Quiz 2 - Neurophysiology Flashcards

Study to ACE quiz 2!

1
Q

What is a microglia responsible for?

A

Immune system function.

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2
Q

What kinds of macroglia are there?

A

Astrocytes (do a little bit of everything)

  • Schwann Cells
  • Radial Glia
  • Oligodendrcytes
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3
Q

What are glia responsible for?

A
  • Act as glue
  • Exchange signals with neurons
  • Help establish synapses
  • Remove neurotransmitters after release
  • Release “gliotransmitters” to regulate activity of neurons.
  • make proteins and pass it on to the neurons.
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4
Q

What is ataxia?

A

Gene mutations of glia result in this neurological disorder.

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5
Q

How can neurons be classified?

A

By structure or function

  • Unipolar
  • Bipolar
  • Multipolar
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6
Q

What are some examples of different types of neurons?

A

Sensory neurons: bring information to the central nervous system.
Inter-nuerons: associate sensory and motor activity in the cns.
Motor neurons: Send signals from the brain and spinal cord to muscles.

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7
Q

Describe the pathway of a neuron.

A
  1. Dendrites
  2. Cell body
  3. Axon hillock
  4. Axon
  5. Presynaptic Terminal
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8
Q

What do reflexes do?

A

pass information to brain.

  • Used to study behavior
  • Automatic
  • Include inhibition and excitation
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9
Q

What are convergence and divergence reflex pathways?

A
  • Convergence (many signals come to one) and divergence (one signal splits to many) pathways.
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10
Q

What is feed forward inhibition?

A

When a excited pathway inhibits a second pathway.

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11
Q

What is feedback inhibition?

A

Excited pathway leads to inhibition of that pathway.

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12
Q

What occurs at the axon hillock?

A

Integration of information.

  • Rich in voltage-sensitive channels
  • EPSPs and IPSPs integrated
  • Action potentials initiated here
  • Depolarize membrane at axon hillock to threshold.
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13
Q

What is the usual membrane potential?

A

-70mV

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14
Q

Does output of signal depend on input?

A

Yes, more input from initial signal = more output (more transmitter release)
- Frequency of firing tells intensity of signal

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15
Q

What is a labeled-line?

A

Each neuron is prewired to carry information from a certain point to the appropriate part of the brain.

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16
Q

Describe ion-channels.

A

Membrane-spanning proteins.

  • regulate ion passage based on size and chemical identity.
  • Gated: voltage, chemically, physically.
  • Studied using patch clamps
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17
Q

What are the factors for ion movement?

A

Concentration gradient and Electrical charge.

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18
Q

How do channels open and close?

A

By changing conformation due to ligands, signals, etc.

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19
Q

What do channels consist of?

A

Built of protein subunits and are distinct from each other.

- Subunits affect the channel kinetics.

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20
Q

Do K+ and Cl- pass readily?

A

Yes.

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21
Q

What are leak channels?

A

Ion channels that are always open and NOT gated.

- EG. K+ leak channel or Na+ leak channel

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22
Q

What is Nernst (equilibrium) potential?

A

E(x) = 57mv/z log [Xout]/[Xin]

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23
Q

What do graded potentials do?

A

Disrupt RMP

  • small voltage fluctuation in cell membrane
  • decay over time and space
  • depolarizing (EPSP) or hyperpolarizing (IPSP)
  • Combined through spatial or temporal summation.
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24
Q

What are the differences between Graded and action potentials?

A

AP: all or none, slower, passive AND active
Graded: decremental, fast, passive

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25
Q

Factors that input depends on.

A
  • Location and size of synapse (greatest at hillock)
  • Proximity to other synapses
  • Relative strength of other synapses
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26
Q

How do PSPs affect membrane voltage?

A

By 0.2 - 0.4 mV

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27
Q

Describe spatial summation.

A

The larger the slower the curve falls off.

- Membrane length constant

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28
Q

Describe temporal summation.

A

Larger = drops off slowly

- membrane time constant

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29
Q

How is the speed of an action potential affected?

A

Speed affected by myelination and diameter of axon.

- Thicker diameter = faster

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30
Q

Describe the steps of an action potential.

A
  1. Depolarization to threshold.
  2. Activation of sodium channels and rapid depolarization (influx of Na+)
  3. Inactivation of sodium channels and activation of potassium channels (efflux of K+) repolarization
  4. Return to normal permeability after hyperpolarization
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31
Q

What is an absolute refractory period?

A

Action potentials can’t generate during this time.

  • Prevent backwards movement
  • Limit rate of firing
  • Na+ channels inactive
  • Occurs during depolarization
32
Q

What is the relative refractory period?

A

K+ channels still active

  • Requires stronger than usual stimulus to trigger an action potential.
  • Occurs during repolarization phase.
33
Q

What is myelin for?

A

Formed by oligodendrocytes in CNS and Schwann cells in PNS

- Speeds up neural impulse.

34
Q

What is the node of Ranvier?

A

Part of axon not covered by myelin

  • occur every 1-2 mm
  • 50x more voltage-sensitive channels here
  • Signal jumps to each node
35
Q

What happens at regions with no myelin?

A

Many interactions between the outside and inside of cell leading to no completed travel of signal.

36
Q

What are chemical synapses?

A

APs open Ca2+ channels

  • Forces vesicles to fuse with membrane
  • chemical released and diffuses across synaptic cleft (20-40 nm)
  • neurotransmitter bins to receptors and causes change in postsynaptic cell
  • slower than electrical synapses (0.3 ms)
  • allows variability and signal amplification
37
Q

What is the purpose of microtubules?

A

Transport structure that carries substances to the axon terminal.

38
Q

What is an ionotropic transmembrane protein?

A

Ion movement through ion channels.

39
Q

What are metabotropic transmembrane proteins?

A

Alter metabolism by changing shapes and effecting interactions inside.

  • Activates second messenger via G protein
  • Hydrolysis of membrane phospholipids (IP3, DAG, arachidonic acid (inflammation))
  • Soluble gases (NO, CO)
  • cAMP
  • 7 domains.
40
Q

What is an example of indirect gating?

A

G-protein coupled receptors

41
Q

What is an example of direct gating?

A

Ion channels

42
Q

Describe neuromusuclar junction

A

Axon branches

  • ACh packaged in vesicles at active zones.
  • ACh released onto unction folds
  • AChE in basement membrane and diffusion rapidly inactivates signal.
43
Q

Describe ACh-Gated Ion channels.

A

Requires 2 ACh to open

  • Permeable to both Na+ and K+
  • Rapid switching between on and off states.
  • Allows 17 million ions to pass/sec
  • Average open time 1 ms
  • Normal stimulation opens ~200,000 channels
44
Q

What are some examples of excitation and inhibition transmitters?

A

Glutamate = excitation

GABA and Glycine = inhibition

45
Q

What do IPSPs do?

A

Inhibit signal.

46
Q

Describe a type 1 synapse (slide 69)

A

Excitatory

  • typically coated on dendrites
  • large active zone
  • wide cleft
  • round vesicles
  • dense material on membranes (a lot)
47
Q

Describe a type 2 synapse (slide 69)

A

Inhibitory

  • typically located on cell body
  • small active zone
  • narrow cleft
  • flat vesicles
  • Sparse material on membranes (little)
48
Q

Postsynaptic Potentials

A

Dendrites contain vlotage-gated Na+ and Ca2+ channels that amplify small EPSPs.
- Channels can also back propagate action potentials to dendrites, but function of this unclear.

49
Q

What is dendrodendritic?

A

Dendrites send messages to other dendrites

50
Q

What is axodendritic?

A

Axon terminal of one neuron synapses on dendritic spine of another.

51
Q

What is axoextracellular?

A

Terminal with no specific target. Secretes transmitter into extracellular fluid.

52
Q

What is axosomatic?

A

Axon terminal ends on cell body

53
Q

What is axosynaptic?

A

Axon terminal ends on another terminal.

54
Q

What is axoaxonic?

A

Axon terminal ends on another axon. (usually inhibitory)

55
Q

What is axosecretory?

A

Axon terminal ends on tiny blood vessel and secretes transmitter directly into blood.

56
Q

Basic pathway of metabotropic receptor.

A
  1. External signal (first messenger)
  2. Receptor (extracellular side)
  3. Transducer
  4. Primary effector
  5. Second messenger
  6. Secondary effector
57
Q

What are some first messenger signals?

A

Norepinephrine, ACh, Histamine

58
Q

What are some receptors?

A

Beta-adrenergic receptor, muscarinic ACh, Histamine receptor

59
Q

What are some primary effectors?

A

Adenylyl cyclase, PLC, PLA2

60
Q

What are some second messengers?

A

cAMP, IP3, DAG, Arachidonic acid

61
Q

What are some transducers?

A

G subunits

62
Q

What are some secondary effectors?

A

cAMP-dependent protein kinase, Ca2+ release, PKC, lipoxygenase

63
Q

What is cAMP?

A

alpha subunit dissociates from G protein to affect target

  • each with unique properties.
  • process continues until transmitter removed.
64
Q

IP3, DAG pathways

A

Membrane phospholipids hydrolyzed, separating polar head group from glycerol and tails

  • most common target is PIP2
  • DAG and IP3 produced
  • DAG activates protein kinase C
  • IP3 releases Ca2+ from storage.
65
Q

What are tyrosine receptor kinases?

A

Activated by peptides: FGF, NGF, BDNF, insulin

  • ligand binding causes dimerization, which activates TRK
  • Activated enzyme ultimately causes long-term, slow-acting changes in gene expression.
66
Q

What are soluble gases and their use?

A

NO, CO

  • Easily cross membranes
  • Don’t use surface receptor
  • Stimulates synthesis of cGMP
  • Retrograde signaling: produced in postsynaptic travels backwards to interact with presynaptic.
  • Must be made and used quickly because it can’t be stored.
67
Q

What does transmitter release depend on?

A

Ca2+ influx to presynaptic terminal

68
Q

There is a ______ number of _____ _____ channels at _____ zone.

A

Large, voltage-gated Ca2+, active

69
Q

What stores neurotransmitters and how are they released?

A
  1. Packed into vesicles.
  2. Vesicles fuse to membrane and release transmitter by exocytosis.
  3. Fusion pore channel vs. complete fusion
70
Q

What are the criteria for neurotransmitters?

A
  1. Synthesized in neuron
  2. Present in synaptic terminal and released to cause effect
  3. Exogenous administration mimics endogenous effects.
  4. Removal mechanism exists
71
Q

Describe small-molecule transmitters.

A
  1. Quick-acting neurotransmitters
  2. Synthesized in axon terminal and pumped into vesicles.
    EG: ACh, Amines (DA,NE, Histamine), Amino acids, ATP
72
Q

Describe neuropeptide transmitters.

A
  1. Multifunctional chain of amino acids that act as neurotransmitter
  2. Synthesized from mRNA; often many different made from single mRNA
  3. Do not bind to ion channels
  4. Cause inhibition, excitation or both
73
Q

What are the similarities and differences between small-molecule and peptide neurotransmitters?

A

Similarities: Send signals, used in most neurons, can coexist in vesicles for peptides
Differences: SM = synthesized locally, vesicles produced at presynaptic terminal and recycled, released by Ca2+ influx at active zones.
Peptides = synthesized in cell body, vesicles derived from golgi and are not recycled, released by non-specific mechanism anywhere in the cell, and requires higher Ca2+ concentration to cause exocytosis (repeated stimulation)

74
Q

Why is the removal of neurotransmitters important?

A

To end current message and allow new message.

75
Q

What are the three mechanisms for removal of neurotransmitters?

A
  1. Enzymatic degradation: ACh esterase
  2. Diffusion: Large molecules (transmitters, polypeptides)
  3. Reuptake: Repackaged and reused (DA, NE, Serotonin)