1.7. Physiology of nerve cells. Synaptic transmission and its regulation. Neurotransmitters. Flashcards

1
Q

I. Physiology of nerve cells
1. What is a nerve cell?

A

An electrically excitable cell that serves as a functional unit of the nervous system

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2
Q

I. Physiology of nerve cells
2. What is the role of a nerve cell?

A

Receives, processes and transmits information in the form of electrical signals

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3
Q

I. Physiology of nerve cells
3. Structure of a typical vertebral neuron (6)

A
  1. Cell body (soma)
  2. Dendrites
  3. Axon
  4. Axon terminal
  5. Axon hillock
  6. Synapse
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4
Q

I. Physiology of nerve cells - Structure of a typical vertebral neuron (6)
3A. The role of Cell body (soma)

A

site of synthesis & degradation of neuronal proteins

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5
Q

I. Physiology of nerve cells - Structure of a typical vertebral neuron (6)
3B. The role of Dendrites

A

receives synapses from other neurons

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6
Q

I. Physiology of nerve cells - Structure of a typical vertebral neuron (6)
3E. The role of Axon terminal

A

forms synapses with another neuron or effector cell, releases NT

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7
Q

I. Physiology of nerve cells - Structure of a typical vertebral neuron (6)
3F. The role of Axon hillock

A

site of nerve impulse generation & summation for incoming signals (high density of VG Na+ channels)

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8
Q

I. Physiology of nerve cells - Structure of a typical vertebral neuron (6)
3C. The role of Axon

A

transmit outgoing signals to axon terminals

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9
Q

I. Physiology of nerve cells - Structure of a typical vertebral neuron (6)
3G. The role of Synapse

A

a site where the information is transmitted form one cell to another
(chemically/electrically)

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10
Q

II. Electrical signals of neurons
1. What is an electrotonic (graded) potential?

A
  • A localized potential resulting from a local change in ionic conductance (cannot speed up to high values – only few mV)
  • Graded = analog signal
  • Typically of a low amplitude
  • Becomes exponentially smaller (decrement) as it spreads along a membrane
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11
Q

II. Electrical signals of neurons
2. What are the 3 examples of electrotonic potential?

A

1/ Receptor potential (generator potential)
2/ Excitatory postsynaptic potential (EPSP)
3/ Inhibitory postsynaptic potential (IPSP)
=> Can be de/hyperpolarized

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12
Q

II. Electrical signals of neurons
3. Characteristics of Action potential

A

Action potential: (a spreading wave of VG
Na+-channel activation)
- A rapid, transient, self-propagating
potential
- Digital signal + defined shape
(depolarization)

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13
Q

III. Receptor potential
1. What is receptor potential?

A
  • A change in voltage across the receptor membrane proportional to the stimulus strength
    -> Resulting from inward current flow (ex: sensory reception, mechanical stimulus)
  • Intensity of the receptor potential determines the frequency of AP
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14
Q

III. Receptor potential
2. What is the mechanism of receptor potential?

A

Stimulus to sensory receptor (need large mechanical stimulus -> open more channels -> more Na+ flows -> higher depolarization)

  1. Electrotonic depolarization (spreads with decrement)
  2. VG Na+-channels will open (threshold reached)
    -> Na+-current influx
  3. AP will spread along fiber
  4. VG K+-channels open, VG Na+-channels inactivated
    -> K+ out = hyperpolarization effect
  5. Repolarization below threshold (sub-threshold)
    - VG Na+-channels return to closed state
    - VG K+ - channels close
  6. Return to ‘’resting state’’
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15
Q

IV. Synaptic transmission - Synapse
1A. What is a synapse?

A

a site where information is transmitted from one cell to another, either electrically (electrical synapse) oR chemically (chemical synapse)

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16
Q

IV. Synaptic transmission - Synapse
1B. What are the differences between electrical and chemical synapses? (Mechanism, direction of transmission, Delay, localization, structure and distance)

A
17
Q

IV. Synaptic transmission
2. What are the 6 steps of synaptic transmission?

A

1) AP reaches the synaptic terminals
-> depolarization of the presynaptic terminal
2) AP causes VG Ca2+-channels to open
-> Ca2+-ions enter the synaptic terminal
3) Ca2+-ions cause synaptic vesicles to fuse with the presynaptic membrane ,which causes the release of the neurotransmitters into the synaptic cleft
4) Neurotransmitters diffuse across the synaptic cleft and bind with the receptors of the ligand-, mediated ion channels on the postsynaptic membrane
-> producing a change in the membrane potential on the postsynaptic cell
5) Change in membrane potential can be either excitatory or inhibitory, depending on the type of neurotransmitter
- Excitatory neurotransmitters -> depolarization of postsynaptic cell (EPSP)
- Inhibitory neurotransmitters -> hyperpolarization of postsynaptic cell (IPSP)

6) The neurotransmitter should be (enzymatically) degraded, diffused away or reuptaken by the presynaptic terminal to remove it from the synaptic cleft

18
Q

IV. Synaptic transmission - Excitatory postsynaptic AP (ESPS)
3A. What are the characteristics of Excitatory postsynaptic AP (ESPS)

A
  • 0,1 – 5mV depolarization for milliseconds
  • Caused by opening of ligand-gated non-selective cation channels
19
Q

IV. Synaptic transmission - Excitatory postsynaptic AP (ESPS)
3B. What is the Most frequent excitatory NT?

A

glutamate

20
Q

IV. Synaptic transmission - Excitatory postsynaptic AP (ESPS)
3C. What are the receptors for Excitatory postsynaptic potential (EPSP)?

A

1/ Inotropic receptors: (ligand-gated ion channels)
- AMPA-R: permeable to univalent cations (Na+/K+)
- NMDA-R: permeable to univalent cations and Ca2+ (Depolarization is required for opening)
2/ Metabotropic receptors: GPCRS. mGlu1-8 (all Gi, except 1 + 5 = Gq)

21
Q

IV. Synaptic transmission - Inhibitory postsynaptic potential (IPSP)
4A. What are the characteristics of Inhibitory postsynaptic potential (IPSP)?

A
  • 0,1 – 5mV hyperpolarization for milliseconds AND/OR stabilization of Em at negative values
  • Caused by the opening of ligand-gated chloride channels (or opening of K+-channels)
22
Q

IV. Synaptic transmission - Inhibitory postsynaptic potential (IPSP)
4B. What is the Most frequent inhibitory NT?

A

GABA (γ-aminobutyric acid)

23
Q

IV. Synaptic transmission - Inhibitory postsynaptic potential (IPSP)
4C. What are the receptors of Inhibitory postsynaptic potential (IPSP)?

A
  • GABA receptor types:
    1/ GABA A receptor: ligand-gated Cl–channel (activated by benzodiazepine)
    2/ GABA B receptor: involved in Gi-protein coupled receptor -> opening of K+-ch.
24
Q

V. Summation of postsynaptic potentials
1. What are the features of summation of postsynaptic potentials?

A
  • One neuron has many inputs/outputs (through synapses)
  • Postsynaptic potentials are summated between the total EPSPs and IPSPs to see which will have the dominant effect, or if they will just cancel each other out
25
Q

V. Summation of postsynaptic potentials
2A. What are the 3 types of summation of postsynaptic potentials

A
  1. Spatial summation
  2. Temporal summation
  3. Cancellation
26
Q

V. Summation of postsynaptic potentials
2B. What are the characteristics of spatial summation?

A

2 potentials from the same origin occur close together in time (f.ex. 2 EPSPs add together to make a stronger EPSP)

27
Q

V. Summation of postsynaptic potentials
2C. What are the characteristics of temporal summation?

A

2 synapses of different origin close to each other add together to have an effect on the postsynaptic potential

28
Q

V. Summation of postsynaptic potentials
2C. What are the characteristics of Cancellation summation?

A

EPSP and IPSP of the same magnitude are added together

29
Q

V. Summation of postsynaptic potentials
3. How can summation of postsynaptic potentials lead to Action Potential?

A

High density of VG Na+-channels on axon hillock
-> if combined EPSPs and IPSPs reach the threshold of Na+-channels -> AP

30
Q

V. Summation of postsynaptic potentials
4. How is AP frequency determined?

A

Amplitude of combined postsynaptic potentials (PSP) determines AP frequency

31
Q

VI. What are the 3 roles of synaptic vesicles

A

1) Synthesis: in the cell body, transported to the axon terminals through axon

2) Axonal transport: along microtubules, with the help of motor proteins (forward with kinesins + backwards with dyneins)

3) Contains…
(1) neurotransmitters
(2) proteins involved in the exocytosis
(3) proteins for transmitter uptake into the vesicle

32
Q

VII. Neurotransmitters
1. What are the 4 characteristics of neurotransmitter?

A
  • Present in presynaptic nerve terminal / synthesized by presynaptic neuron
  • Released in response to presynaptic depolarization
  • Specific receptor on the postsynaptic cell
  • Response in target cell (administered substance is also effective /
    Specific inhibitor prevents the response)
33
Q

VII. Neurotransmitters
2. How are catecholamines and transmitter amino acids taken up into vesicles?

A

Catecholamines (ex: NE, E), ACh and transmitter amino acids are taken up into vesicles in an energy-dependent manner:
- ATPase cleaves ATP and pumps H+ into the vesicle -> Concentration gradient created
- Neurotransmitter-H+ exchanger pumps H+ out and NT into the cell (secondary active transport)
Specific inhibitor prevents the response)

34
Q

VII. Neurotransmitters
3A. What are the 3 types of neurotransmitters?

A
  1. Small molecule neurotransmitters
  2. Peptide neurotransmitters
  3. Gas neurotransmitters
35
Q

VII. Neurotransmitters
3B. Examples of small molecule neurotransmitters

A
36
Q

VII. Neurotransmitters
3C. Examples of peptide neurotransmitters

A
37
Q

VII. Neurotransmitters
3D. Examples of gas neurotransmitters

A
  1. NO
  2. CO
  3. H2S
38
Q

VII. Neurotransmitters
4. What is the effect of termination of transmitter?

A
  1. Diffusion
  2. Reuptake by presynaptic terminal (in general, cotransport with Na+)
    - E.g, cocain inhibits catecholamine reuptake
  3. Enzymatic breakdown (acetylcholinesterase)
39
Q

VII. Explain frequency coding of nervous system

A
  • Maintained receptor potential induces repetitive AP firing without the neuron entering the resting state
  • The amplitude of receptor potential determines AP frequency
    -> In case of a maintained / strong stimulus, as soon as the VG K+-channels bring the membrane potential to sub-threshold level, VG Na+-channels fire again, thus
    decreasing the interval between each spike (increasing frequency)
    -> The stronger the stimulus  the higher the amplitude of receptor potential -> the higher the AP frequency