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A Physiology > 8.1. Physiology of nerve and glia cells. > Flashcards

8.1. Physiology of nerve and glia cells. Flashcards

1
Q

I. Neurons
1. What are neurons?

A

Functional cellular units of the nervous system

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2
Q

I. Neurons
2. What is the role of neurons?

A

Specialized for receiving information, making decisions and transmitting signals

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3
Q

I. Neurons
3. What is the role of cellular body (soma/perikaryon) of neurons?

A

responsible for housekeeping functions

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4
Q

I. Neurons
4. What is the role of Dendrites of neurons?

A
  • Possess receptors that bind and respond to the NT released by presynaptic membranes of neighboring neurons
  • The dendrites receive synapses from other neurons and then conduct an electrical signal to another location via their axon, and form a synapse with a different cell at the axon terminal
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5
Q

I. Neurons
5. What is the role of Axons of neurons?

A

Axons: originates from the axon hillock, often myelinated, sends signals down to the axon terminal

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6
Q

I. Neurons
6. What is the role of synapses?

A

The synapses use NTs as signaling molecules, and they may be excitatory or inhibitory molecules

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7
Q

II. Information coding in the nervous system
1. What are the 3 factors in Information coding in the nervous system?

A

1) Labelled lines
2) Spatial maps
3) Pattern of nerve impulses

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8
Q

II. Information coding in the nervous system
2A. What are the features of labeled lines?

A
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9
Q

II. Information coding in the nervous system
2B. Give an example of labeled lines?

A

E.g. electrical stimulation of the visceral system produces visual sensation

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10
Q

II. Information coding in the nervous system
3. What are the features of spatial map?

A
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11
Q

II. Information coding in the nervous system
4. What is the pattern of nerve impulses?

A

Temporal pattern or timing of APs (or AP bursts) of a single axon conveying information

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12
Q

III. Neural network function
1. Describe the input (Neural network function)

A
  • A neuron receives information from excitatory + inhibitory axon terminals via a synapse
  • Information is carried in the form of NTs
  • Depending on the types of NTs the neuron receives, EPSPs and IPSPs are generated
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13
Q

III. Neural network function
2. Describe the Computation (Neural network function)

A
  • EPSPs and IPSPs are summed
  • If depolarization reaches the threshold at the axon hillock (↑ density of VG-Na+-Ch. here) => AP generated
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14
Q

III. Neural network function
3. Describe the Output (Neural network function)

A
  • AP is conducted by the axon to the axon terminals, and influences the synaptic input of further neurons
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15
Q

IV. Postsynaptic potentials
1. What are the 2 types of Postsynaptic potentials?

A
  1. Excitatory postsynaptic potential (EPSP)
  2. Inhibitory postsynaptic potential (IPSP)
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16
Q

IV. Postsynaptic potentials - Excitatory postsynaptic potential (EPSP)
2. What are the features of Excitatory postsynaptic potential (EPSP)?

A
  • 0,1 – 5mV depolarization for milliseconds (makes postsynaptic neuron more likely to fire an AP)
  • Typically caused by the opening of ligand-gated non-selective cation channels
  • Most frequent: glutamate (Glu)-
  • Glutamate receptors:
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17
Q

IV. Postsynaptic potentials - Excitatory postsynaptic potential (EPSP)
3A. What are the glutamate receptors for Excitatory postsynaptic potential (EPSP)?

A
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18
Q

IV. Postsynaptic potentials - Excitatory postsynaptic potential (EPSP)
3B. What are the role and features of Ionotropic receptors (glutamate receptors)?

A
  1. AMPA: permeable to univalent cations (Na+-influx)
  2. NMDA: permeable to univalent cations and Ca2+ s
    o Depolarization is required for opening (EC Mg2+-plug)
    o Inhibitors: phencyclidine (PCP)
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19
Q

IV. Postsynaptic potentials - Excitatory postsynaptic potential (EPSP)
3C. What are the features of metabotropic receptors (glutamate receptors)?

A

Metabotropic receptors: (G protein, 7TM)
8 total: 1+5 = Gq, rest = Gi

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20
Q

IV. Postsynaptic potentials - Inhibitory postsynaptic potential (IPSP)
4. What are the features of Inhibitory postsynaptic potential (IPSP)?

A
  • 0,1 – 5mV hyperpolarization for milliseconds AND/OR stabilization of Em at negative values
  • Typically caused by the opening of ligand-gated chloride channels/K+-channels
  • Most frequent NT: GABA (gamma-aminobutyric acid)
  • GABA receptor types
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21
Q

IV. Postsynaptic potentials - Inhibitory postsynaptic potential (IPSP)
5A. What are the GABA receptor types?

A
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22
Q

IV. Postsynaptic potentials - Inhibitory postsynaptic potential (IPSP)
5B. What are the features of GABA-A receptor?

A
  • GABAA receptor: ligand-gated Cl—channel
  • Can be activated by benzodiazepines/barbiturates
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23
Q

IV. Postsynaptic potentials - Inhibitory postsynaptic potential (IPSP)
5C. What are the features of GABA-B receptor?

A

GABAB receptor: 7TM
- Gi-coupled
- Open the inward-rectifying K+-channels

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24
Q

IV. Postsynaptic potentials - Summation of postsynaptic potentials
6. What are the features of Summation of postsynaptic potentials?

A
  • Occurs at the axon hillock
  • 1 neuron can receive/send multiple inputs/outputs
  • 3 summation types: temporal, spatial, cancellation
  • The amplitude of combined PSPs is encoded in the AP frequency
  • Stimulation of 1 excitatory synapse is not enough to bring the neurons to depolarization = no AP
  • AP frequency is directly proportional to the summed PSP amplitude => if there is a small summated EPSP, there will be a low frequency of APs – and vice versa
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25
Q

IV. Postsynaptic potentials - Summation of postsynaptic potentials
7A. What are the types of Summation of postsynaptic potentials?

A

3 summation types: temporal, spatial, cancellation

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26
Q

IV. Postsynaptic potentials - Summation of postsynaptic potentials
7B. What are the features of temporal summation?

A
  • 1 presynaptic neuron releases NTs many times over a short period of time
  • PSPs are added together as another PSP starts to develop on top of the previous PSP
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27
Q

IV. Postsynaptic potentials - Summation of postsynaptic potentials
7C. What are the features of Spatial summation?

A
  • Summation of PSPs from different inputs at the same time, which has a more powerful effect than temporal summation
    -> consequent PSPs add up together: if strong enough = reach threshold of VG-Na+-channels => AP
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28
Q

IV. Postsynaptic potentials - Summation of postsynaptic potentials
7D. What are the features of Cancellation?

A

EPSP and IPSP at the same magnitude are added together

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29
Q

IV. Postsynaptic potentials - Summation of postsynaptic potentials
8. How is The amplitude of combined PSPs encoded?

A

The amplitude of combined PSPs is encoded in the AP frequency

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30
Q

IV. Postsynaptic potentials - Summation of postsynaptic potentials
9. Is Stimulation of 1 excitatory synapse enough to bring the neurons to depolarization ?

A

NO!!! Stimulation of 1 excitatory synapse is not enough to bring the neurons to depolarization = no AP

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31
Q

IV. Postsynaptic potentials - Summation of postsynaptic potentials
10. What is the factor that determine the AP frequency?

A

The amplitude of summated postsynaptic potentials
=> AP frequency is directly proportional to the summed PSP amplitude -> if there is a small summated EPSP, there will be a low frequency of APs – and vice versa

32
Q

V. Spiking patterns of isolated neurons
1. Why do we have Spiking patterns of isolated neurons?

A

Different types of neurons receiving the same long excitatory stimulus can either undergo ‘’adaption’’ or ‘’rhythmic bursting’’ based on their ion channel repertoire

33
Q

V. Spiking patterns of isolated neurons
2. What are the 3 types of Spiking patterns of isolated neurons?

A
  1. Non-adapting
  2. Adapting
  3. Rhythmic bursting
34
Q

V. Spiking patterns of isolated neurons
3. What are the features of Non-adapting?

A

Quickly depolarize and repolarize, can maintain a high frequency of APs (quick VG Na+- and K+-channels)

35
Q

V. Spiking patterns of isolated neurons
4. What are the features of Adapting?

A
  • Also have slowly-activating VG K+-channel that open
    => ↑hyperpolarizing current
    => Makes the AP frequency decrease despite a long stimulus
36
Q

V. Spiking patterns of isolated neurons
5. What are the features of Rhythmic bursting?

A

1

37
Q

V. Spiking patterns of isolated neurons
6. What are the features of Burst (thalamus neurons)?

A

Different types of neurons receiving the same long excitatory stimulus can either undergo ‘’adaption’’ or ‘’rhythmic bursting’’ based on their ion channel repertoire

38
Q

VII. Presynaptic inhibition
1. What is Presynaptic inhibition?

A
  • A mechanism that suppresses the release of NTs from axon terminals.
  • Importance: selective inhibition of a given excitatory input (remember α2-AR (Gi) mentioned in 1st semester)
39
Q

VII. Presynaptic inhibition
2. What is the mechanism of Presynaptic inhibition?

A
40
Q

VIII. Retrograde signaling
1. What is Retrograde signaling?

A

When the postsynaptic cell influences the presynaptic activity

41
Q

VIII. Retrograde signaling
2. What are the molecule and receptor involved in Retrograde signaling?

A
  • Cannabinoid receptors (CB1R)
  • 2-arachidonylglycerol (2-AG)
42
Q

VIII. Retrograde signaling
3. What is the mechanism of Retrograde signaling?

A
43
Q

IX. Describe Synaptic plasticity

A
44
Q

X. Synaptic strength
1. What is Synaptic strength?

A

It mean amplitude of the postsynaptic response

45
Q

X. Synaptic strength
2. What happen if Synaptic strength↑?

A
46
Q

X. Synaptic strength
3. What happen if Synaptic strength↓?

A
  • Habituation: in response to inactivity or relatively low frequency stimulation
  • Depression: after high or persistent low AP frequency stimulation
  • Long term depression (LTD)
47
Q

X. Synaptic strength
4. What are the feature(s) and mechanism of Synaptic facilitation?

A
  • Shorter effect than 1 second
  • Mechanism: AP series -> presynaptic [Ca2+] remains high -> because more Ca2+ remain, more NTs are released in response to a single AP
48
Q

X. Synaptic strength
5A. What are the features of Long term potentiation (LTP)?

A
  • Hours to days (seen in hippocampus)
  • A long-term increase in synaptic strength
49
Q

X. Synaptic strength
5B. What is the mechanism of Long term potentiation (LTP)?

A

Mechanism: in one synapse = AMPA and NMDA ionotropic glutamate receptors
1. Low presynaptic AP frequency: only AMPA-R opens (Na+-influx, weak depol.)
2. High presynaptic AP frequency: sustained AMPA-R activity

50
Q

X. Synaptic strength
5C. What happen if there is Low presynaptic AP frequency

A

only AMPA-R opens (Na+-influx, weak depol.)

51
Q

X. Synaptic strength
5D. What happen if there is High presynaptic AP frequency

A

sustained AMPA-R activity
=> stronger depol.
=> NMDA-R opens
=> Ca2+-influx
=> activation of Ca2+/calmodulin- dependent protein kinase (CamKII)
=> phosphorylation of target proteins (AMPA receptor)
=> postsynaptic sensitivity to transmitter↑

52
Q

XI. Glial cells
1. What are the features of Glial cells?

A
  • Constitute half of the volume of the brain and outnumber neurons
  • ‘’nerve glue’’, provides support for neurons
  • Intimate partners with neurons in virtually every function of the brain
53
Q

XI. Glial cells
2. What can neuroglia subdivide into?

A
  • Neuroglia can be subdivided into macroglia, which can again be subdivided to astrocytes (star-shaped appearance), oligodendrocytes and microglial cells
54
Q

XI. Glial cells
3. What are the cell types of glial cells?

A
55
Q

XI. Glial cells
4. What is the role of astrocytes?

A
  • Elaborate processes that closely approach both blood vessels and neurons
  • May transport substances between the blood and neurons
56
Q

XI. Glial cells
5. Describe the structure of astrocytes?

A
  • Dense processes of an individual astrocyte define its spatial domain
  • Specific intermediate filament: composed of glial fibrillar acidic protein (GFAP)
  • Shape and function (e.g. NT receptors) vary among astrocytes from different brain regions
57
Q

XI. Glial cells
6A. What are the 4 special forms of astrocytes?

A
  1. Radial glial cell
  2. Müller cells (span the entire width of the retina)
  3. Bergmann glial cells (their processes run parallel to the processes of Purkinje cells)
  4. Ependymal cells (ventricular lining)
58
Q

XI. Glial cells
6B. What are the features of Radial glial cell?

A
  • From the ventricle to the pial surface in the developing brain
  • Neuroblast guidance during development
59
Q

XI. Glial cells
6C. What are the features of Müller cells?

A

span the entire width of the retina

60
Q

XI. Glial cells
6D. What are the features of Bergmann glial cells?

A

their processes run parallel to the processes of Purkinje cells)

61
Q

XI. Glial cells
6E. What are the features of Ependymal cells?

A

ventricular lining

62
Q

XII. FUNCTIONS OF ASTROCYTES
1. What are the 5 functions of astrocytes?

A
  1. Astrocytes supply fuel (lactose) to neurons: (substrate buffering, 2nd energy reservoir)
  2. Regulate [K+] (and pH) of the brain EC fluid (BECF): acidemia ↔ hyperkalemia
  3. Take up the synaptically released glutamate, then release glutamine into the BEFC (Glutamate-glutamine cycle)
  4. Modulate cerebral blood flow (e.g. neural activity induced vasodilation)
  5. Secrete trophic factors that promote neuron survival and synaptogenesis:
63
Q

XII. FUNCTIONS OF ASTROCYTES
2A. How can astrocytes supply fuel (lactose) to neurons?

A
  • Astrocytes supply fuel (lactose) to neurons: (substrate buffering, 2nd energy reservoir)
  • Neurons can either
    a) Obtain glucose directly from the blood plasma
    b) Obtain lactate (LAT) from astrocytes: (trans-astrocyte path)
64
Q

XII. FUNCTIONS OF ASTROCYTES
2B. How can neurons Obtain glucose directly from the blood plasma?

A
  • GLU enters neuron through GLUT3
  • GLU converted to pyruvate to provide energy (glycolysis)
65
Q

XII. FUNCTIONS OF ASTROCYTES
2C. How can neurons obtain lactate (LAT) from astrocytes?

A
  • Astrocytes supply fuel (lactose) to neurons: (substrate buffering, 2nd energy reservoir)
  • Neurons can either
    a) Obtain glucose directly from the blood plasma
    b) Obtain lactate (LAT) from astrocytes: (trans-astrocyte path)
66
Q

XII. FUNCTIONS OF ASTROCYTES
3A. How can astrocytes regulate [K+] (and pH) of the brain EC fluid (BECF)?

A
  • Frequent depolarization of neurons leads to high [K+]EC and low [Na+] locally
  • Astrocytes regulate that via 3 transporters:
    1. Na+/K+-ATPase (K+ in, Na+ out) - Primary transport
    2. Na+/K+/2Cl—transporter - Secondary transport
    3. K+-channels allow influx of K+ - passive transport (this is an exception because K+ always moves outward)
    => Spatial buffering of K+ by astrocyte syncytium
67
Q

XII. FUNCTIONS OF ASTROCYTES
3B. In regulation of [K+] (and pH) of the brain EC fluid (BECF), why is an influx of K+ by K+ chennales an exception?

A
68
Q

XII. FUNCTIONS OF ASTROCYTES
4A. Astrocytes are able to take up the synaptically released glutamate
=> Explain this function

A
69
Q

XII. FUNCTIONS OF ASTROCYTES - Take up the synaptically released glutamate, then release glutamine into the BEFC
4B. Glutamate is taken up by the presynaptic terminal (the same one it was released from) through ____

A

an excitatory AA transporter (EEAT)

70
Q

XII. FUNCTIONS OF ASTROCYTES
5A. How can astrocytes .Modulate cerebral blood flow?

A
71
Q

XII. FUNCTIONS OF ASTROCYTES
6. What are the role of types of trophic factors secreted by astrocytes?

A

Secrete trophic factors that promote neuron survival and synaptogenesis:
- Brain-derived neurotrophic factor (BDNF)
- Glial-derived neurotrophic factor (GDNF)

72
Q

XIII. Oligodendrocytes and Schwann cells
1. What is the role of Oligodendrocytes and Schwann cells?

A

Make and sustain the myelin sheath

73
Q

XIII. Oligodendrocytes and Schwann cells
2. What are the features of oligodendrocytes?

A
  • CNS: oligodendrocytes
  • 15 – 30 processes myelinates many axons
  • BECF pH regulation, iron metabolism
74
Q

XIII. Oligodendrocytes and Schwann cells
3. What are the features of Schwann cells?

A
  • PNS: Schwann cells
  • A single myelin segment to a
    single axon of a myelinated nerve
  • BECF pH regulation, iron metabolism
75
Q

XIV. Microglial cells
1. What are Microglial cells?

A

the macrophages of the CNS

76
Q

XIV. Microglial cells
2. What are the features of Microglial cells?

A
  • Derive from the cells related to the monocyte-macrophage lineage
  • ~20% of the total glial cells
  • Most effective antigen-presenting cells within the brain (activated T lymphocytes are able to cross the BB)
77
Q

XIV. Microglial cells
3. What happen when Microglial cells are activated?

A
  • Proliferate
  • Change shape
  • Become phagocytic
  • Release cytokines, free radicals and NO

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