Week 3 Flashcards Preview

Neuro > Week 3 > Flashcards

Flashcards in Week 3 Deck (74):
1

Postsynaptic terminal can be:

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

2

Where can synaptic communications between neurons occur?

cell body
dendrites
axon

3

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

opening of membrane ion channels

4

What generates a local postsynaptic potential?

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

5

Axaxonic activity produces:

presynaptic effects

6

Postsynaptic potentials can be either:

excitatory
inhibitory

7

Excitatory:

from a local depolarization

8

Inhibitatory:

from a local hyperpolarization

9

What are presynaptic effects?

facilitation
inhibition

10

A local depolarization is what?

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

11

What is a local hypepolarization?

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

12

Spatial summation:

simultaneous potentials from different locations across the cell body

13

Temporal summation:

not absolutely simultaneous but overlapping potential at a given time

14

When is an action potential triggered?

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

15

When does presynaptic effect occur?

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

16

What is presynaptic facilitation?

More neurotransmitter is released

17

When does presynaptic facilitation occur?

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

18

What is presynaptic inhibition?

Less neurotransmitter is released.

19

When does presynaptic inhibition occur?

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

20

What can intensify pain experience?

presynaptic faciliation through signals interpreted as pain
mentally focusing on pain can increase the level of activity of brain areas associated with the pain

21

What are the two classes of neurotransmitters?

small molecule neurotransmitters
peptide neurotransmitters

22

What are the two families of receptors?

iontropic (ligand gated ion channels)
metabotropic: receptor activating second messenger systems

23

What is a neurotransmitter?

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

24

What is a neuromodulator?

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

25

What is the effect of a neuromodulator?

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

26

What does neurotransmitters do to the postsynaptic neuron?

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

27

What are the types of neurotransmitters?

fast acting (act directly)
slow acting (act indirectly

28

How much transmission time does a fast acting neurotransmitter require?

1/1000 of a second

29

How much transmission time does a slow acting neurotransmitter require?

1/10 of a second to minutes

30

Fasting acting:

ACh
Amino acids

31

Acetylcholine

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

32

Glutamate

amino acid
excitatory and elicits neural changes that occur with learning and development

33

Glycine and gamma-aminobutyric acid (GABA)

inhibitory and have preventive effect on excessive neural activities

34

Slow acting:

Amines
peptides
nitric oxide

35

What are some amines:

widely distributed throughout nervous system
dopamine, norepinephrine (NE), serotonin and histamine.

36

Peptides:

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

37

Examples of peptides:

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

38

Nitric oxide:

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

39

What is Substance P?

One of the most common neuropeptides
Stimulates nerve endings at the site of injury

40

Sustance P in the CNS?

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

41

Implication of substance P inCNS?

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

42

Synaptic receptors produce:

direct or indirect action

43

Synaptic receptors acting directly:

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

44

Synaptic receptors acting indirectly:

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

45

Three mechanisms of postsynaptic receptors to transduce signals:

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

46

What is modifiability?

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

47

Where can plasticity occur?

at synapses, neuronal circuits or neural systems

48

What is neuroplasticity?

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

What does neuroplasticity encompass?

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

50

What is habituation?

a decrease in response to a repeated, benign stimulus
-short term and reversible

51

What does habituation describe in PT/OT?

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

52

What is experience-dependent plasticity?

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

53

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

long term potentiation (LTP)
long term depression (LTD)

54

What is a silent synapse?

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

55

What is an active synapse?

when mobile AMPA receptors are inserted into the synaptic membrane

56

What does induction of LTP require?

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

57

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

1. voltage-dependency of NMDA mediated currents
2. permeability of NMDA channels to Ca2+

58

What is long term depression?

a conversion of an active synapse to a silent synapse

59

What causes a LTD?

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

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

Axons

61

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

cell body

62

What are the degeneration changes following axonal injury/

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

What is sprouting?

regrowth of damaged axons

64

What are the two forms of sprouting?

collateral and regenerative

65

What is collateral sprouting?

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

66

What is regenerative sprouting?

occurs when an axons and its target cell have been damaged

67

What causes the functional regeneration of axon?

production of nerve growth factor by Schwann cells

68

Why does sprouting not occur in CNS axons?

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

69

Synaptic changes following CNS injury:

- recovery of synaptic effectiveness
- denervation hypersensitivity
- synaptic hypereffectiveness
- unmasking of silent synapses

70

Recovery of synaptic effectiveness:

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

71

Denervation hypersensitivity:

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

Synaptic hypereffectiveness:

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

Unmasking of silent synapses:

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

What is excitoxicity?

cell death caused by overexcitation of neurons