Neurons Flashcards

1
Q

Neurons

A

Building blocks and instrument of communication in brain

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2
Q

Synaptic potential

A

Inputs from other neurons from dendritic tree to cell body ‘soma’

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3
Q

Action potential

A

Signal flows away from soma to synaptic boutons (axon terminal), communicate with other neurons

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4
Q

Neurons consist of

A

Soma (cell body), Dendrites, usually 1 axon

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5
Q

Purkinje cell

A

Found in cerebellum

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6
Q

Cerebellum

A
  • Receives infro from sensory systems, spinal cord, other parts of brain
  • Coordinates voluntary responses,
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7
Q

Pyramidal cell

A

Found in cerebral cortex

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8
Q

Cerebral cortex

A

Outer layer of cerebrum

Important role in consciousness, thinking, action

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9
Q

Resting Membrane Potential (RMP)

A
  • Electrical potential difference across cell membrane which results form separation of charge
  • Absence of synaptic and action potentials
    (-50 -> -70 mV)
  • Cytoplasm more negative than extracellular space
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10
Q

How and what parts of the body are excitable

A

Neurons, muscle fibres, some endocrine cells

Respond with short-term change of potential by Action Potential, in response to a stimulus

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11
Q

What causes RMP

A

Unequal conc. of Na+ and K+ inside and outside cell

Unequal permeability of cell membrane to these ions

Small contribution:
Electrogenic action of Na-K pump

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12
Q

Unequal conc. of Na+ and K+

A

Carrier protein, Na-K pump, ‘salty banana’
3 Na OUT, 2 K IN
Primary active transport
ATP needed]

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13
Q

Explaining unequal permeability

A
Selective permeability of ions:
non-gated 'leak'
channels
- 40:1 ratio, K to Na 
- Open @ rest

Gated (voltage, ligand) channels
- Closed @ rest

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14
Q

Equilibrium potential of Na and K

A

K outside = 5 mM
Na inside = 15 mM
K inside = 100 mm
Na outside = 150mM

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15
Q

Nernst equation for each ion at equilibrium potential

A

61.5 x log( [Ion] outside/ [ion] inside)

E(K) = -80 mV
E(Na) = + 60 mV

Only applies if cell membrane permeable to ONLY ONE ION

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16
Q

RMP rule

A

Higher permeability of cell membrane to particular ion (e.g. K+), RMP closer to equilibrium for that ion, (e.g. E(K+)) = -80 mV

  • closer to -80 mV than to E(Na+) which is +30 mV
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17
Q

Goldman Equation

A

Calculates RMP taking into account:

  • Both concentration gradients
  • Relative permeability of cell membrane to K+ and Na+ ions
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18
Q

Action Potential

A

Brief fluctuation in membrane potential caused by transient opening of voltage-gated ion channels (mainly Na+ and K+) that spread like a wave along neuron

  • Occurs after threshold of -55 mV reached
  • Can also be transmitted along muscle fibres
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19
Q

Significance of Action Potentials

A

Information is coded in the frequency of action potentials
- AP’s regarded as ‘language’ which neurons communicate by

Key element of signal transmissions along axons (often v. long)

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20
Q

First stage of AP

A
Fast depolarisation
- After threshold of -55mV reached
- Overshoot from -55mV to +30 mV
- Voltage-gated Na+ channels open very fast
P(Na+) > P(K+) in a 20:1 ratio
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21
Q

Stimulus

A

Detectable change in internal/external environment

  • Physical
    (light, electric current, stretch)
  • Chemical
    (drug, synaptic excitation)
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22
Q

2nd stage of AP

A

Repolarisation

  • Na+ channels inactivate, and are short lived
  • Transient opening of K+ channels repolarise membrane potential
  • P(K+) > P(Na+) in a 100:1 ratio
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23
Q

Why doesn’t membrane potential reach +60 mV @ 1st stage

A

MP shifts towards E(Na+) as Na: K ratio is 20:1

  • Na+ channels short lived and quickly inactivate
  • Transient opening of K+ voltage-gated channels

Leads to repolarisation and AHP

MP shifts towards E (K+) which is -80mV as P(K+) > P(Na+) 100:1

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24
Q

3rd stage of AP

A

After Hyperpolarisation (AHP)
Voltage-gated K+ channels open for a while then close
- Dips belows -70mV (RMP) as it wants to get closer to E(K+) which is -80mV
- P(K+) > P(Na+)

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25
Q

Hyperpolarisation

A

If Membrane potential becomes MORE negative
(e.g. -70mV to -75mV)

Potential inside cell moves closer to E(K+) and away from E(Na+)

Results from slow closing of voltage gated K+ channels

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26
Q

Depolarisation

A

If Membrane potential becomes LESS negative
(e.g. -70mV to -60mV)

Potential inside cell moves closer to E(Na+) and away from E(K+)

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27
Q

Are Neuron potentials constant

A

NO

Change when conc. of ions or membrane permeability change

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28
Q

Activation/ Deactivation of Na+ channel

A

1) RMP (negative MP) Voltage sensor/ ACTIVATION GATE opens when it senses depolarisation
2) Depolarisation to threshold (less negative MP)

3) Fraction of a millisecond later inactivation occurs by INACTIVATION GATE
(+ MP)

4) Back to initial state when membrane repolarises
activation gate back, inactivation gate released

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29
Q

SUPRAthreshold

A

Stimulus large enough in magnitude to produce an AP in excitable cells

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30
Q

How can AP evoked (awaken)

A

1) Outside from + to - (extracellular fluid) - electrolytes etc.
2) Across membrane and inside axon

ONLY path 2) can change RMP

Current generated by OUTSIDE source flows through cell membrane from OUTSIDE -> INSIDE
(Hyperpolarisation- more -ve)

INSIDE -> OUTSIDE
Depolarisation (MP less -ve)

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31
Q

Which way does current flow

A

Current flow is shown by direction/ movement of cations

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32
Q

How are AP’s first generated in CNS neurons

A

AP’s first generated in axon initial segment (axon hillock) which has the lowest threshold so acts as a ‘trigger zone’ for AP’s

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33
Q

How does depolarisation occur in CNS neurons

A

Caused by excitatory postsynaptic potentials (EPSP’s), spread passively from dendrites to axon initial segment

Once AP generated, it is transmitted ACTIVELY along axon, away from soma

34
Q

Chemical potential

A

Difference in solute concentrations across a membrane

35
Q

Electrical potential

A

Difference in charge across a membrane

36
Q

Electrochemical gradient

A

Sum of chemical and electrical gradients for that particular ion

37
Q

How does repolarisation of membrane potential occur during action potential of a neuron?

A

K+ efflux (leaves cell)

as Na+ channels are closed so can’t enter or leave

38
Q

Where are action potentials regenerated as they propagate along a myelinated axon?

A

At nodes

Voltage-gated sodium channels are largely restricted to the nodes between myelinated internodes.

39
Q

Myelinated axons

A

Larger diameter than unmyelinated (5-10 um)

AP’s transmission is fast and
saltatory (large steps)

20 to 100 m/sec

40
Q

Which type of axon will velocity of action potential conduction be the fastest?

A

Myelinated axons with the largest diameter

41
Q

What changes occur to voltage-gated Na+ and K+ channels at the peak of depolarization?

A

Inactivation gates of voltage-gated Na+‎ channels close, while activation gates of voltage-gated K+‎ channels open.

42
Q

Unmyelinated axons

A
Small diameter (1 um)
AP transmission must be REGENERATED at EVERY POINT on membrane therefore is conduction velocity is slow and continuous

1 m/sec

43
Q

Action potential transmitted in unmyelinated axons

“battery”

A

1) Action potential
2) Passive current flow
3) Depolarisation of ADJACENT parts of membrane to threshold
4) Voltage-gated Na+ channels in adjacent parts of membrane open
5) New FULL SIZE AP generated in adjacent parts of membrane

44
Q

AP transmission of myelinated axons

A

Increase efficiency of passive thread
Only regenerated @ NODES OF RANVIER

Current flows passively between nodes ‘saltatory conduction’

45
Q

What is the Myelin Sheath formed from

A

Formed by two types of glia cells

Oligodendrocytes in CNS

Schwann cells in PNS

46
Q

Myelin

A

‘Insulates’ axon, NO AP generated here, as no flow of current
LESS current dissipation along axon

47
Q

Under physiological conditions why does AP only flow in one direction

A

Due to absolute refractory period (nerve cell can’t respond to another stimulus)

Na+ channels still INACTIVATED

By the time ARP is over, AP has already moved down axon towards next NoR

48
Q

How long does absolute refractory period last

A

1-2 ms

Occurs during stage 1+2 of AP

49
Q

Why don’t we have all myelinated axons in our body

A

Although they transmit AP faster, they are larger in size, so we would fit less axons into smaller spaces (e.g. skull)

50
Q

Receptor Potential concept

A

When stimulus acts on receptors in SENSORY neurons, AP’s are not immediate

1) Graded depolarisation (aka receptor potential) at sensory endings

Receptor potential PASSIVELY spreads to TRIGGER ZONE

51
Q

Trigger Zone

A

Where AP’s are generated in sensory neurons

Contains Na+ and K+ voltage gated channels for depolarisation

52
Q

Sensory Neurons

A

Unipolar
Can be myelinated or non-myelinated
AP’s travel towards CNS

53
Q

Muscle spindles

A

Gated channels by mechanical force
Stretch of membrane opens channel
Non-selective cation channels, Na+ moves in more than K+ wants to leave

54
Q

Stretch of stimulus on sensory muscle spindle

A

Coded by amplitude of receptor potential and frequency of AP’s

55
Q

Most abundant class of neuron in the central nervous system is

A

Multipolar

56
Q

Branches along axons

A

Collaterals

57
Q

Extensive damage to oligodendrocytes in CNS can cause

A

Loss of sensation and motor control

58
Q

Synaptic transmission

A

Process of transferring information between neurons or between neuron and muscle fibres

59
Q

Two ways synaptic transmission occurs between neurons

A

1) Chemical synapses

2) Electrical synapses (via pores called ‘gap junctions’)

60
Q

Where do Chemical Synapses occur

A

Between

  • Neurons in brain
  • Neurons and muscle fibres
61
Q

Neuromuscular junction

AKA ‘end plate’

A

Synapse between neuron and muscle fibre

62
Q

Two main types of chemical Synapses

A

Excitatory Synapse

Inhibitory Synapse

63
Q

Excitatory Synapses

EPSP

A

Depolarisation of Post synaptic neuron

Excitatory Postsynaptic Potential

64
Q

Mechanism and Neurotransmitters of Excitatory synapses

A

Transient opening of channels selective for Na+, K+ and Ca2+

Glutamic acid (glutamate)
Ach
65
Q

Mechanism and Neurotransmitters of Inhibitory synapses

A

Transient opening of K+ channels

GABA (gamma-aminobutyric acid)
Glycine

66
Q

Inhibitory Synapse

IPSP

A

Hyperpolarisation (more -ve, further away from threshold) of postsynaptic membrane

Increase in cell membrane permeability to K+

67
Q

What are Neurotransmitters

A

Chemical ‘messengers’ that open (sometimes close) ion channels

Lead to depolarisation or hyperpolarisation

Each neurotransmitter can bind to many different receptors each have different neuron function

68
Q

Small Molecule (Classical) Neurotransmitters and examples

A
Fast action (milliseconds)
Directly act on postsynaptic membrane

Examples:
Amino acids
(glutamate, GABA, glycine)

Acetylcholine

Noradrenaline, Dopamine, serotonin

69
Q

Neuropeptides (neuromodulators)

A
Large molecule
Slow (sec -> minutes)
Indirectly act on PSM
Modulatory action
- no effects themselves, but alter other neurotransmitter effects
Examples:
Enkephalin
Substance P
Neuropeptide Y (NPY)
Kisspeptin
70
Q

Factors determining synaptic action

A

Type of neurotransmitter
Type of receptor/ channel in PSM
Amount of neurotransmitter receptor present

71
Q

Glutamate receptors and function in CNS

A

4 receptors in PSM, all allow Na+, K+ in

TOO much–> excessive activation of neurons

AMPA
NMDA (also allows Ca2+)
Kainate
‘metabotropic’ glutamate receptor (slower action)

72
Q

Excitotoxicity

A
Excess Ca2+ from NMDA
Neuron damage leading to 
- Stroke
- Brain damage
- Epilepsy
73
Q

Synaptic Plasticity

A

ability of synapses to strengthen/weaken over time, in response to increases or decreases in their activity

LTP - long-term potentiation
LTD- long-term depression

How we learn, study, memorsie

74
Q

Direct gating

A

Neurotransmitter directly binds to receptor/ ion channel

Depolarisation or hyperpolarisation of membrane as ions flow in

Fast (< 1 msec)
Short (msec range)

75
Q

Indirect gating

A

Transmitter binds to G-coupled ‘metabotropic’ receptors activating a pathway involving G-proteins

Protein kinases activated by second messengers phosphorylate ion channels to open/close
- change MP

slow and long-lasting (sec-min)

76
Q

Spatial summation

A

involves multiple AP on pre-SN that are active simultaneously

EPSP’s arrive at several places on neuron causing build up of depolarisation

77
Q

EPSPs and IPSPs are integrated at the

A

Axon hillock

78
Q

Temporal summation

A

When EPSPs arrive in rapid succession on ONE presynaptic neuron causing buildup of depolarization

More frequency of AP, higher chance total may exceed threshold

79
Q

1st way of neurotransmitter inactivation

A

1) diffusion

- all NT removed from synaptic cleft to some degree by diffusion

80
Q

2nd way of NT inactivation

A

2) Enzymatic degradation
- Ach removed by Achsterase (< 1ms)

Monoamine Oxidase (MAO) degrades amines

Peptidases cleave neuropeptides

81
Q

3rd way of inactivation

A

3) Re-uptake
Specific neurotransmitter transporters in presynaptic membrane or adjacent glia cells

E.g. glutamate transporter takes gluatamate to different places

82
Q

End plate potentials

A

Ionic channels to both Na+ and K+ (non-selective cationic channels)