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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
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

Neuro (23 decks)

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