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1. Foundations of Medicine PoNF > Nerves > Flashcards

Nerves Flashcards

1
Q

What are the subdivisions of the nervous system

A
  • CNS: Brain, Spinal cord
  • PNS: Autonomic (symoathetic/parasympathetic/enteric), Somatic

See diagram

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2
Q

Lable parts of brain (name them)

See sheet for diagram

A
  • Meninges
  • Gyrus vs. sulcus
  • Cerebellum
  • Cerebrum- frontal lobe, temporal lobe, parietal lobe, occipital lobe
  • Diencephalon- thalamus, hypothalamus
  • Brainstem- midbrain, pons, medulla oblongata
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3
Q

Number of pairs of spinal nerves

A

31

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4
Q

give the arrangement of spinal nerves

A
  • 8 cervical (although 7 vertebrea)= neck, shoulders and arms
  • 12 thoracic= chest and abdomen
  • 5 lumbar= hips and legs
  • 5 sacral= genitalia and gastrointestinal tract
  • 1 coccygeal
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5
Q

Lable the spinal chord cross section

A

See diagram

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6
Q

Nerve afferent

A

Sensory info (go in)

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7
Q

Nerve efferent

A

Motor (go out)

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8
Q

What is grey matter/what makes it grey

A

cell bodies

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9
Q

Why is white matter white

A

myelin - white fibres

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10
Q

Anatomy of a neuron

A
  • dendrites- receive information
  • cell body (soma)- contains the nucleus
  • initial segment (axon hillock)- triggers action potential
  • axon- sends action potential
  • axon (presynaptic) terminals- releases neurotransmitter

see picture

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11
Q

Types of neuron

A

Afferent (sensory) neurons PNS —> Interneurons CNS —> efferent (motor) neurons PNS

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12
Q

Moorphology of neurons

A
  • afferent (sensory) neurons= bipolar, pseudounipolar
  • interneurons= multipolar, anaxonic
  • efferent (motor) neurons= multipolar
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13
Q

what are glia

A

Cells that support neurons (non-neuronal cellsof the brain/nervous system)

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14
Q

Types of glia cells in CNS

A

astrocytes, oligodendrocytes, microglia, ependymal cells

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15
Q

What do astrocytes do

A
  • Maintain external environment for the neurons
  • Surround blood vessels and form blood brain barrier
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16
Q

What do oligodendrocytes do

A

Form myelin sheaths in the CNS

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17
Q

what do microglia do?

A

macrophages of the CNS, hoover up infection

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18
Q

What do ependymal cells do?

A

produce the cerebrospinal fluid

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19
Q

Tyopes of glial cells in PNS

A

Schwann cells and satellite cells

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20
Q

What do Schwann cells do?

A

form myelin sheath in PNS

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21
Q

What do satellite cells do?

A

support neuron cell bodies

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22
Q

What does a neuron look like?

A

see picture

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23
Q

How do neurons send electrical signal

A

Action potentials= transmit signals over long distances

Graded potentials= decide when an action potential should be fired

Resting membrane potentials= keeps cell ready to respond

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24
Q

What is the resting membrane potential

A
  • Inside potential of cell relative to outside
  • Outside taken as 0mV and inside relative to this (usually -70mV in neurons)
  • Aka potential difference
  • Inside is negative
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25
Q

How do we create a resting membrane potential

A
  1. Phospholipid bilayer impermeable to water and ions
  2. Assume equal concentrations of NaCl and KCl inside and outside the cell
  3. Everything is balanced inside and outside the cell - No membrane potential

Then…

  1. Na/K pump uses ATP to pump K into and Na out of the cell
  2. charges still balanced (ish) - still no membrane potential

Then…

  1. Add “leaky K” channel
  2. Some K leaks out cell down its conc gradient
  3. Builds up electrical gradient
  4. Equilibrium is reached when electrical gradient is equal and opposite to conc gradient
  5. Have resting membrane potential
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26
Q

Explain the movement of K+ in terms of conc and electrical gradient

A
  • Conc gradient - K+ beign pulled out
  • Electrical grad - K+ being pulled in
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27
Q

How is resting membrane potential determined

A

By size of initial conc gradient:
* Small conc grad = small resting membrane potential
* Large resting membrane potential = need lots of K+ to leak out to reach equilibrium

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28
Q

What is the equilibrium potential

A

The equilibrium potential is the membrane potential at which the electrical gradient is exactly equal and opposite to the concentration gradient

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29
Q

Nernst equation

A

equation predicts the equilibrium potential for a single ion species

see picture

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30
Q

What is the nernst equation usually at 37 degrees

A

for K+, approx -90 mV, for most neurons it is closer to -70 mV due to other “leaky” channels, especially Na+ and Cl-

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31
Q

What does the Goldman-Hodgkin-Katz (GHK) equation do

A

Predict the equilibrium potential generated by several ions

see picture

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32
Q

why is the Na/K+ ATPase not completely responsible for generating the resting membrane potential?

A
  • Exchanges 3 Na+ for 2 K+ meaning it is Electrogenic (makes the inside of the cell slightly negative)
  • Only contributes about 5 mV Na+/K+ pump is needed to set up the ion gradients
  • Without leaky K+ channels, only a small membrane potential would be generated
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33
Q

What is resting membrane potential dominated by

A

The permeability of the resting membrane to K+

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34
Q

briefly summarise leaky K+ channels

A

K+ continually leaks out the cell down its conc gradient (against electric grad), which was established by Na/K pumps. Why resting membrane potential close to K+ equilibrium potential - only close due to other leaky channels

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35
Q

Blood-brain barrier

A

Capillaries in brain which prevent polar substances from crossing through/between endothelial cells. Protects brain from changes in plasma ion conc

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36
Q

What does the resting membrane potential produce

A

Evoked potentials (graded or action)

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37
Q

2 types of potential

A
  1. graded
  2. action
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38
Q

Graded potential

A

any change in electric potential of a neuron that is not propagated along the cell (as is an action potential) but declines with distance from the source

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39
Q

What do graded potentials decide?

Jotted down, might not be “true”

A

Whether a cell is depolarised past a threshold to fire an action potential - decide when action potential is fired

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40
Q

examples of graded potentials

A
  • Generator potentials- at sensory receptors
  • Postsynaptic potentials- at synapses
  • End plate potentials- at neuromuscular junction
  • Pacemaker potentials- in pacemaker tissues (heart)
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41
Q

How do graded potentials respond to small and large stimuli

A
  • Small stimulus opens a few channels and evokes a small response (small depolarisation)
  • Strong stimulus opens many channels and evokes a large response (large depolarisation)
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42
Q

What does this mean graded potentials can also signal (what other bit of info can they share)

A

Stimulus intensity in their amplitude

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43
Q

What is a key propety of graded potentials

think how they change

A

They are decremental

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44
Q

Why are graded potentials decremental?

A

Become smaller as they travel along the membrane, therefore only useful over very** short distances**, this is why graded potentials are also called local potentials

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45
Q

What 2 things can graded potentials be

A

Depolarising or hyperpolarising

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46
Q

explain depolarising and hyperpolarising of graded potentials

A

Neurotransmitters can open channels that depolarise the cell, or different channels that hyperpolarise the cell. Since firing an action potential depends on reaching a firing threshold. Graded potentials at synapses can therefore excite or inhibit a cell

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47
Q

What does depolarising a cells do/mean

graded potentials

A

Less negative value - Exitory postsynaptic potential (EPSP)

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48
Q

What does hyperpolarising a cell do

graded potentials

A

Away form threshold (less likely to fire action potiential) - Inhibitory postsynaptic potential (IPSP)

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49
Q

What can multiple graded potentials do together?

A

Summate

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50
Q

how can graded potentials summate?

A
  • A single neuron has lots of synapses, evoking their own postsynaptic potential - 1 neuron can have hundreds of neurons attached on dendrites
  • If two occur at the same time, they can add to together
  • This is important for synaptic integration
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51
Q

Ionic bases of graded potentials

summary

A
  • We already know that at rest there are lots of leaky K+ channels - continually allow K+ into cell down conc grad (generates resting membrane potential)
  • That explains why the RMP is close to the K+ equilibrium potential of -90 mV
  • The opening of other ion channels generates other ion gradients
  • We can predict what would happen in each case
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52
Q

What can happen with ion channels in relation to graded potential

A

Can open/close them to hyperpolarise or depolarise the cell

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53
Q

Ionotripic receptor

A

ligand gated ion channels (ion channel + receptor) - through which ions pass in response to a neurotransmitter

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54
Q

Metabotropic recepor

A

metabotropic receptors require G proteins and second messengers to indirectly modulate ionic activity in neurons

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55
Q

what are the properties of graded potentials?

A

graded, decremental, depolarising or hyperpolarising, can summate

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56
Q

What causes a fast IPSP (hyperpolarising)

A

ionotropic receptor (Cl- into cell)

57
Q

What causes a slow IPSP

A

metabotropic receptor (K+ out)

58
Q

Non-specific monovalent cation channel

A

For aqueous pathway for single positively charged ions to flow down their electrochemical gradient into/out of a cell

59
Q

What causes fast EPSP

A

ionotropic receptor (for Na/K…)

60
Q

What causes a slow EPSP

A

metabotropic receptor (stops movenet of K+ out of cell - closes)

61
Q

What does the G-protein act as with metabotropic receptors

A

Doorman: to find and close “leaky” K channels (Na/K pump still going so cell depolarises

62
Q

How are EPSPs generated?

A

EPSPs generated by opening (non-specific monovalent) Na+/K+ channels or closing leaky K+ channels

63
Q

how are IPSPs generated?

A

IPSPs generated by opening Cl- channels or opening K+ channels

64
Q

What is EPSP

A

an excitatory postsynaptic potential, a local depolarization of the cell membrane of the neuron. Summation of EPSPs can lead to the generation of an action potential.

65
Q

What is an IPSP

A

inhibitory post synaptic potential,
hyperpolarization of cell membrane of neuron

66
Q

What is the principle inhibitory neurotransmitter in the CNS?

A

GABA

67
Q

Would GABA hyperpolarise or depolarise neurons

A

As an** inhibitory neurotransmitter**, GABA usually causes hyperpolarization of the postsynaptic neuron to generate an inhibitory postsynaptic potential (IPSP) while

68
Q

Glutamate - neurotranmitter action

A

glutamate causes depolarization of the postsynaptic neuron to generate an excitatory postsynaptic potential (EPSP)

69
Q

What are GABA and glutamate

A

GABA - princible inhibitory neurotransmitter in CNS
Glutamate - principle exitory neurotransmitter in CNS

70
Q

Can GABA/Glutamate act on more than one type of recepor (gating an ion channel)

A

Yes

71
Q

Is depolarising EPSP or IPSP

A

EPSP

72
Q

Is hyperpolarising EPSP or IPSP

A

IPSP

73
Q

What does each neuron have hundreds of

A

exitory and inhibitory synapses

74
Q

What does each exitory/inhibitory synapse evoke

A

Fast or slow EPSP’s and fast or slow IPSP but each is only a few mV high

75
Q

What does adding together all the tiny EPSP/IPSPs do

A

Either push cell to threshold and fire an action potential or keeps cell away from threshold and tells it to shutup

76
Q

Synaptic integration definition

A

The summation of the synaptic inputs to decide in the initial segement will reach threshold and fire action potential

77
Q

What happens for synapses that are distant from the initial segment (axon hillock) in terms on firing activity/

A

Have less of an influence on the firing activity of the cell than those that are closer.

78
Q

When are action potentials used

A

over long distances

79
Q

Steps in firing of an action potential

A
  1. Depolarisation
  2. Repolarisation
  3. Undershool (more -ve) and then hyperpolarise
80
Q

Give the steps of firing an action potential in more detail

A
  1. Leaky K+ channels maintain membrane potential
  2. Voltage-gated Na+ channels open, leading to a influx of Na+ into the cell
  3. Rapid depolariseation of cell occurs
  4. Voltage-gated K+ channels open (letting K+ out) and Na+ ones close, allowing for a slow repolarisation of the cell
  5. K+ channels open when reach -55mV
  6. K+ channels close and cell returns to resting membrane potential

+ ball and chain blocking channels where appropriate

81
Q

How does the ball and chain function in action potentials

A

Closes voltage-gated Na/K channels, preventing the entry/exit of ions into the cell

82
Q

What are the 2 periods in the firing of an action potential - describe both

A
  • Absolute refractory period - Is the period of time during which a second action potential ABSOLUTELY cannot be initiated, no matter how large the applied stimulus is
  • Relative refractory period - Is the interval immediately following the Absolute Refractory Period during which initiation of a second action potential is INHIBITED, but not impossible.
83
Q

Properties of action potentials

A
  1. Have a threshold
  2. All-or-none (always same amplitude)
  3. Self-propagating - keeps going
  4. Have refractory period - ball/chain inactivation gate
  5. Travel slowly
84
Q

What can action potentials only encode

A

Stimulus intensity in firing frequency, not amplitude

85
Q

What are all action potentials mediated by

A

Voltage-gated channels (as opposed to ligand-gated channels that generate postsynaptic potentials)

86
Q

What will a stronger stimulus show in an action potential

A

More action potentials fire

87
Q

Explain the movement of action potentials down the axon

A
  1. Cell -ve at rest
  2. Na+ channels open, allowing influx of Na+ into cells at that point on the membrane—> depolarisation
  3. Now, neighbouring Na+ channels open, depolarising this part of the membrane
  4. Initial Na+ channels blocked by ball and chain, close off, stopping influx of Na+ - clamps channels closed and stops signals going the wrong way down the neuron
  5. Process continues and signal moves all the way along the neuron
88
Q

What mediates the depolarising, repolarising and hyperopolarising phase

A
  • Depolarising - Voltage-gated Na+ channels
  • Repolarising - Voltage-gated K+ channels
  • Hyperpolarising - Voltage-gated K+ channels
89
Q

Benefit but also drawback of action potentials

A

Self-propagating = grate but slow

90
Q

How can we spped up conduction velocity of action potentials

2 ways

A
  1. Larger diameter axons
  2. Myelination
91
Q

Explain how large (diameter) axons increase conduction velocity

A
  • Current flows more easily along large axon where axial resistance is lower
  • Allows the Na+ channels to be more spaced out along the membrane
92
Q

Explain how myelination increases conduction velocity

A
  • Schwann cells in PNS and oligodendrocytes in CNS
  • Wrap layers of myelin arounf axons
  • Inc membrane resistance - less current leaks out of membrane
  • Dec membrane capacitance -less current wasted charging up membrane
  • Action potential spreads passively from nod to node and still reach threshold
  • Known as saltatory conduction
93
Q

Essentially, what does myelination do?

A

Allows action potentials to “jump” from one node to the next

94
Q

What are some consequences of demyeination

A
  • multiple sclerosis in CNS and Guillain-Barre syndrome in PNS
  • both demyelinating diseases that attack the myelin sheath
  • Dec membrane resistance and inc membrane capacitance
  • ** Conduction fails** - depolarisation fails to spread
95
Q

How can nerve fibres differ?

nerve fibre types

A

Axons different:
* small and large unmyelinated and myelinated axons

all conduct at different velocities, genertes a compound action potential

96
Q

Give nerve fibre types going from fastest to slowest

A
  • Large myelinated (Aa) - proprioception, motor neurons
  • Large myelinated (AB) - Touch, pressure
  • Small myelinated (Ay) - motor neurons of muscle spindles
  • Smallest myelinated (A#) - touch, cold, “fast” pain
  • Unmyelinated (C) - warmth, “slow” pain
97
Q

What do extracellular recording from a nerve (bundle of axons) generate

A

A compound action potential - looks nothing like an action potential

98
Q

Compare action potential to compound action potential

A

Action potential:
* Intracellular recording
* microelectrode through membrane
* relative to outside the cell

Compound action potential:
* extracellular recording
* electrodes outside axons
* relative to earth
* each action potential very small but add up to large waves

99
Q

thus, differennces in axon anatomy will lead to differences in …

A

Conduction velocity

100
Q

What correlates with an axons function

A

Anatomy and conduction velocity

101
Q

Nodes of Ranvier

A

specialized regions in the axonal membrane that are not insulated by myelin

102
Q

Briefly summarise the neuromuscular junction and why we have it

A

Synapse between motor neuron and skeletal muscle
First step in triggering muscle contraction is to evoke an action potential in the skeletal muscle membrane (the sarcolemma)

103
Q

Describe the anatomy of the nmj moving across the junction

A
  1. Preynaptic terminal filled with vesicles containing acetylcholine (ACh)
  2. Synaptic cleft
  3. Postsynaptic end plate of the skeletal muscle fibre

Fold in end plate - allows greater uptake

104
Q

What does depolarisation of a motor neuron do

A

Depolarises skeletal muscle (nmj) —> action potenital being evoked leading to contraction of muscle

105
Q

Give steps of firing of the nmj

12 steps

A
  1. Action potential in motor neuron - mediated by voltage-gated Na channels (depolarises)
  2. Opens voltage-gated Ca2+ channels in presynaptic terminal - Ca2+ pulled in by conc and elec gradient
  3. Fusion of vesicles (Ca2+ dependent exocytosis)
  4. ACh diffuses across synaptic cleft
  5. ACh binds to ACh (nicotinic) receptors - ionotropic (non-specific cation channels)
  6. opens ligand-gated Na+/K+ channles —> pull into cell
  7. Evokes end plate potential (graded potential), very large
  8. (Always) depolarises membrane to a threshold
  9. Opens voltage-gated Na+ channels
  10. Evokes action potential
  11. Action potential propagated along muscle cell membrane leading to muscle contracts
  12. Acetylcholine (ACh) cleared up by acetylcholinesterase
106
Q

Describe acetylcholine (ACh) receptors

A

Contain integral ion channel - ligand gated (non-specific monovalent cation channel) - muscarinic or nicotinic

107
Q

What are some key characteristics of the nmj

A
  • Ligand gated Na/K (2 diff channels) channels evoke the end plate potential
  • Very large graded potential which is always bid enough to reach threshold
  • Thus, no synaptic integration - nmj acts like a switch
  • Post-junctional folds inc number of voltage-gated Na+ channels close to where it is evoked
108
Q

What is the end plate potential (with nmj)

A

very large

109
Q

What do post-junctional folds allow for

A

The end plate potential has a short distance to travel to the voltege-gated Na+ channels

110
Q

how is the sequence of events similar/different in CNS synapses to that in NMJ

A

Same, however CNS synapses have added complexities

111
Q

CNS synapses compared to NMJ in terms of neurotransmitters

A

NMJ: acetylcholine
CNS: many inc amines (adrenaline/noradrenaline/dopamine, serotonin (5HT), histamine), amino acids (glutamate, GABA, glycine), peptides (endorphins, cholecystokimim. substance P), purines (ATP, adenosine), gases (nitric oxide)

112
Q

How can postsynaptic potentials be in the CNS

A

exitory, inhibitory, fast or slow
(e.g. slow IPSP or fast EPSP)
this range allows for complex synaptic integration

113
Q

How may postsynaptic potentials are there in the NMJ

A

1

114
Q

How can CNS synapses be arranged (3)

A
  1. Axo-dendritic - typically exitory
  2. Axo-somatic - typically inhibitory
  3. Axo-axonal - can be both but usually inhibitory (work by regulating how much neurotransmitter is released)
115
Q

How is CNS synapse anatomy different to that of NMJ

A

CNS: 3 arrangements
NMJ: 1

116
Q

How can are synapses connected in the CNS and how does this differ to the NMJ

A
  • Divergence - influences cells further down
  • Convergence

NMJ: Only have divergence (1 motor neuron synaps onto multiple muscle fibres)

117
Q

Do NMJ have feedback inhibition

A

No

118
Q

Explain feedback inhibition in relation to CNS synapses

A
  • When action potential fired, collateral (branch) activates an inhibitory interneuron
  • Inhibitory neurotransmitter released
  • Initial neuron hyperpolarises
  • it is prevented from repeated firing

Net effect: initial neuron inhibited from repeated firing of action potential

119
Q

Give an overview of the complexity of pathways in the CNS

A

Monosynaptic reflex: stereotyped: detect stimuli and fire action potential, limited scope for synaptic integration or for the behaviour of motor neuron to be influenced bu convergent pathways (simple)
Polysynaptic reflex: multiple sites of peotential synaptic integration so multiple neurons where behaviour will be influenced by convergent pathways. Much more complex decisions made and less likely to be stereotyped (same every time)

120
Q

Explain inhibitory reflex pathways in the CNS

A

Inhibitory interneuron releases inhibitory neurotransmitter (e.g. GABA) and stops efferent (motor) neuron intitiating a response

121
Q

What is synaptic plasticity

A
  • Ability of synapses to change their strength.
  • can be activity-dependent
  • Many diff types of synaptic plasticity:

Long-term potentiation (LTP involved in learning and memory)
Long-term depression

122
Q

Overall, what makes CNS synapses more complicated than the nmj?

A
  • Range of neurotransmitters
  • Range of postsynaptic potentials
  • Arrangement of synapses
  • Arrangement of wiring
123
Q

Synaptic pathway

A

hormones are produced in the neuron, secreted, and travel along the axon to the synapse where they are released and taken up by a nearby neuron with the appropriate receptors to exert an effect, enter via afferent (sensory) neuron and leave via afferent (motor) neuron

124
Q

how do we classify nerve fibre types

A

divided into three types on the basis of the relationship between their diameter and conduction velocity: group A, group B and group C nerve fibres.

125
Q

What is a synapse in basic terms

A

Jucntion between neurons and a way of communicating between neurons

126
Q

Common exitory neurotransitter

A

Glutamate

127
Q

Common inhibitory neurotransitter

A

GABA

128
Q

What can we call the process of 1 neuron releasing a neurotransmitter at its synapse which evokes a reponse in the next neuron

A

signal transduction

129
Q

Where are interneurons found

A

The CNS only

130
Q

function of acetylcholinesterase

A

to terminate neuronal transmission and signaling between synapses to prevent ACh dispersal and activation of nearby receptors. - breaksdown ACh

131
Q

Function of graded potential (postsynaptic, generator potential, end-plate potential)

A

to determine when/weather a cell will fire its action potential

132
Q

Where does Acetylcholinesterase remove ACh from

A

Acetylcholinesterase does not directly remove ACh from the receptors. Instead it continuously removes ACh from the synaptic cleft so there is less chance of ACh activating the receptors.

133
Q

Synaptic integration in the CNS

A

In the CNS the EPSP evoked at a single synapse is likely to be in the order of 1-5mV. It is therefore not going to let the cell reach threshold. Instead, summation of EPSPs from many synapses is required. This is the concept of synaptic integration.

Also IPSP’s so add/subtract

134
Q

When does the equilibrium potential for an ion occurs

A

when the concentration gradient for the ion is matched by an equal and opposite electrical gradient

135
Q

Multiple sclerosis

A

demyelinating disease which impairs the ability of the action potential to be conducted from one node of Ranvier to the next

136
Q

Can action potentials summate?

A

No (graded postsynaptic potentials can)

137
Q

What effect would inc extracellular [K+] have on the resting membrane potential

A

Will decrease the K+ concentration gradient. This will sustain a smaller electrical potential at equilibrium and therefore depolarise the resting membrane potential.

138
Q

effect of poisining Na/K pumps

A

The electrogenic nature of the Na+/K+ pump (pumping 3 Na+ ions for every 2 K+ ions) makes only a small contribution (about 5mV) to the resting membrane potential. Setting up the K+ concentration gradient is far more important. Poisoning the pump will therefore only cause a small immediate decrease in membrane potential. The remainder of it decays slowly as the K+ concentration gradient gradually runs down.

139
Q

What could we say is at the NMJ (in terms or 1 motor neurone innervatign multiple muscle fibres)

A

Divergence

1. Foundations of Medicine PoNF (22 decks)

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