52
Q

What does Baclofen do?

A

It is a mm relaxant

It increases the presynaptic release of GABA

53
Q

What is ACh

a) Slow or fast
b) Excitatory or Inhibitory

A

A cholinergic NT

a) Slow and Fast
b) Fast-acting is Excitatory and Slow-acting is inhibitory

54
Q

What are nicotinic and muscarinic receptors associated with?

55
Q 
Nicotinic Receptor
A) what does it bind
b) What is it linked to
c) What type of response
d) Located where?
e) Mediates (excitation/inhibition?)
A

A) Nicotine

b) Ion channels
c) Fast and brief
d) Neuromuscular junction, autonimic ganglia, some CNS
e) Exciation

56
Q 
Muscarinic Receptor
A) what does it bind
b) What is it linked to
c) What type of response
d) Located where?
e) Mediates (excitation/inhibition?)
A

a) Muscarine
b) 2nd messenger G protein
c) Slow and prolonged response
d) Myocardial mm, smooth mm, and some CNS
e) Both inhibition and excitation

57
Q

T or F: ACh is a NT and a NM

A

True - as a neuromodulator it regulates locomotion and arousal, facilitates attention, memory and learning

58
Q

Dopamine

a) NT Type
b) Excitatory or Inhibitory
c) What is it involved in
d) Where is it produced

A

a) Amine
b) Inhibitory in CNS
c) Motor A, motivation/reward, cognition
d) SNc of BG

59
Q

List the different types of amines

A

Histamine
Norepinephrine
Serotonin
Dopamine

60
Q

What is the dopamine projection system

A

a) BG - Movement
b) Limibic - Reward/wanting & addiction
c) prefrontal - working memory, attn

61
Q

Which Neuro conditions are from an increase in dopamine

A

1) Lack of motivation Behaviours

2) Schizophrenia

62
Q

Which Neuro Conditions are from dec. DA

A

1) PD (dec. in BG)
2) Depression/cognitive
3) Drug addiction

63
Q

What are the body’s natural pain killers?

A

Peptides - the endogenous opioids

64
Q

Opiopeptins

a) NT Type
b) Excitatory or Inhibitory
c) What is it involved in
d) How can the body increase these concentrations

A

A) Peptides
B) Inhibitory
c) Pain killing and altering the perception of pain
d) EXERCISE

65
Q

What is Substance P

A

A peptide that acts as both a NT and NM

66
Q

Substance P’s role as a NT

A

Binds NK-1 receptors in SC that then relay this info up the spinothalamic tract up to Broadman areas 1,2

67
Q

What nerve cells release Substance P as a NT

A

Primary afferent C and A delta nerve fibers

68
Q

What does Substance P co-transmit w/ and what does it do

A

Glutamate and substance P work together to cause pain signals to be sent to the brain and prolong the depolarization caused by glutamate

69
Q

What is the dual role in pain management played by Substance P

A

It increases sensitivity to pain indirectly by its inflammatory effects AND it directly increases the recognition of pain

70
Q

What is the centralization of pain vs peripheralization

A

Pain moving towards the center of the spine vs laterally away from the center of the spine/down the extremity

UM - Neuro Science (9 decks)

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