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Neuro > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Postsynaptic terminal can be:

A

another neuron, muscle cell, gland or any cell of an organ

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2
Q

Where can synaptic communications between neurons occur?

A

cell body
dendrites
axon

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3
Q

What can chemical stimulation of the receptors of postsynaptic memebrane result in?

A

opening of membrane ion channels

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4
Q

What generates a local postsynaptic potential?

A

If the synapse is neuromuscular, axosomatic, or axodendritic, the flux of ions in the postsynaptic membrane

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5
Q

Axaxonic activity produces:

A

presynaptic effects

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6
Q

Postsynaptic potentials can be either:

A

excitatory

inhibitory

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7
Q

Excitatory:

A

from a local depolarization

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8
Q

Inhibitatory:

A

from a local hyperpolarization

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9
Q

What are presynaptic effects?

A

facilitation

inhibition

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10
Q

A local depolarization is what?

A

an excitatory postsynaptic potential; sum of many can generate an AP; release ACh at synapse between neuron and a muscle cell

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11
Q

What is a local hypepolarization?

A

an inhibitory postsynaptic potential (IPSP) that decreases the possibility of firing an action potential

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12
Q

Spatial summation:

A

simultaneous potentials from different locations across the cell body

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13
Q

Temporal summation:

A

not absolutely simultaneous but overlapping potential at a given time

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14
Q

When is an action potential triggered?

A

Only if the overall summation (both EPSPs and IPSPs) is sufficient to depolarize the cell to threshold at the axon hillock

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15
Q

When does presynaptic effect occur?

A

when the amount of neurotransmitter released by a neuron is influenced by previous activity in an axoaxonic synapse

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16
Q

What is presynaptic facilitation?

A

More neurotransmitter is released

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17
Q

When does presynaptic facilitation occur?

A

Occurs when a presynaptic axon releases a neurotransmitter that slightly depolarizes the axon terminal of a second neuron, more Ca++ than normal enters the presynaptic neuron (2), causing more transmitter released to the cleft

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18
Q

What is presynaptic inhibition?

A

Less neurotransmitter is released.

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19
Q

When does presynaptic inhibition occur?

A

Occurs when an axon releases a neurotransmitter that slightly hyperpolarizes the axonal region of a second neuron

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20
Q

What can intensify pain experience?

A

presynaptic faciliation through signals interpreted as pain

mentally focusing on pain can increase the level of activity of brain areas associated with the pain

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21
Q

What are the two classes of neurotransmitters?

A

small molecule neurotransmitters

peptide neurotransmitters

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22
Q

What are the two families of receptors?

A

iontropic (ligand gated ion channels)

metabotropic: receptor activating second messenger systems

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23
Q

What is a neurotransmitter?

A
  • is released by a presynaptic neuron into the synaptic cleft
  • acts directly on postsynaptic ion channels or activates proteins inside the postsynaptic neuron
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24
Q

What is a neuromodulator?

A

released into extracellular fluid and adjust the activity of many neurons. Alter neural function by acting at a distance away from the synaptic cleft

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25
Q

What is the effect of a neuromodulator?

A

Effects manifest more slowly and usually last longer than those of neurotransmitters, which happen in seconds; the effects last from minutes to days

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26
Q

What does neurotransmitters do to the postsynaptic neuron?

A

may excite or inhibit it, depending on the molecules released and the receptors they interact with

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27
Q

What are the types of neurotransmitters?

A 
fast acting (act directly)
slow acting (act indirectly
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28
Q

How much transmission time does a fast acting neurotransmitter require?

A

1/1000 of a second

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29
Q

How much transmission time does a slow acting neurotransmitter require?

A

1/10 of a second to minutes

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30
Q

Fasting acting:

A

ACh

Amino acids

31
Q

Acetylcholine

A

usually excitatory; used by motor neurons that synapse with muscle fibers to elicit fast-acting effects on muscle membranes

32
Q

Glutamate

A

amino acid

excitatory and elicits neural changes that occur with learning and development

33
Q

Glycine and gamma-aminobutyric acid (GABA)

A

inhibitory and have preventive effect on excessive neural activities

34
Q

Slow acting:

A

Amines
peptides
nitric oxide

35
Q

What are some amines:

A

widely distributed throughout nervous system

dopamine, norepinephrine (NE), serotonin and histamine.

36
Q

Peptides:

A

can affect neuronal signaling by acting as hormones, neurotransmitters or neuromodulators

37
Q

Examples of peptides:

A

substance P, calcitonin gene-related peptide, galanin, opioid peptides

38
Q

Nitric oxide:

A

diffusible transmitter, and does NOT require a receptor to bind for activation

39
Q

What is Substance P?

A

One of the most common neuropeptides

Stimulates nerve endings at the site of injury

40
Q

Sustance P in the CNS?

A

it acts as a neurotransmitter carrying information from the spinal cord to the brain

41
Q

Implication of substance P inCNS?

A

Strongly implicated as a neuromodulator in the pathophysiologic response to pain syndromes, which involves the perception of normally innocuous stimuli as painful

42
Q

Synaptic receptors produce:

A

direct or indirect action

43
Q

Synaptic receptors acting directly:

A

when the receptor and ion channel make up a single functional unit

44
Q

Synaptic receptors acting indirectly:

A

using a cascade of intracellular molecules to activate ion channels or cause other changes within the postsynaptic neuron

45
Q

Three mechanisms of postsynaptic receptors to transduce signals:

A

directly: opens ion channels
indirectly (fast)
indirectly: opens ion channels (slow)
Activates a cascade of intracellular events, including activating genes (slow synaptic transmission

46
Q

What is modifiability?

A

the ability of neurons to change in function, chemical profile (amount/types of neurotransmitters produced), or structure

47
Q

Where can plasticity occur?

A

at synapses, neuronal circuits or neural systems

48
Q

What is neuroplasticity?

A

the basis of all functions involving changes

  • acquisition of new skills
  • regaining skills lost due to injury to nervous system
  • acquisition of cognitive skills such as language, music, learning and memory
49
Q

What does neuroplasticity encompass?

A
  1. Habituation
  2. Experience-dependent plasticity: learning and memory
  3. Cellular recovery after injury
50
Q

What is habituation?

A

a decrease in response to a repeated, benign stimulus

-short term and reversible

51
Q

What does habituation describe in PT/OT?

A

techniques and exercises intended to decrease the neural response to a stimulus

52
Q

What is experience-dependent plasticity?

A

a complex process involving persistent, long-lasting changes in the strength of synapses between neurons and within neural networks
-learning and memory

53
Q

What are the two main types of plasticity in learning and memory formation?

A

long term potentiation (LTP)

long term depression (LTD)

54
Q

What is a silent synapse?

A

characterized by lack of functional glutamate AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) receptors

55
Q

What is an active synapse?

A

when mobile AMPA receptors are inserted into the synaptic membrane

56
Q

What does induction of LTP require?

A

activation of NMDA (N-methyl-D-aspartate) subtype of glutamate receptor

57
Q

What are the two factors the explain the necessity of NMDA receptors for the induction of LTP?

A
  1. voltage-dependency of NMDA mediated currents

2. permeability of NMDA channels to Ca2+

58
Q

What is long term depression?

A

a conversion of an active synapse to a silent synapse

59
Q

What causes a LTD?

A

removal of AMPA receptors from the postsynaptic membrane, making the membrane less likely to be depolarized when glutamate is released from the presynaptic neuron

60
Q

Injuries that damage or sever _____ cause degeneration but may not result in cell death; some neurons have the ability to regenerate this.

A

Axons

61
Q

Injury that destroys what of a neuron leads to death of the cell?

A

cell body

62
Q

What are the degeneration changes following axonal injury/

A
  1. axon terminal degenerates
  2. myelin breaks down and froms debris
  3. cell body undergoes metabolic changes
  4. presynaptic terminals retract from dying cell body
  5. postsynaptic cells degenerate
63
Q

What is sprouting?

A

regrowth of damaged axons

64
Q

What are the two forms of sprouting?

A

collateral and regenerative

65
Q

What is collateral sprouting?

A

occurs when a denervated targe is reinnervated by branches of intact axons of neighboring neurons

66
Q

What is regenerative sprouting?

A

occurs when an axons and its target cell have been damaged

67
Q

What causes the functional regeneration of axon?

A

production of nerve growth factor by Schwann cells

68
Q

Why does sprouting not occur in CNS axons?

A

glial scars or an absences of nerve growth factor and release of many different growth-inhibiting factors

69
Q

Synaptic changes following CNS injury:

A
  • recovery of synaptic effectiveness
  • denervation hypersensitivity
  • synaptic hypereffectiveness
  • unmasking of silent synapses
70
Q

Recovery of synaptic effectiveness:

A

occurs with the reduction in local edema that interfered with synthesis and transport of neurotransmitter and action potential conduction.

71
Q

Denervation hypersensitivity:

A

occurs after destruction of presynaptic neurons deprives postsynaptic neurons of an adequate supply of neurotransmitter. The postsynaptic neurons develop new receptors at the remaining terminals. An increased or hypersensitive response occurs to neurotransmitter released by other nearby axons

72
Q

Synaptic hypereffectiveness:

A

occurs after some presynaptic terminals are lost. Neurotransmitter accumulates in the undamaged axon terminals, resulting in excessive release of transmitter at the remaining terminals

73
Q

Unmasking of silent synapses:

A

When a synapse is silent, only N-methyl-D-aspartate (NMDA) receptors are present on the postsynaptic membrane, and synaptic transmission does not occur. The synapse becomes unmasked when alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors move into the postsynaptic membrane and the synapse becomes active

74
Q

What is excitoxicity?

A

cell death caused by overexcitation of neurons

Neuro (23 decks)

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