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YEAR 2 - The Nervous System > 20. Sensory Systems > Flashcards

20. Sensory Systems Flashcards

1
Q

Describe the basics of sensory perception.

A
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2
Q

Define somatoensory.

A
  • Relating to or denoting a sensation (such as pressure, or warmth) which can occur anywhere in the body, in contrast to one localized at a sense organ (such as sight, balance, or taste).
  • Pain is usually considered an extreme form of somatosensory stimulation, and it is often considered separately from somatosensory systems.
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3
Q

What are the main modalities encompassed by somatosensory systems and what nerve fibres are they carried by?

[IMPORTANT]

A
  • Proprioception (Aα) -> Muscle stretching, tension
  • Touch (Aβ) -> Pressure, vibration
  • Thermal sensation (Aδ and C)
  • Itch (C)

Pain is also modulated by Aδ and C fibres

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4
Q

For all of the types of sensory fibres involved in somatosensory and mechanoreception, state:

  • Names
  • Myelination
  • Diameter
  • Speed
  • Function
A

Aα:

  • Myelinated
  • 12-20μm
  • 70-120m/s
  • Proprioception of skeletal muscle

Aβ:

  • Myelinated
  • 5-12μm
  • 30-70m/s
  • Mechanoreceptors of skin

Aδ:

  • Myelinated
  • 1-5μm
  • 5-30m/s
  • Pain, temperature

C:

  • Unmyelinated
  • 0.2-1.5μm
  • 0.5-2m/s
  • Pain, temperature, itch
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5
Q

Explain how the names of sensory fibre types varies depending on their origin.

A
  • If the fibres originate from the skin, they are the Aα, Aβ, Aδ and C fibres
  • If the fibres originate from the muscle, they are instead called group I, II, III and IV respectively

These are just differences in nomeclature -> They refer to the same thing.

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6
Q

Do somatosensory systems respond to change or rate of change?

A

They detect change, which is a binary event, and then look at the rate of change (the rate of firing of action potentials).

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7
Q

How do receptors allow for graded response to a touch stimulus, for example?

A
  • Force applied determines the number of channels opening, which determines the depolarisation
  • Increased depolarisation leads to increased action potential firing per second (i.e. increased rate of change)
  • This increases the likelihood of onward signal propagation via the spinal cord and up to conscious perception
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8
Q

Explain the principle of different sensitivity of different sensory receptors.

A

Some receptors must be more sensitive to stimuli than others. For example, nociceptors cannot be activated by very light stimuli, since this would cause unnecessary pain.

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9
Q

Describe the importance of diversity within somatosensory receptors.

A
  • Not only do we require different receptors for different modalities (e.g. touch and heat), but we also require diversity within each receptor type
  • This allows for more accurate perception of the stimulus
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10
Q

What is the receptive field?

A

The area of skin (or other organ) on which a somatosensory receptor can detect stimuli.

i.e. It is like the range of the receptor

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11
Q

Name some ways in which receptors can allow for diverse responses within, for example, mechanoception.

A
  • Different receptive fields
  • Different thresholds
  • Adaptation vs non-adaptation
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12
Q

Describe the concept of receptor adaptation.

A
  • In the presence of a continued stimulus, an adaptive receptor produces action potentials with decreasing frequency
  • A non-adaptive receptor produces action potentials with continued frequency
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13
Q

Describe the connective tissues within a spinal nerve.

A
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14
Q

Where do afferent neurons originating from somatosensory receptors have their cell bodies?

A

In dorsal root ganglia (DRG).

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15
Q

Where is pain from the viscera referred to?

A

The midline, in areas that are not sharply defined.

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16
Q

Explain the concept of 2 point discrimination.

[EXTRA]

A
  • Sensory receptors are not evenly distributed across the body
  • Some locations have a higher density than others
  • This means that in places with a high density of receptors, you can distinguish touch between two points a shorter distance apart
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17
Q

Compare the receptive fields of superficial and deep receptors in the skin.

A

Superficial receptors have a smaller receptive field than deep receptors.

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18
Q

How can increased sensitivity of receptors be achieved?

A

Convergence of receptive fields:

  • Multiple individual receptors clustered into small hotspot can send signals to a single DRG afferent
  • This means that the sensitivity is increased, since there is summation
  • An example of this is with Meissner’s corpuscle mechanoreceptors
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19
Q

What is proprioception?

A

A sense of the body’s position in space, essential for locomotion and balance.

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20
Q

What fibres carry proprioceptive information?

A

Aα fibres (and to a lesser extent Aβ)

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21
Q

What are the two proprioprioceptors?

A
  • Muscle spindles
  • Golgi tendon organs
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22
Q

What are muscle spindles and Golgi tendon organs?

A

They are stretch receptors that detect tension in muscles.

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23
Q

Compare the position muscle spindles and Golgi tendon organs.

A

Muscle spindles lie in parallel to muscle fibres, whereas Golgi tendon organs lie in series.

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24
Q

What important process are muscle spindles involved in? How does this work?

A
  • The muscle stretch reflex (muscle contraction in response to stretching within the muscle).
  • This involves activation of synergistic muscles and inhibition of antagonistic muscles (vi inhibitory interneurons)

(Note: There will be more flashcards on this later).

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25
Q

What fibres types do muscle spindles and Golgi tendons send information via?

A
  • Muscle spindles -> Type Ia (Aα) and II (Aβ)
  • Golgi apparatus -> Type Ib (Aα)

(Remember how the I system corresponds to the Aα when in muscle. Aα fibres include both Ia and Ib fibres.)

Therefore, note how Aβ fibres are also minorly involved in proprioception despite not always being mentioned.

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26
Q

What are the two fibre types that take afferent information from muscle spindles? What is the function of each?

A
  • Ia (Aα) -> Adapting, fast-responding discharge, which allows immediate reflex response to changes in length
  • II (Aβ) -> Non-adapting, slower discharge, which allows constant tension depending on current stretch

Ia fibres arise from dynamic and static fibres, while II fibres arise from static fibres only.

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27
Q

What are the targets of fibres carrying information from muscle spindles?

A
  • Synergistic α-motorneurons
  • Ia inhibitory interneurons that synapse onto antagonistic α-motor neurons
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28
Q

How do Aα neurons enable rapid reflexes?

A
  • They synapse not only on motor neurons that innervate the muscle that needs to contract, but also on interneurons that are inhibitory to the antagonistic muscle.
  • Since Aα fibres are responsible for propriception, when there is stretch of the muscle, the agonist will contract slightly, while the antagonist will relax.
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29
Q

What important process are Golgi tendon organs involved in? How does this work?

A
  • Negative feedback during muscle contraction
  • This is done via inhibitory interneurons that prevent the muscle from over-contracting
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30
Q

What are the fibre types that take afferent information from Golgi tendon organs?

A

Ib (Aα) fibres

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31
Q

What are the targets of fibres carrying information from Golgi tendon organs?

A

Ib inhibitory interneurons in the ventral horn -> These then inhibit synergistic α-motor neuron activity, allowing negative feedback of muscle contraction.

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32
Q

What is another name for touch?

A

Somatosensation

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33
Q

What are the main receptor types in the skin?

A
  • Meissner corpuscle
  • Ruffini corpuscle
  • Merkel cells
  • Pacinian corpuscle
  • Free nerve endings

These are essentially the major mechanoreceptors.

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34
Q

Give a summary of the main receptor types in the skin, in terms of:

  • Stimuli detected
  • Location in skin
  • Afferent response
  • Stimulus shape
  • Receptive field
  • Perceptual functions
A
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35
Q

What is glabrous skin and how are the mechanoreceptors in it distributed?

A
  • Skin that does not contain hair follicles, such as that over the palms and soles.
  • On the ridges of your fingerprint, there are Merkel cells and Meissner corpuscles
  • This means that when you run your finger along a surface, the ridges vibrate and the stimulus can be detected
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36
Q

What fibre types carry afferent information from mechanoreceptors?

A

Aβ

(And also some Aδ fibres from free nerve endings)

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37
Q

Compare the receptive field for:

  • Meissner’s corpuscles
  • Merkel cells
  • Pacinian corpuscles
  • Ruffini endings
A
  • Meissner’s corpuscles and Merkel cells have a small receptive field since they are quite superficial
  • Pacinian corpuscles and Ruffini endings have a larger receptive field since they are deeper
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38
Q

Compare whether these are rapidly or slow-adapting:

  • Meissner’s corpuscles
  • Merkel cells
  • Pacinian corpuscles
  • Ruffini endings
A
  • Meissner’s corpuscles -> Rapidly-adapting
  • Merkel cells -> Slow-adapting
  • Pacinian corpuscles -> Fast-adapting
  • Ruffini endings -> Slow-adapting
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39
Q

Describe how mechanoreceptor diversity allows a range of responses to touch.

A
  • There are two more superficial receptors (Meissner’s and Merkel), with a smaller receptive field, and two more deep receptors (Pacinian and Ruffini), with a large receptive field
  • Of each category, one of the receptors is rapidly-adapting (Meissner’s and Pacinian), while the other is slow-adapting (Merkel and Ruffini)
  • This means that a range of responses is possible
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40
Q

What are the different types of ion channels in the membrane of mechanoreceptors?

[EXTRA?]

A
  • 1 and 2 are opened by physical distortion
  • 3 is opened by an indirect process
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41
Q

For a Meissner’s corpuscle, state:

  • Function
  • Location
  • Receptive field
  • Rapidly/Slow adapting
  • Number of receptors per DRG cell
A
  • Function -> Light touch
  • Location -> Superficial epidermis, High density in fingertips
  • Receptive field -> Small
  • Rapidly/Slow adapting -> Rapidly adapting
  • Number of receptors per DRG cell -> 10-25
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42
Q

Draw the structure of a Meissner’s corpuscle.

A
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43
Q

What makes a Meissner’s corpuscle special?

A
  • It has the lowest highest sensitivity to low frequency vibrations.
  • This is due to a low threshold and 10-25 Meissner’s corpuscles per DRG cell.
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44
Q

For a Merkel disc, state:

  • Function
  • Location
  • Receptive field
  • Rapidly/Slow adapting
  • Number of receptors per DRG cell
A
  • Function -> Deep touch, Pressure
  • Location -> Superficial epidermis, High density in fingertips
  • Receptive field -> Small
  • Rapidly/Slow adapting -> Slowly adapting
  • Number of receptors per DRG cell -> 10-25
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45
Q

Give some experimental evidence relating to the function of Merkel discs.

A

(Maricich, 2009):

  • Identified that a gene involved in Merkel disc development is Atoh1
  • Atoh1 knockout mice allow us to see the importance of Merkel discs
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46
Q

For a Pacinian corpuscle, state:

  • Function
  • Location
  • Receptive field
  • Rapidly/Slow adapting
  • Number of receptors per DRG cell
A
  • Function -> Vibration
  • Location -> Deep in the dermis, High density in finger tips
  • Receptive field -> Large
  • Rapidly/Slow adapting -> Rapidly adapting
  • Number of receptors per DRG cell -> 1
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47
Q

Draw the structure of a Pacinian corpuscle.

A
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48
Q

Give some experimental evidence relating to the structure and function of the Pacinian corpuscle.

[EXTRA]

A

(Lowenstein, 1959):

  • Experiment 1 showed that the lamellae are not required, just the nerve ending inside
  • Experiment 2 showed that interruption of the action potential transmission causes no response, but does not interrupt the generator voltage
  • Experiment 3 showed that partial degeneration of the nerve ending prevents the generator voltage

Therefore, the mechanoreceptive component is the nerve ending within the Pacinian corpuscle.

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49
Q

Give some experimental evidence relating to the function of the lamellae in a Pacinian corpuscle.

A

This showed that the lamellae are important for rapid adaptation, so that the receptor can respond to a high frequency of signal.

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50
Q

For a Ruffini ending, state:

  • Function
  • Location
  • Receptive field
  • Rapidly/Slow adapting
  • Number of receptors per DRG cell
A
  • Function -> Stretch (involved in hand position)
  • Location -> Deep dermis, Fewer in fingers
  • Receptive field -> Large
  • Rapidly/Slow adapting -> Slow adapting
  • Number of receptors per DRG cell -> 1
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51
Q

What receptor type is this?

A

Pacinian corpuscle

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52
Q

What receptor type is this?

A

Merkel disc

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53
Q

What receptor type is this?

A

Ruffini ending

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54
Q

What receptor type is this?

A

Meissner’s corpuscle

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55
Q

Describe the arrangement of Ruffini corpuscles.

A

They are arranged along tissue planes on the hand.

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56
Q

What are thermoreceptors?

[IMPORTANT]

A

Free nerve endings

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57
Q

What are the proteins on free nerve endings that allow perception of heat?

A

Transient Receptor Potential (TRP) family of proteins often located on free nerve endings (Aδ and C fibres) in mammals.

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58
Q

What are the two types of thermreceptors?

A
  • Cold fibres
  • Warm fibres

These have different firing rates at different temperatures. They both fire equally at around 37 degrees (the desired body temperature).

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59
Q

What is the diameter of cold and warm thermoreceptors?

A
  • Cold -> 5-10mm
  • Warm -> 15mm
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60
Q

Name some different TRP proteins on free nerve endings and what they respond to.

A
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61
Q

Describe how spicy foods cause a strong response via TRP receptors.

A
  • Spicy foods (and heat) open TRPV1, giving it slight permeability to cations
  • However, prolonged exposure to spicy foods or heat causes phosphorylation, which induces a transition to a dilated state, in which permeability to large cations is increased
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62
Q

What TRP protein is responsible for extreme hot thermoreception?

A

TRPV2 -> It responds to stimuli over 52*C. Unlike the capsaicin receptor TRPV1, TRPV2 has no response to capsaicin or acid.

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63
Q

What TRP protein is responsible for extreme cold thermoreception?

A

TRPM8

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64
Q

What are some agonists of hot and cold thermoceptors?

A
  • Cold (TRPM8) agonists -> Menthol, Eucalyptol
  • Hot (TRPV1) agonists -> Capsaicin
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65
Q

Give some experimental evidence for the importance of the TRPM8 receptor in cold thermoreception.

A

(Bautista, 2007):

  • Showed that mutant TRPM8 mice have difficulty differentiating between a hot and cold space
  • However, below around 10*C, they can detect a cold space, which shows that there is likely to be another thermoreceptive protein for low temperatures
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66
Q

What ultimately determines the function of any given free nerve ending?

A

The receptors embedded in the membrane.

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67
Q

Describe what stimuli can activate free nerve endings and what fibre type each of these travel down.

A
  • Thermoreceptive-> Aδ and C fibres
  • Mechanoreceptive -> Aδ fibres
  • Specific nociceptive -> Aδ and C fibres
  • Polymodal nociceptive -> C fibres
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68
Q

Compare the sort of pain that Aδ and C fibres mediate.

A
  • Aδ -> Sharper pain with reflex withdrawal, Fast-adapting (coding change)
  • C -> Spreading pain, Slow-adapting
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69
Q

What are some chemicals that can act on nociceptors?

A

(More on this later, hopefully)

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70
Q

What is nociception?

A
  • It is pain
  • It is essentially the perception of extreme thermal, chemical and mechnical stimuli that could be damaging
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71
Q

What are the main types of nociceptor?

A
  • Mechanical nociceptors -> Respond to strong stimuli and mediate sharp pain
  • Thermal nociceptors -> Respond to cold and warm stimuli
  • Polymodal nociceptors -> Respond to a variety of stimuli and evoke slow burning pain
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72
Q

What are the functions of the spinal cord?

A
  • Receives sensory information from sensory neurons
  • Provides motor information to motor neurons
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73
Q

What does the spinal cord receive sensory information from and where does it enter?

A

From the central axons of dorsal root ganglion neurons -> Into the grey matter of the dorsal horn

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74
Q

On this diagram of the spinal cord, what are the grey and white sections?

A
  • Central H-shaped grey matter -> Neuron cell bodies
  • White matter -> Myelinated axon tracts

There is also the central CSF-filled canal.

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75
Q

Label the GREY MATTER of spinal cord with the main sensory and motor areas.

A
  • In the dorsal half, there are the sensory interneurons
  • In the ventral half, there are the:
    • Lateral motor column (a.k.a. pool)
    • Medial motor column (a.k.a. pool)
    • Motor interneurons
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76
Q

Describe how the grey and white matter of the spinal cord work together.

A

Horn (grey matter):

  • The dorsal horn receives sensory information
  • This can then be taken within the grey matter along a reflex arc or through segmental interneurons
  • Alternatively, it can be passed into the white matter

White matter:

  • The white matter is made of axons and it is divided into tracts that carry information up the spinal cord and back down from the spinal cord
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77
Q

Draw the position of the main ascending and descending white matter columns.

A

Ascending (sensory):

  • Dorsal column
  • Spinocerebellar tracts
  • Anterolateral system

Descending (motor):

  • Corticospinal tracts (lateral + anterior)

[YOU NEED TO KNOW THIS IS MUCH MORE DETAIL. MAKE SURE YOU’VE MADE MORE NOTES ON IT.]

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78
Q

Draw the main nuclei and laminae in the grey matter of the spinal cord. [IMPORTANT]

A

Dorsal horn:

  • Marginal zone
  • Substantia gelatinosa
  • Nucleus proprius

Lateral horn (in thoracic region?):

  • Thoracic nucleus (Clarke’s column)
  • Intermediolateral nucleus

Ventral horn:

  • Lateral motor pool
  • Medial motor pool
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79
Q

What sort of sensory fibres enter the dorsal horn of the spinal cord? From what direction? What is their function?

A

Large diameter axons:

  • Enter medially and possess ascending collaterals
  • Aα -> Proprioception
  • Aβ -> Mechanoceptors

Fine diameter axons:

  • Enter laterally and project across several segments -> Lissauer’s tract (LT)
  • Aδ -> Nociception, Thermal
  • C -> Nociception, Thermal, Itch
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80
Q

For Aα fibres, describe where they originate and terminate.

A
  • Originate in muscle spindles, from where they carry sensory proprioception information
  • Terminate at lamina 6 to 9, which includes interneurons in the dorsal horn and motor neurons in the ventral horn
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81
Q

For Aβ fibres, describe where they originate and terminate.

A
  • Originate from cutaneous receptors and static proprioceptors
  • Terminate in the laminae 3 to 6 of the dorsal horn (a.k.a. the nucleus proprius)
  • They synapse onto wide dynamic range neurons (interneurons involved in polysynaptic reflexes)
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82
Q

Where do Aδ and C fibres (nociceptive fibres) synapse?

A
  • Aδ -> At the marginal zone of the dorsal horn (lamina 1) and nucleus proprius (laminae 3-5)
  • C -> At the substantia gelatinosa of the dorsal horn (lamina 2)

Note: Each of these fibres can synapse at multiple heights in the spinal cord.

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83
Q

Compare the direction from which proprioceptive/mechanoreceptive (Aα and Aβ) and nociceptive (Aδ and C) enter the spinal cord.

A
  • Proprioceptive/mechanoreceptive (Aα and Aβ) -> From medial side
  • Nociceptive (Aδ and C) -> From lateral side
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84
Q

Which laminae do each of these fibres synapse at:

  • Aα
  • Aβ
  • Aδ
  • C
A
  • Aα -> 6-9
  • Aβ -> 3-6
  • Aδ -> 1, 4 and 5
  • C -> 2
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85
Q

Do large diameter afferent fibres (Aα and Aβ) supply just one point along the spinal cord?

A
  • No, they can enter and course up and down the spinal cord, innervating more than one motor/interneuron. However, all the motor neurons innervated tend to have synergistic action.
  • They do this via the ascending tracts
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86
Q

Where do Aα neurons synapse?

A
  • On interneurons that are inhibitory to antagonistic muscles (in the dorsal horn)
  • On motor neurons in the ventral horn (for stretch reflex)

They also send out branches without synapsing which ascend in the ascending dorsal columns to inform higher centres (conscious proprioception).

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87
Q

Draw a diagram to show where the collateral branches of large diameter sensory fibres originate. What do these form?

A
  • These form the dorsal ascending tracts that carry proprioceptive and mechanoreceptive information up to the brain.
  • This allows for conscious perception of body position and touch.
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88
Q

Describe transmission through the dorsal column tracts. [IMPORTANT]

A

It carries afferent proprioceptive and mechanoreceptive information:

  • Dorsal root ganglion axons have ascending branches that travel cranially in the dorsal column
  • These then synapse at the dorsal column nuclei in the medulla
  • The fibres then decussate (cross to the other side of the body)
  • They then travel up the medial lemniscus through the midbrain and to the thalamus
  • Relay neurons take the information from the thalamus to the somatic sensory cortex
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89
Q

Explain the concept of orders of neurons.

A
  • First-order neurons carry signals from the periphery to the spinal cord
  • Second-order neurons carry signals from the spinal cord to the thalamus
  • Third-order neurons carry signals from the thalamus to the primary sensory cortex
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90
Q

Compare the orders of neurons carried by the dorsal column and anterolateral systems.

A
  • Dorsal column system carries 1st order neurons, since synapsing and decussation only happens in the medulla
  • Anterolateral system carries 2nd order neurons, since synapsing and decussation occur within the spinal cord
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91
Q

What are the two fascicles of the dorsal column?

A

These correspond to the cuneate and gracile nuclei in the medulla, which these join up with.

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92
Q

Describe transmission through the spino-cerebellar tracts. [IMPORTANT]

A

It carries afferent proprioceptive information from the lower limb:

  • Dorsal root ganglion axons at the lumbar region, which receive information from the lower limb, have branches that ascend up to the thoracic region
  • At the thoracic region, they terminate at Clarke’s column (a.k.a. thoracic nucleus)
  • This sends out relay neurons to the dorsal spino-cerebellar tracts
  • These take the information to the cerebellum on the same side of the body -> This is important for unconscious perception and response to the stimulus
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93
Q

Give a summary of proprioception and mechanoception. [IMPORTANT]

A
  • Proprioception is mediated by Aα fibres (from muscle spindles), while mechanoception is mediated by Aβ fibres (from mechanoreceptors)
  • These fibres then do two things:
    • Take the information directly to the grey matter of the spinal cord to allow reflex response
      • Aα fibres synapse at laminae 6 to 9, in both the dorsal and ventral horns
      • They synapse with motor neurons in the ventral horn and interneurons in the dorsal horn (which are inhibitory to the antagonistic muscle) -> Allows reflex reactions so muscles to maintain position
      • Aβ fibres synpase in laminae 3 to 6 of the dorsal horn (a.k.a. the nucleus proprius)
      • These are projection neurons that decussate and enter the anterolateral system (in particular the anterior spinothalamic tract), which take the information to the thalamus (the anterolateral tracts carry CRUDE touch information)
    • Send out branches before they reach the grey matter, which travel up to the brain to give conscious and unconscious perception of the stimulus (and also innervate muscles at different spinal levels e.g. if the biceps needs to contract then lots of muscle bundles need to be recruited)
      • These form the dorsal column tracts (thes carry proprioception and FINE touch):
        • Fibres synapse at the dorsal column nuclei in the medulla
        • The fibres then decussate (cross to the other side of the body)
        • They then travel up the medial lemniscus (a bundle of fibres) through the midbrain and to the thalamus
        • Relay neurons take the information from the thalamus to the somatic sensory cortex -> CONSCIOUS PERCEPTION
      • There are also the spino-cerebellar tracts, which carry afferent proprioceptive information from the lower limb:
        • Fibres ascend up to the thoracic region
        • At the thoracic region, they terminate at Clarke’s column (a.k.a. thoracic nucleus)
        • This sends out relay neurons to the dorsal spino-cerebellar tracts
        • These take the information to the cerebellum on the same side of the body -> UNCONSCIOUS PERCEPTION
        • Note how there is no decussation in this case

Note how crude touch is carried by the anterolateral system (anterior spinothalamic tract), while fine touch is carried by the dorsal column system along with proprioception. Proprioception is also carried to the cerebellum via the spinocerebellar tracts.

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94
Q

What enables nociceptive fibres (Aδ and C) to terminate at more than one height in the spinal cord?

A
  • They are carried by Lissauer’s tract up and down, before they enter the grey matter.
  • This allows ampification of the signal, which does not happen with proprioception/mechanoreception since these need to be localised
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95
Q

What is Lissauer’s tract?

A

An ascending tract to the lateral side of the dorsal horn that takes the axons of nociceptive fibres up to higher spinal levels for synapsing.

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96
Q

Describe what happens after nociceptive fibres (Aδ and C) synapse in the spinal cord.

A

The sensory fibres travel up the spinal cord via Lissauer’s tract, then they synapse at various levels in the spinal cord.

Aδ:

  • Some synapse at the marginal zone of the dorsal horn (lamina 1) and nucleus proprius (laminae 3-5) with projection neurons:
    • Projection neurons send an axon across to the contralateral side of the spinal cord
    • These axons then join the anterolateral system, which takes the signal to the thalamus
    • Relay neurons take the information from the thalamus to the somatic sensory cortex

C:

  • Some synapse at the substantia gelatinosa of the dorsal horn (lamina 2) with interneurons:
    • These send axons to the nucleus proprius, which contains projection neurons
    • Projection neurons send an axon across to the contralateral side of the spinal cord
    • These axons then join the anterolateral system, which takes the signal to the thalamus
    • Relay neurons take the information from the thalamus to the somatic sensory cortex
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97
Q

How do axons of neurons from the nucleus proprius get to the other side of the body?

A

They pass via the anterior white commissure.

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98
Q

Describe transmission through the anterolateral column.

A

It carries afferent nociceptive (and some mechanoreceptive) information:

  • Wide dynamic range neurons in the nucleus proprius send axons across the midline (via the anterior white commissure)
  • The fibres then travel via the anterior and lateral spinothalamic tracts to the medulla, where the spinal leminiscus
  • This carries the information to the thalamus
  • Relay neurons take the information from the thalamus to the somatic sensory cortex
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99
Q

Give a summary of nociception. [IMPORTANT]

A
  • Nociception is mediated by Aδ and C fibres
  • These fibres then travel up to multiple levels in the spinal cord using Lissauer’s tract (this allows for amplification)
  • Each each level, they enter the grey matter from the lateral side and synapse in the grey matter.
  • Aδ fibres:
    • Synapse at the marginal zone of the dorsal horn (lamina 1) and nucleus proprius (cell bodies in lamina 5 with dendrites in laminae 3-5) with projection neurons:
      • Projection neurons arise from laminae 1 and 5, send an axon across to the contralateral side of the spinal cord
      • These axons then join the anterolateral system, which takes the signal to the thalamus
      • Relay neurons take the information from the thalamus to the somatic sensory cortex
  • C:
    • Synapse at the substantia gelatinosa of the dorsal horn (lamina 2) with interneurons:
      • These send axons to the nucleus proprius, which contain projection neurons
      • Projection neurons send an axon across to the contralateral side of the spinal cord
      • These axons then join the anterolateral system, which takes the signal to the thalamus
      • Relay neurons take the information from the thalamus to the somatic sensory cortex
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100
Q

Compare the dorsal column (proproception and mechanoception) and anterolateral (nociception) systems.

A
  • In the dorsal column, the DRG afferents do not synapse, but send fibres straight up the tract, while in the anterolateral, the DRG afferents synapse and the wide dynamic range neurons send fibres up the tract (i.e. dorsal column contains 1st order axons, while the anterolateral system contains 2ns order axons)
  • In the dorsal column, the decussation occurs in the medulla at the dorsal column nuclei, while in the anterolateral decussation occurs at the spinal level where synapsing occurs
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101
Q

Label this spinal cord cross-section.

A
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102
Q

What is Clarke’s column? [IMPORTANT]

A
  • A bundles of nerve cells in the thoracic region of the spinal cord.
  • It is in the LATERAL horn of the grey matter [IMPORTANT]
  • It receives ascending fibres from lumbar dorsal root ganglion neurons, and then passes this information on to the dorsal spino-cerebellar tracts (then to the cerebellum)
  • Therefore, it plays a role in UNCONSCIOUS perception of proprioceptive information
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103
Q

What are the important zones in the dorsal horn of the grey matter and what laminae do these include? [IMPORTANT]

A
  • Lamina 1 -> Marginal zone (a.k.a. posteromarginal zone)
  • Lamina 2 -> Substantia gelatinosa
  • Laminae 3-5 -> Nucleus proprius (a.k.a main sensory nucleus)
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104
Q

Compare proprioceptive/mechanoreceptive (Aα and Aβ) and nociceptive (Aδ and C) fibres in terms of where how many heights they synapse.

A
  • Proprioceptive/mechanoreceptive fibres -> These synapse at just one height in the spinal cord (and although they send out collateral fibres, these synapse in the brain, unless it is in Clarke’s column)
  • Nociceptive fibres -> These can synapse at multiple heights in the spinal cord, with each axon terminating at more than one dorsal root
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105
Q

Describe the importance of the nucleus proprius.

A
  • The nucleus proprius (laminae 3-5) receives combined input from Aβ (mechanoreceptive) and Aδ fibres (nociceptive)
  • The wide dynamic range (WDR) neurons in the nucleus proprius cross the midline (via the anterior white commissure) and ascend in the anterolateral columns.
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106
Q

Where in the brain does sensory information pass to from the spinal cord? How?

A
  • It goes to the thalamus, which relays it to the primary sensory cerebral cortex (all senses except smell).
  • Some also goes to brainstem structures, which allows for reflex and unconscious behaviours,
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107
Q

What are the two main ascending spinal pathways you need to know about?

A
  • Dorsal column system
  • Anterolateral system
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108
Q

For proprioception, touch, thermoreception and nociception, summarise:

  • Receptors
  • Fibre types
  • Termination in spinal cord
  • Ascending pathway
  • Higher nuclei
  • Conscious perception
A
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109
Q

What is decussation and why is it important?

A
  • It is the crossing of ascending and descending tracts to the contralateral side of the body.
  • Knowing where tracts decussate is important because it allows us to understand the consequences of various lesions.
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110
Q

Do the cerebral and cerebellar hemispheres receive information from the ipsilateral or contralateral side of the body?

A
  • Cerebral hemispheres -> Receive information from the contralateral side (therefore conscious perception is contralateral)
  • Cerebellar hemispheres -> Receive information from the ipsilateral side (therefore unconscious perception is ipsilateral)
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111
Q

What is Brown-Séquard syndrome and what symptoms does it present with?

A
  • A lesion of half of the spinal cord at a given level
  • It can be caused by gunshot/knife wounds, tumours or spinal disc herniation

Symptoms:

  • Loss of proprioception/mechanoreception on the ipsilateral side -> This is because the dorsal column system decussates in the medulla, so they have not decussated yet
  • Loss of nociception, thermoreception and crude touch on the contralateral side, at a lower spinal level -> This is because the nociceptive, thermoreception and crude touch information decussates in the spinal cord and then travels up via the anterolateral system. The loss starts at a lower spinal level because Lissauer’s tract carries fibres up to several levels before decussation.
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112
Q

What information do the dorsal column and anterolateral systems carry? Why?

A

Dorsal column:

  • Proprioception and fine touch
  • This is due to the ascending collateral fibres (first order) that are Aα and Aβ fibres.

Anterolateral systems:

  • Nociception, temperature and crude touch
  • Nociception and temperature are due to Aẟ and C fibres that synapse in the nucleus proprius and supply second order fibres that arise in the. Crude touch is due to Aβ fibres that do the same.
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113
Q

Compare the speed of the dorsal column and anterolateral systems.

A

The dorsal column system is faster and less susceptible to modulation, since there are fewer synapses.

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114
Q

Explain the concept of the anterolateral system.

A
  • Aẟ, C and Aβ fibres synapse in the dorsal horn at various locations (these are covered in earlier flashcards, but don’t worry too much since it is a complicated topic)
  • All of these either synapse directly onto projection neurons or use interneurons to converge onto projection neurons.
  • Projection neurons cross the midline via the anterior white commisure.
  • The main projection neurons arise from laminae 1 (marginal zone) and 5 (part of the nucleus proprius), but there are also some on laminae 6 and 7
  • The projection neurons form three main tracts that make up the anterolateral system -> Different tracts arise from different laminae
  • The spinothalamic tract is the main tract, going directly to the thalamus for conscious perception of pain, while the other two tracts synapse at lower structures and are involved in altertness and pain-control mechanisms
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115
Q

What are the three tracts that form the anterolateral system? Where does each terminate?

A
  • Spino-reticular
  • Spino-mesencephalic
  • Spino-thalamic
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116
Q

For the spino-reticular tract (part of the anterolateral system), where does it originate and terminate? What is the role?

A
  • Origin: Medial laminae (6-8) of grey matter
  • Terminates: Reticular formation (throughout the brainstem) -> This passes to the thalamus after this

Roles:

  • Increases alertness in response to pain -> ‘Reticular activating system’ -> Projects to higher centres and alerts the cerebral cortex about stimuli.
  • Increases reflex activity (e.g. in muscles) -> Via influencing the reticulospinal tracts

(Note: You can try and check where these fibres from laminae 6-8 arise from, but it probably doesn’t matter that much. Just assume that interneurons brought information there.)

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117
Q

For the spino-mesencephalic tract, where does it originate and terminate? What is the role?

A
  • Origin: Laminae 1 and 5
  • Terminates: The periaqueductal grey matter

Roles:

  • Pain-control mechanisms -> Via the periaqueductal grey in the midbrain, which has pathways that come back down the spinal cord
  • Unconscious body orientation (e.g. moving the eyes towards the painful stimulus) -> Via the superior collicitus in the midbrain, which influences the tectospinal tracts
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118
Q

For the spino-thalamic tract, where does it originate and terminate? What are the roles?

A
  • Origin: Laminae 1 and 5 (also 6-7)
  • Terminates: Thalamus (in the ventral posterior lateral nucleus and central lateral nucleus)

Roles:

  • Conscious perception of pain and its location
  • Also carries mechanoreceptive information (from Aβ fibres that synapse in the nucleus proprius)
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119
Q

Where do anterolateral projections originate from?

[IMPORTANT]

A

Main sensory nucleus (a.k.a. nucleus proprius) of the dorsal horn. Also from the marginal zone.

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120
Q

Where do fibres decussate to give rise to the anterolateral system?

[IMPORTANT]

A

Anterior white commissure

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121
Q

What are the two parts of the spinothalamic tract?

A
  • Anterior spinothalamic tract -> Crude touch and pressure
  • Lateral spinothalamic tract -> Pain and temperature
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122
Q

Where do the nociceptive fibres terminate in the brain?

[IMPORTANT]

A
  • Central lateral (CL) nuclei -> a.k.a. Intralaminar nuclei of the thalamus
  • Ventral posterior lateral (VPL) nuclei
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123
Q

Describe the difference between the old (archi) and new (neo) spinothalamic tracts.

A

These are divisions of the lateral spinothalamic tract?

Old (archi) spinothalamic tracts:

  • Take fibres from the nucleus proprius of the dorsal horn
  • The nucleus proprius receives information from Aδ fibres (direct) and C (indirect via interneurons in layer 2)
  • The tract goes up to the central lateral nucleus of the thalamus -> From there go to diffuse and ‘emotional’ areas of cortex (anterior insula/cingulate)

New (neo) spinothalamic tracts:

  • Take fibres from the marginal zone (lamina 1) of the dorsal horn
  • The fibres that supply the marginal zone are direct Aδ fibres
  • The tract goes up to the ventral posterior lateral nucleus of the thalamus -> From there go to sensory SI cortex for the location of a painful stimulus
124
Q

After the thalamic nuclei, where does information from the anterolateral tracts go?

[IMPORTANT]

A
  • Central lateral (interlaminar) nuclei -> Goes on to the insula cortex [IMPORTANT] as well as the diffuse and cingulate cortex.
  • Ventral posterior lateral (VPL) thalamus -> Go on to the primary and secondary sensory cortex for localisation of touch
125
Q

Describe how pain sensation is centrally mediated.

A
  • The hypothalamus and amygdala supply the periaqueductal grey
  • The periaqueductal grey mediates nociception via:
    • Control of raphe 5-HT (serotonin) cells of the medulla -> This modulates laminae 1,2 and 5
    • Control of noradrenergic cells of the locus coeruleus (pons) -> This modulates laminae 1 and 5
126
Q

What are the two dorsal columns called?

A
  • Cuneate fasciculus -> More lateral
  • Gracile fasciculus -> More medial

Remember it as “GG” in the middle.

127
Q

Where do the fibres in the dorsal column system synapse?

A

In the dorsal column nuclei in the medulla -> These are called the cuneate and gracile nuclei.

(Remember, these are 1st order fibres so they have not synapsed yet).

128
Q

Explain the concept of lateral inhibition in the dorsal column nuclei.

[IMPORTANT]

A
  • The dorsal column nuclei are the first points of synapse for mechanoreceptive (and proprioceptive) information
  • We want to be able to tell exactly where the information is coming from (e.g. in fine touch)
  • Lateral inhibition allows this:
    • A strongly excited second order neuron causes inhibition of neighbouring neurons
    • This can occur by feed-forward or feed-back inhibition
    • Therefore, only a single signal remains, allowing for high acuity
129
Q

Does lateral inhibition occur in the anterolateral system?

A

No, because it is more important for amplification to occur (via Lissaeur’s tract), so acuity can be sacrificed.

130
Q

When do the fibres of the dorsal columns decussate?

A
  • After they synapse at the dorsal column nuclei (in the medulla)
  • They cross the midline as internal arcuate fibres, then form the medial lemniscus.
131
Q

After decussating at the dorsal column nuclei, what do the fibres of the dorsal columns continue as?

A

Medial lemniscus

132
Q

On an axial (horizontal) section of the midbrain, label the medial leminiscus and spinothalamic tract.

A

(Anterior is at the top of the image)

133
Q

Where in the brain does the medial lemniscus (a continuation of the dorsal columns) terminate?

[IMPORTANT]

A

Ventral posterior lateral thalamus

134
Q

What is somatotopy?

A
  • The point-for-point correspondence of an area of the body to a specific point on the central nervous system.
  • i.e. A certain part of the white matter may carry innervation from the feet.
135
Q

Describe somatotopy throughout the dorsal columns and in the medial lemniscus.

[IMPORTANT]

A

Dorsal columns:

  • From medial to lateral, the innervation becomes more superior (i.e. medial = legs, lateral = arms)
  • This is because low down we start with just the gracile fascicles and then the cuneate fascicles join

Medial lemniscus:

  • In medulla -> Arms to legs in a dorsal to ventral direction
  • In pons -> Arms to legs in medial to lateral direction
  • In mibrain -> Arms to legs in ventral to dorsal direction

(In the medial lemniscus it is as if the person is doing a sommersault)

136
Q

What is the role of the thalamus in somatosensation?

A

Thalamus is a relay station, the gateway for sensory & motor information to reach the cerebral cortex (and thereby conscious perception)

137
Q

How does the thalamus send information to the cerebral cortex?

A

Via the internal capsule, which is made of the white matter that goes around the lateral ventricles.

138
Q

Draw the somatotopy of the primary somatosensory cortex in the post-central gyrus.

[IMPORTANT]

A
139
Q

Give some experimental evidence for the somatotopy of the primary somatosensory cortex.

A

(Penfield, 1937):

  • Stimulated various parts of the brain of a patient about oto undergo surgery
  • Asked the patient to report what was felt every time he stimulated a part of the primary somatosensory cortex
140
Q

What provides somatosensory innervation of the face to the somatosensory cortex?

A

Trigeminal nerve (CN V)

141
Q

Give the names of the three branches of the trigeminal nerve and draw their sensory territories.

A
142
Q

Describe how the trigeminal nerve carries somatosensory information from the face to the brain. Include nuclei.

[IMPORTANT]

A

Proprioceptive input:

  • Αα information from the muscles of mastication passes ‘locally’ to the midbrain mesencephalic nucleus
  • Then it passes to motor nucleus V, in the pons, which is involved in reflexes, etc.

Mechanoreception:

  • Aβ skin mechanoceptors synapse in the principal trigeminal nucleus
  • Then cross to join medial lemniscus and terminating ventral posterior medial nucleus

Pain and temperature:

  • Aδ axons pass down on the ipsilateral side to spinal nucleus
  • Here they synapse and decussate to join the contralateral anterolateral system
143
Q

To what important nucleus does most somatosensory information from the face go?

[IMPORTANT]

A

Ventral posterior medial nucleus (in the thalamus)

144
Q

Summarise the somatosensory thalamic nuclei. Draw their positions.

A
  • Ventral posterior lateral (VPL) thalamus -> Main somatosensory and nociceptive nucleus receiving input from the body (via from dorsal column and spinothalamic tracts). Projects on to the primary and secondary sensory cortex for localisation of touch.
  • Ventral posterior medial (VPM) thalamus -> Receives mechanoreceptive and nociceptive input from the face. Projects on to the primary and secondary sensory cortex.
  • Central (intralaminar) nuclei -> Receives nociceptive inputs (from the spinothalamic tract). Projects to insular, cingulate and diffuse cortex for the affective aspects of nociception.
145
Q

What are S1 and S2?

A
  • S1 = Primary somatosensory cortex
  • S2 = Secondary somatosensory cortex
146
Q

Where are the primary and secondary somatosensory cortexes?

A

They are just behind the central sulcus (the groove that runs laterally across the superior surface of the brain) in the central gyrus (the buldge just behind the sulcus).

147
Q

What are the main parts of the primary somatosensory cortex (S1)?

A

They are called Brodmann’s areas:

  • 1
  • 2
  • 3a
  • 3b

(Note: The whole cerebral cortex is divided into Brodmann’s areas - these are just the 4 in S1)

148
Q

Which Brodmann’s area is considered to be the true somatosensory cortex?

A

3b (because this is where most of the mechanoreceptive input goes)

149
Q

Is the receptive field of area 3b of the primary somatosensory cortex have conserved receptive fields?

A

Yes, there is a high fidelity, allowing precise localisation of touch.

150
Q

Draw the different Brodmann areas of the primary somatosensory cortex.

A
151
Q

Describe the input to the different areas of the primary somatosensory cortex.

A

Most input from the thalamus goes to areas 3a and 3b:

  • 3a -> Proprioception
  • 3b -> Mechanoreception

Some input to areas 1 and 2:

  • 1 -> Mechanoreception from receptors + Texture information from 3b
  • 2 -> Muscle and joint sensory feedback from receptors (mechano and proprio?) + Size and shape information from 3b

i.e. Areas 1 and 2 receive mechanoreceptive information from 3b, allowing it to be integrated, so that we have a wider understanding of the object we are touching.

152
Q

Does the primary somatosensory cortex deal with nociception?

A

Not really -> Even though nociceptive information passes to the thalamus, from there it passes to the insular, cingulate and diffuse cortex.

153
Q

Describe an experiment to show how fidelity of the sensory receptive fields is changes throughout the somatosensory cortex.

A
  • When fingertips are used to trace some letters on a rotating cylinder, the action potentials in the 3b area of S1 correspond to a precise tracing of the letters
  • As you progress further through the brain (areas 1 and 2), this signal is degraded, since the receptive fields are not conserved
  • This leads to degradation of the quality of the trace
154
Q

Areas 1 and 2 of the primary somatosensory cortex (S1) receive input largely from 3a and 3b, but have lower fidelity. What is the purpose of this?

A

Although they do not have as high fidelity (i.e. the receptive fields are larger due to convergence of fibres), they allow for integration of information from a wider areas of the body.

155
Q

Summarise the different roles of the primary somatosensory cortex (S1) when trying to work out the identity of an object in our pocket.

A
  • Area 3a -> Receives proprioceptive information, so it tells us where the hand is in space
  • Area 3b -> Receives mechanoreceptive information, so it gives detailed information about touch
  • Area 1 -> Receives some texture information, but mostly involved in combining mechanoreceptive information (from 3b), to get a more global picture of the shape of the object
  • Area 2 -> Receives combined sensory information from muscles and joints, plus mechanoreceptve information from 3b, so it gives a 3D picture of the object

The information is then passes to the posterior parietal cortex (areas 5 and 7), which is involved in memory of the object.

156
Q

Describe the onwards processing of information after the primary somatosensory cortex (S1).

[GOOD AS A SUMMARY]

A

After entering mostly at areas 3a and 3b, the information has high fidelity. It then passes to areas 1 and 2, which are involved in integrating the information from various receptors into a more complete picture. All of these S1 areas then send information to:

  • S2 (secondary somatosensory cortex), which passes it to the temporal lobe -> This is involved in knowing what a stimulus represents (tactile memory - “this is a book!”)
  • Posterior parietal cortex (areas 5 and 7), which combines it with visual information it receives and also passes it to the other side of the body via the corpus callosum -> This is involved in knowing where a stimulus (“this is where the book is!”)

Note: The pulvinar is a nucleus in the thalamus, involved in attention, so that you are attentive to the stimulus.

157
Q

Describe the columnar organisation of the primary somatosensory cortex (and the neocortex in general).

[IMPORTANT]

A

Inputs to the primary somatosensory cortex (from the thalamus) travel in columns from each receptor. These columns are divided into layers:

  • Layer 4 -> This receives information from the thalamus, then passes it up to layers 2/3
  • Layers 2/3 -> Passes the information to S2 or back down to layers 5/6
  • Layer 5 -> Cells project down to brainstem and spinal cord
  • Layer 6 -> Cells project down to thalamus

It is also worth noting that layer 1 is composed of just axons that can travel to different parts of the cortex (e.g. between Brodmann areas).

158
Q

Describe what is meant by the concept of canonical cortical circuits.

[IMPORTANT]

A

In each column of the prrimary somatosensory cortex, cellular responses of neurons are input specific.

(Check what this means and add more!)

159
Q

What are the effects of a broad S1 lesion?

[IMPORTANT]

A

Deficits in:

  • Sense of position
  • Ability to discriminate size, texture and shape
  • Also deficits in hand function (due to lack of descending feedback)

There is also altered but not absent nociceptive sensation.

160
Q

What are the effects of an area 3b lesion of S1?

A

Problems with discrimination of texture, size and shape.

161
Q

What are the effects of an area 1 lesion of S1?

A

Problems with assessment of texture.

162
Q

What are the effects of an area 2 lesion of S1?

A

Problems with assessment of size and shape.

163
Q

What are the effects of an S2 lesion?

[EXTRA]

A
  • Severe impairment
  • Cannot learn new tactile discrimination based on shape
164
Q

What are some causes of lesion of the primary somatosensory cortex (S1)? How do they differ?

A

They are frequently caused by stroke:

  • Anterior cerebral artery -> Foot, leg and trunk somatosensation lost
  • Middle cerebral artery -> Arm, hand and face somatosensation lost

This is because of the parts of S1 that each artery supplies.

165
Q

What is the descending contribution of the somatosensory cortex?

A

The somatosensory cortex uses the corticospinal (CST) tract to provide control of the ascending sensory systems (in addition to motor control).

166
Q

Give some experimental evidence for the role of the somatosensory cortex in descending pathways.

A

(Hikosaka, 1985)

167
Q

Give some experimental evidence for plasticity of the somatosensory cortex.

A
  • In patients who have a hand amputation during development, the part of the somatosensory cortex that would usually correspond to the hand is now encoded by the face.
  • This means that the face covers a wider area.
168
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual/potential tissue damage.

169
Q

What is nociception?

A

The perception of noxious stimuli.

170
Q

What are nociceptors?

A

Free nerve endings of primary sensory neurons activated by chemicals, heat, or mechanical pressure, that lead to a sensation of pain.

171
Q

What is analgesia?

A

The alleviation or the absence of pain.

172
Q

What is hyperalgesia?

A

Lowered threshold and excessive response to noxious stimuli (i.e. heightened pain).

173
Q

Give an example of hyperalgesia.

A

Pressure sensitivity of bruised tissue

174
Q

What is allodynia?

A

Pain resulting from stimuli that are not normally noxious.

175
Q

Give an example of allodynia.

A

Pain upon movement of joints in rheumatoid arthritis.

176
Q

What are the two main types of pain (based on their origin)?

A
  • Peripheral pain -> Due to activation of nociceptors in the skin or soft tissue by tissue injury.
  • Neuropathic pain -> Not due to nociceptor activation, but due to damage of peripheral and/or central nerves.
177
Q

Give some examples of peripheral and neuropathic pain.

A
178
Q

What are some factors that influence pain sensitivity?

A

Genetic, epigenetic and environmental factors.

179
Q

What are some types of pain treatment (for peripheral and neuropathic pain)?

A
180
Q

Compare the types of afferent fibres involved in nociception in terms of the pain type they carry.

A
  • Aẟ fibres -> Acute sharp (‘pricking’) pain -> Precisely localized and short duration
  • C fibres -> Burning pain -> Slower onset, diffuse, longer in duration.
181
Q

Compare the myelination of Aẟ and C fibres.

A
  • Aẟ -> Lightly myelinated
  • C -> Unmyelinated
182
Q

What fibres are polymodal?

A

C fibres, which are also a source of itch (aside from pain).

183
Q

What fibres are responsible for detecting temperature and how is this enabled?

A
  • Transient receptor potential (TRP) channels exist on nociceptive fibres (Aδ and C type)
  • Each type of TRP displays distinct temperature thresholds, but note that not all generate nociception
  • Also, some TRPs may be pain-generating mechanoreceptors
184
Q

What are some different chemicals that are involved in exciting nociceptive fibres in response to tissue damage and inflammation (e.g. when hitting your finger with a hammer)?

A
185
Q

Summarise how nociceptive nerve endings sense various molecules.

[IMPORTANT]

A

Ionotropic receptors:

  • Lead to cation entry -> This depolarises the cell
  • ATP binds to P2X receptors
  • Protons bind to ASIC and TRPV1 receptors
  • Capsaicin, endovanilloids and noxious heat activate TRPV1 receptors

Metabotropic receptors:

  • Lead to downstream cascades that affect ion channels
  • Bradykinin binds to B2 receptors -> Activates PKC, which phosphorylates TRPV1 channels and increases their sensitivity
  • Prostaglandins bind to prostanoid receptors -> Activates PKA, which phosphorylates voltage-gated sodium channels and increases their likelihood of causing depolarisation
  • Opiods, cannabinoids and noradrenaline -> Decrease PKA, which leads to decreased activation of voltage-gated sodium channels and increased activation of potassium channels, leading to hyperpolarisation
  • Nerve growth factors (NGF) -> Activates tyrosine kinase receptor, which increases the gene expression of the TRPV1 and VGSC in the membrane

This allows us to see which receptors cause nociception, and which simply sensitise to it.

186
Q

What are some things that can lead to hyperalgesia?

A

Heightened response to noxious stimuli can be caused by:

  • Diffusion of chemicals from site of injury
  • Axon reflexes causing neurogenic inflammation -> Transmission through pain fibres causes feedback release of inflammatory factors (Histamine, 5-HT and substance P -> See diagram)
  • Chemical sensitization of nociceptors (Bradykinin, prostaglandins and NGF)
  • ‘Wind-up’ of synaptic transmission in the spinal cord -> Increase in pain intensity over time when a given stimulus is delivered repeatedly above a critical rate
187
Q

Describe the entry of nociceptive fibres into the spinal cord and where they synapse.

A
  • They enter into the dorsal horn
  • C fibres terminate mostly in lamina 2 (substantia gelatinosa), while Aδ fibres terminate both in lamina 1 (marginal zone) and laminae 3-5 (nucleus proprius)
  • After synapsing, the second order fibres decussate and carry the fibres up the spinal cord
188
Q

Draw the results of histochemistry experiments showing the different neurotransmitters involved in pain transmission.

[EXTRA]

A
189
Q

What is the effect of enkephalins on pain?

[IMPORTANT]

A
  • Enkephalins are endogenous opioid peptides
  • They can be released into the synapse between a sensory nociceptive fibre and a projection neuron that travels up the spinal cord
  • They inhibit nociception (e.g. in descending control of nociception)

(ADD MORE FLASHCARDS ON THIS)

190
Q

What is wind-up? Which fibres show “wind-up” and why?

A
  • Wind-up is the increase in pain intensity over time when a given stimulus is delivered repeatedly above a critical rate.
  • Aδ fibres do not show wind-up
  • C fibres do show wind-up
  • This is suggested to be because glutamate released from the sensory fibre acts on NK-1 receptors (Gq-coupled) on the second-order projection neurons in the spinal cord, leading to an increase in intracellular calcium
  • This calcium leads to increased sensitivity of the second-order neuron, possibly due to insertion of more ionotropic glutamate receptors into the membrane
191
Q

Describe the descending control of nociceptive pathways.

[IMPORTANT]

A
  • The pariaqueductal grey sends fibres to the locus coeruleus and nucleus raphe magnus.
  • The locus coeruleus releases noradrenaline onto the inhibitory enkephalin interneurons in the spinal cord.
  • The nucleus raphe magnus also releases 5-HT and enkephalins onto inhibitory enkephalin interneurons in the spinal cord.
  • The inhibitory enkephalin interneurons release enkephalins that are inhibitory to a synapse between the first and second order nociceptive neurons in the spinal cord. (Check this cos it doesn’t quite agree with what Trev-dog says)
192
Q

What is the periaqueductal grey and what is its importance in pain?

[IMPORTANT]

A
  • The PAG is a nucleus in the midbrain that surrounds the central aqueduct
  • It is involved in descending control of pain perception, inhibiting synapses between first and second order nociceptive neurons
193
Q

Give some examples of drugs used in the treatment of pain.

A

Those highlighted are in the spec. Others in the spec that are not mentioned here:

  • Tramadol (a type of opioid)
  • Anxiolytics (anti-anxiety drugs)
194
Q

What are some examples of NSAIDs?

A
  • Aspirin
  • Ibuprofen
  • Paracetamol (weak)
195
Q

How do NSAIDs work?

A
  • NSAIDs are cyclo-oxygenase (COX) inhibitors that reduce the synthesis of prostaglandins
  • Prostaglandins are inflammatory mediators that sensitise the nociceptive nerves to excitation by increasing the likelihood of opening of voltage-gated sodium channels
196
Q

What is a downside of NSAID use?

A
  • COX-1 is constitutively active (eg. produces prostaglandins to support the gastric mucosa) while COX-2 is activated by inflammation -> Thus, COX-2 selective inhibitors (celecoxib) were developed as analgesics to avoid peptic ulcers associated with NSAID treatment
  • But there is current concern over cardiovascular harm associated with COX-2 inhibition (Vioxx controversy)
197
Q

What is the mechanism of action of paracetamol?

A
  • It is a NSAID
  • It is a weak COX-1/COX-2 inhibitor, but the mechanism of action is uncertain
198
Q

What are some examples of opioid analgesics?

A
  • Morphine
  • Codeine
  • Tramadol
199
Q

How do opioid analgesics work?

A
  • They stimulate opioid receptors in:
    • Dorsal horn (at the synapse between first order and second order nociceptive neurons) -> Lead to
    • Higher pain centres (e.g. the periaqueductal gray)
    • Nociceptive sensory fibre endings
  • This leads to downregulation of nociception
200
Q

What are some downsides of opioid analgesic use?

A
  • Adverse effects:
    • Sedation
    • Nausea
    • Constipation
    • Respiratory depression
    • Coma
  • Addiction -> Associated with long-term use and increased mortality
201
Q

What is migraine and what is the pathophysiology?

A
  • A headache disorder characterized by cluster of symptoms including nausea, sensory sensitivity, aura, severe headache and vertigo.
  • Pathophysiology likely involves changes in cerebrovasculature, inflammation and neural networks (including the hypothalamus, cerebral cortex and trigeminal nucleus)
  • Changes in circulating 5-HT and peptides are thought to play a role.
202
Q

What are some current treatments for migraine?

A
  • Triptans (5-HT1 agonists) [IMPORTANT]
  • NSAIDS (acute migraine) [EXTRA]
  • 5-HT2 receptor antagonists (migraine prophylaxis) [EXTRA]
203
Q

How do migraine treatments work?

A
  • Only triptans are mentioned in the spec: They are 5-HT1 antagonists
  • They:
    • Are vasoconstrictors of extracerebral vasculature
    • Reduce neuropeptide release from C fibres in the periphery
    • Stimulate inhibitory 5-HT1 receptors in the trigeminal nucleus
  • NSAIDs block inflammation via COX inhibition
  • 5-HT2 antagonists also lead to vasoconstriction
204
Q

What triptan used in migraine treatment is mentioned in the spec?

[IMPORTANT]

A

Sumatriptan

205
Q

What is the mechanism of action of local anaesthetics?

[IMPORTANT]

A

They are voltage-gated sodium channel inhibitors, so they stop nociceptive fibre action potential transmission.

206
Q

What are the mechanisms of the main analgesic classes?

[PARTLY EXTRA]

A
207
Q

Why is there a need for so many different types of analgesic drugs?

A
  • Analgesics have different strengths (strongest opiates) to match different levels of pain severity (headache versus cancer pain)
  • Analgesics have different durations of action (acute versus chronic pain)
  • Side effects of specific analgesics can limit their use in vulnerable patient groups (eg NSAIDs contra-indicated in patients with peptic ulcers)
  • Certain analgesics most useful in specific pain states:
    • Local anaesthetics for surgical repair of wounds
    • Triptans for migraine
    • Antidepressants and anticonvulsants for neuropathic pain
208
Q

What is chronic pain?

A

Pain that outlives acute pain’s ‘warning’ role (3-4 months) -> i.e. The system gone wrong

209
Q

What are some facts relating to chronic pain?

[EXTRA]

A
  • 1:5 people suffer from chronic pain
  • On average, sufferers live with chronic pain for 7 years (20% >20 years)
  • One in five reports losing a job or have been diagnosed with depression as a result of their pain
  • Conservative estimate annual costs $560-635b USA/€200b Europe
210
Q

What is the relationship between pain and nociception?

A

Nociception leads to pain -> How much pain is experienced varies.

211
Q

What are some reasons why the relationship between nociception and pain is not always linear?

[IMPORTANT?]

A

These can be studied using imaging techniques that allow us to see the activity of the brain upon nociceptive inputs.

212
Q

Describe the structure of nociceptors and their location in the skin.

A

They are free nerve endings that go all the way into the epidermis (more superficial than the mechanoreceptors).

213
Q

Describe how different types of pain are seen on an graph after the stimulus.

A
214
Q

Draw a graph of the sensitivities of different TRP channels at different temperatures.

A
215
Q

What TRP channels can menthol and capsaicin activate?

A
  • Menthol -> TRPM8
  • Capsaicin -> TRPV1
216
Q

What are the 3 main pathways for nociceptive signals in the spinal cord?

A
  1. Nociceptive afferents from periphery may synapse directly with neurons of the ascending anterolateral pathway
  2. Afferents may synapse with excitatory interneurons, which relay nociceptive inputs to ascending fibres
  3. Afferents may synapse with inhibitory inputs which inhibit or block completely transmission of nociceptive impulse

This explains a lot clinical implications of pain, such as referred pain, and also gave rise to the gate theory of pain.

217
Q

Describe the gate theory of pain.

[IMPORTANT]

A
  • The gate theory of pain states that when a nociceptive C fibre fires, if an Aβ fibres simultaneously, the Aβ fibre will stimulate an inhibitory interneuron
  • The inhibitory interneuron releases enkephalin [IMPORTANT]
  • This inhibits the second order nociceptive neuron, so that the nociception is reduced
  • Thus, it can be seen that pain can be reduced by providing some gentle touch stimulation to the same area (e.g. rubbing a wound after falling over)
218
Q

What are the 3 main tracts involved in taking pain information to the brain? What is the role of each?

[IMPORTANT]

(Flashcards on this earlier too)

A
  • Spinothalamic -> The big one, responsible for conscious perception of pain
  • Spinoreticular -> Arousal in response to pain “wow yeah I should do something about this”
  • Spinomesencephalic -> Via the brainstem, involved in descending control of nociception “this is a bit hardcore, I should modulate it”
219
Q

What is trigeminal neuralgia and what causes it?

[IMPORTANT]

A
  • Spontaneous episodes of chronic pain in the distribution of one or more branches of the trigeminal nerve.
  • These episodes may be triggered by weak mechanical stimulation in same region.
  • Major contributing factor appears to be mechanical damage to the trigeminal ganglion by an artery that impinges on the ganglion.
  • Surgical displacement of the artery can resolve the condition.
220
Q

Aside from trigeminal neuralgia, what is another condition associated with cranial nerves?

A

Migraine

221
Q

Compare the anterolateral and dorsal column systems in terms of:

  • Modalities
  • Location in spinal cord
  • Level of decussation
  • Brain stem terminations
  • Cortical terminations
A
222
Q

How can we study pain in babies?

[EXTRA]

A
223
Q

What are the 3 main categories of chronic pain? Give some examples of each.

A
224
Q

What keeps people in chronic pain?

A
  1. Constant firing of nociceptive fibres
  2. Amplification/Sensitisation of these pain signals in CNS -> Could be due to decreased descending inhibition or increased descending stimulation
  3. Maladaptive plasticity (when the brain has hindered functional recovery or the development of an unwanted symptom that can lead to pain)
  4. Vulnerability towards developing chronic pain
225
Q

What are some different ways of measuring pain in patients?

A
226
Q

Describe the multifactorial approach often used to treat pain.

A

These are used together:

  • Drugs
  • Cognitive behavioural therapy
  • Physical therapy
227
Q

What causes taking a shower to be painful after sustaining sunburn?

A

There is sensitisation of the nerves by inflammatory mediators (see Trevor’s lecture).

228
Q

State some substances that can activate or sensitize nociceptive nerves.

A

(See also: Trevor’s lecture)

229
Q

What is sensitisation and what are the two types?

A
  • Sensitisation is the enhancement of nociceptive pathways so that a smaller or even innocuous stimulus can produce pain
  • Peripheral sensitisation occurs at the level of the nociceptors themselves, where release of various substances from the damaged tissue cause the nociceptor to be more primed for firing (see all the substances in Trevor’s lectire)
  • Central sensitisation occurs within the CNS at the level of the afferent nerve terminal of the second order neuron in the dorsal horn (not dorsal column!), where various mechanisms mean that the second order neuron receives greater input
230
Q

Explain primary and secondary hyperalgesia.

A
  • Primary hyperalgesia is increased sensitivity at a wound or area of damage -> Mostly due to peripheral sensitisation (but central sensitisation can occur too)
  • Secondary hyperalgesia is increased sensitivity in the area surrounded a wound or area of damage-> Due to central sensitisation
231
Q

Describe how central sensitisation occurs.

A

There are multiple suggested mechanisms that can contribute:

  • Wind-up -> High rates of C-fibre firing lead to an increase in intracellular calcium in the post-synaptic nerve terminal, which causes more ionotropic glutamate receptors to be inserted into the membrane (or their phosphorylation) -> This leads to primary hyperalgesia.
  • Aβ fibres that innervate the area around the wound sprout to synapse onto the same post-synaptic neuron as Aẟ and C fibres. The same mechanism as wind-up means that mechanoreception is perceived as pain -> This leads to secondary hyperalgesia and allodynia.
  • Prostaglandins in the spinal cord can bind to PGE2 receptors on the post-synaptic membrane, causing more phosphorylation of glutamate receptors, as well as on the pre-synaptic membrane, causing more glutamate release.
  • Injury to the nociceptive peripheral nerve axons causes insertion of α2ẟ channels in the membrane, leading to increased glutamate release.
  • Synaptic disinhibition -> Decreased GABAergic descending inhibition and increased descending stimulation (from e.g. the PAG).
232
Q

Secondary hyperalgesia is indicative of…

A

Central sensitisation (since peripheral sensitisation doesn’t really cause it)

233
Q

Give some clinical relevance of α2ẟ channels on nociceptive fibres.

[EXTRA]

A
  • α2ẟ channels are calcium channels on the membrane of first order nociceptive fibres in the periphery
  • They lead to calcium influx that stimulates glutamate release and therefore downstream pain perception
  • They can be targeted by inhibitors such as gabapentin, which reduce pain
234
Q

How can we modulate descending inhibition of nociceptive pathways?

[EXTRA]

A
  • Descending inhibition occurs via noradrenergic nerves that synapse onto enkephalin-containing nerves, which in turn inhibit the synapse between the first and second order neurons
  • Tricyclic antidepressants and SSRNIs (selective serotonin-norepinephrine reuptake inhibitors) can be used to increase this noradrenergic control, leading to suppression of nociception
235
Q

What is unusual about damage to nociceptive fibres?

A
  • Usually, when sensory fibres are damaged, there will be loss of function (e.g. loss of vision).
  • However, when nociceptive fibres are damaged, they fire ectopically and therefore show increased activity.
  • We do not know why this happens.
236
Q

Give some examples of neuropathic pain caused by lesions at different levels in the spinal cord.

A
237
Q

What is referred pain?

A

Sensation of pain in area of body DISTANT from site of origin of the original nociceptive receptor activation.

238
Q

What causes referred pain?

[IMPORTANT]

A
  • Most commonly, it is experience of cutaneous, muscle or bone pain through activation of visceral nociceptor nerve endings
  • Occurs through existence of common central points of convergence of nociceptive afferent inputs from viscera and somatic structures.
  • Same second-order neuron receives input from viscera AND the skin.
239
Q

How can we very easily reduce expected pain in every day life? How does this work?

[IMPORTANT?]

A
  • We can make use of psychology by, for example, psyching ourselves up in advance of pain
  • This impacts the descending inhibition of nociception (from the brainstem), causing pain to be reduced
  • This might have potential in treatment
240
Q

What is a way in which psychological modulation of pain might work?

[IMPORTANT?]

A
  • The brainstem sends down stimulatory and inhibitory control of the nociceptive pathway
  • Therefore, the brainstem can control how much pain is perceived at a given time
241
Q

Give some clinical evidence for the placebo effect in pain.

[EXTRA]

A

(Beard, 2017):

  • Compared patients receiving (a) no treatment, (b) shoulder surgery known as subacromial surgery, and (c) sham surgery (i.e. the placebo)
  • They compared the pain scores at 6 and 12 month follow up
  • The two surgery group showed very similar pain outcomes, and the no treatment group showed slightly worst pain
  • It was suggested that it was the act of coming into hospital, going into surgery, etc. was rresponsible for the outcome
  • This placebo effect might be modulated by the brainstem sending increased inhibition of nociception down the spinal cord in response to the brain thinking that surgery had happened
242
Q

What are some different categories of clinical pain syndromes and how can they be treated?

A
243
Q

Is neuropathic pain usually acute or chronic?

A

Chronic

244
Q

Can neuropathic be treated using analgesics (e.g. NSAIDs)?

A

No

245
Q

What are some symptoms of neuropathic pain?

A
  • Numbness and sensory loss
  • Spontaneous, on-going and paroxysmal pain
  • Stimulus-evoked pain:
    • Hyperalgesia or Allodynia
    • Evoked by hot, cold or mechanical stimuli
  • Common pain descriptors:
    • Burning
    • Shooting
    • Electrical
246
Q

Describe how the pain in multiple sclerosis (MS) can be treated and why this works.

A
  • Pain affects are 2/3rd of patients with MS (Amatya, 2018)
  • Approximately 50% of the patients with MS use THC or CBD for treatment.
  • CBD does not bind directly to cannabinoid receptors, but instead it inhibits FAAH (fatty acid amide hydrolase), which usually breaks down anandamide (the ligand for the CB1 receptor)
  • Therefore, CBD increases the concentration of the ligand for the cannabinoid receptor.
  • Monoacylglycerol lipase (MAGL) is a key enzyme in the hydrolysis of the endocannabinoid 2- arachidonoylglycerol (CB2 ligand) -> Potential target for treatment
247
Q

How can pain caused by heat be studied in animal models?

[EXTRA]

A

Hargreaves test:

  • A mouse is placed in a chamber where it is free to move
  • A warm laser is placed beneath the mouse
  • The laser is shon onto the mouse’s paw, causing it to heat up gradually
  • The time taken for the mouse to move away from the heat is a measure of the pain hyperalgesia in that mouse
248
Q

How can pain caused by mechanical stimuli be studied in animal models?

[EXTRA]

A
  • Von Frey hairs are used
  • These are hairs of various diameters, allowing different forces to be applied
  • They can be used in combination with a Hargreaves-style chamber
249
Q

What are different types of genetic disorders of painlessness?

A
  • Degenerative disorders of nociceptive pathways where nociceptor function is progressively lost.
  • Non-functional nociceptors such as in congenital insensitivity to pain (CIP) due to mutations in voltage-gated sodium channels resulting in nociceptors being unable to detect tissue damage.
  • Disorders of failed nociceptor neurodevelopment where pain-sensing neurons do not develop.
250
Q

Evaluate use of NK1 antagonists as analgesics.

[EXTRA]

A
251
Q

How are microglia involved in pain?

A
  • Microglia are activated in pain
  • They produce inflammatory mediators that act on afferent neurons, stimulating nociception
252
Q

Olfaction and taste are forms of…

A

Chemoreception (Ability to recognise and respond to environmental and internal chemicals, such as hormones and neurotransmitters)

253
Q

In order for chemoreceptors to detect a chemical stimulus, what must happen to it?

A
  • It must be taken up by ingestion, inhalation or skin contact
  • It must be dissolved in aqueous fluids (mucus, saliva, blood, interstitial fluid)
254
Q

Where is the olfactory mucosa?

A

Upper posterior side of the lateral wall of the nasal cavity.

255
Q

What are turbinates/conchae and what is their function?

A

Ridges in the nasal cavity that direct air to the olfactory mucosa. They warm and humidify the air.

256
Q

What is the area of the olfactory mucosa in humans?

A

Around 10cm2

257
Q

Describe the structure of the olfactory mucosa and the cells involved.

A

Olfactory mucosa = Olfactory epithelium + Mucus

Cells in olfactory epithelium:

  • Olfactory receptor neurons/sensory neurons (OR/SN)
  • Basal cells (stem cells)
  • Supporting cells
258
Q

Where is olfactory mucus secreted from?

A

Secreted from Bowman’s gland.

259
Q

What is the function of the olfactory mucus?

A
  • Contains antibodies, enzymes, salt and odorant binding proteins
  • Dissolves odorants, enabled them to be sensed
260
Q

Describe the structure of an olfactory receptor neuron (a.k.a. sensory neuron).

A
  • Each olfactory receptor neuron has a cell body and dendritic knob.
  • There are specialised cilia that carry odorant receptors.
261
Q

How do olfactory receptors work?

A
  • They are GPCR
  • Each neuron expresses only one type of GPCR
  • The receptive range of this gene can be broad or narrow, partly depending on conditions, such as concentration
262
Q

Where do olfactory receptor neurons output to?

[IMPORTANT]

A

They send unmyelinated axons that penetrate the cribiform plate of the ethmoid bone to contact the olfactory bulb.

263
Q

Describe how transduction in the olfactory system works.

A
  • Odorant dissolves in mucus and binds to olfactory receptor
  • This leads to Gαolf activation, which in turn activates adenylate cyclase III
  • This increases cAMP, which opens cyclic nucleotide gated channels, leading to an influx of calcium and sodium
  • This depolarises the cell and calcium activates chloride channels that further depolarise the cell
  • This can trigger the firing of an action potential, which leads to release of NT onto the olfactory bulb
264
Q

How can transduction in olfactory receptor neurons be terminated?

A

It can be terminated in several ways:

  • Unbinding of the odorant
  • Extrusion of calcium
  • Calcium-dependent adaptation (weakened response over time)
265
Q

Describe the different layers of the olfactory bulb.

A
266
Q

What are glomeruli in the olfactory bulb?

A

They are spherical sites in the olfactory bulb that houes synapses between olfactory receptor neurons and mitral cells.

267
Q

How are different smells mapped in the olfactory bulb?

A
  • Each glomerulus receives input from one type of olfactory receptor neuron. This means that an increase in odorant concentration increases the activity at that relevant glomeruli.
  • However, at high concentrations of odorant there may be non-specific activation of other olfactory receptor neurons, leading to activation of other glomeruli too.
268
Q

Onto what cells do olfactory receptor neurons release neurotransmitter?

A

Mitral cells in the olfactory bulb.

269
Q

Draw and describe the connectivity of different cells in the olfactory bulb.

A
  • Olfactory receptor neurons contact mitral cells which are the projection neurons of the olfactory bulb.
  • These output directly to the primary olfactory cortex.
  • Periglomerular and granule cells provide lateral inhibition.

(You do not need to know the details. Just remember the ORNs and mitral cells.)

270
Q

Where are the olfactory bulbs?

A
271
Q

What is the output from the olfactory bulbs via?

A

The mitral cell axons form the olfactory tracts.

272
Q

Describe where the olfactory tracts output to.

[IMPORTANT]

A

The olfactory divides into medial and lateral stria at the level of the optic chiasm:

  • Medial stria
    • Goes to the contralateral olfactory bulb via the anterior commissure.
  • Lateral stria
    • Goes to the fibres to the primary olfactory cortex (NOT via the thalamus), which outputs to the secondary olfactory cortex, limbic system and hypothalamus.
    • Goes to the secondary olfactory cortex (via medio-dorsal thalamus)
273
Q

Where are the primary and secondary olfactory cortices?

[IMPORTANT]

A
  • Primary olfactory cortex -> Temporal lobe
  • Secondary olfactory cortex -> Orbitofrontal cortex
274
Q

Summarise the main targets of the olfactory tracts.

A
  • Primary olfactory cortex (NOT via thalamus) -> Then secondary olfactory cortex, hypothalamus and limbic system
  • Secondary olfactory cortex (via medio-dorsal thalamus)
  • Opposite olfactory bulb
275
Q

What is the function of the primary olfactory cortex?

A

Emotional, motivational, autonomic and endocrine response to the smell (partly via output to the limbic system and hypothalamus).

276
Q

What is the function of the secondary olfactory cortex?

A

Conscious discrimination of different smells.

277
Q

What are pheromones?

A
  • A substance that is utilised for intra-species communications
  • Released by one individual and received by conspecifics
  • Send information about sex, strain and species to receiver
  • Are meaningful or informative for species
278
Q

Give some examples of disorders of smell.

[EXTRA]

A
  • Anosmia -> Inability to detect presence of odour:
    • Conductive loss -> Obstruction of nasal passage
    • Sensorineural causes -> Damage to olfactory epithelium
    • Central dysfunction -> In relation to CNS disease
  • Dysosmia -> Difficulty with odour discrimination
  • Parosmia -> Sensation of odour distinct from that present
  • Phantosmia -> Perception of odour in absence of odour source

Causes:

  • Aging (neurodegenerative diseases!)
  • Upper respiratory tract infections
  • Head trauma
  • Sinonasal disease
  • Congenital (rarely)
279
Q

Describe the properties of tastants (i.e. the taste equivalents of odours).

A
  • Non-volatile
  • Hydrophilic
  • Soluble in saliva
  • Detection threshold high
280
Q

Describe the structure of the tongue’s taste apparatus.

A
  • On the tongue, there are papillae which have trenches to concentrate the tastant
  • In the trenches of the papillae, there are taste buds
  • Each taste buds contains 50-150 taste receptor cells
  • The taste receptor cells have taste receptors on their surface.
281
Q

What are the 5 main tastes? What is the function of each?

A
  • Salty -> Enables detection of electrolytes
  • Sour -> Warning of noxious chemicals
  • Bitter -> Warning of noxious chemicals
  • Sweet -> Enables detection of energy dense foods
  • Umami -> Enables detection of amino acids
282
Q

Describe the distribution of different type of papillae on the tongue.

[EXTRA?]

A
283
Q

Describe the structure of taste buds.

A
  • Taste receptor cells
  • Support cells
  • Basal cells (stem cells)

The taste buds are surrounded by epithelial cells. The taste buds themselves are essentially equivalent in structure to olfactory receptor mucosa, except the taste receptor cells release NT onto afferent nerve cells.

284
Q

Describe the structure of taste receptor cells.

A
  • Have apical microvilli that have receptors for tastants that enable sensory transduction
  • Release NT on the basal side
285
Q

What neurotransmitters do taste receptor cells release and onto where?

A
  • Possibly ATP or 5-HT
  • Onto afferent nerve cells
286
Q

Describe how different flavour taste receptors are distributed within a taste bud.

[EXTRA]

A

This model has the strongest evidence in mice, but there is still some controversy.

287
Q

Describe how each of the types of taste receptor detect their flavour.

A
  • Salty
    • Have ENaC channels that detect sodium
  • Sour
    • Have unknown receptors for H+
  • Sweet, Bitter and Umami (shown in diagram)
    • Have GPCRs that lead to increases in IP3
    • This leads to calcium release from intracellular stores
    • The calcium leads to influx of sodium via TrpM5 channels, which depolarises the cell and leads to NT release
288
Q

What are the different GPCR that are the taste receptors for sweet, bitter and umami?

A
  • Sweet → T1R2 + T1R3
  • Bitter → T2R
  • Umami →T1R1 + T1R3, mGluR4
289
Q

What nerves carry taste information and from where?

[IMPORTANT]

A
  • Facial nerve (VII) -> From anterior 2/3rd of tongue
  • Glossopharyngeal nerve (IX) -> From posterior 1/3rd of tongue

(Remember this by their positions in this diagram)

290
Q

Where do the facial nerve (VII) and glossopharyngeal nerve (IX) carry taste information?

[IMPORTANT]

A

To the nucleus of the solitary tract (a.k.a. nucleus solitarius or nucleus tractus solitarii).

291
Q

Describe the taste pathway in detail.

[IMPORTANT]

A
  • Taste receptors release neurotransmitter onto the afferent nerves (facial nerve on the anterior 2/3rd of the tongue, glossopharyngeal on the posterior 1/3rd of the tongue)
  • The facial nerve (VII) and glossopharyngeal nerve (IX) output to the nucleus of the solitary tract
  • Nucleus of the solitary tract outputs to:
    • Primary taste cortex (via the ventral-posterior thalamus), then to the secondary taste cortex
    • Hypothalamus (for endocrine responses to food)
292
Q

Where is the nucleus of the solitary tract?

A

Medulla

293
Q

Where is the primary taste cortex?

A

Anterior insula on the insular lobe and the frontal operculum on the inferior frontal gyrus of the frontal lobe.

294
Q

Where is the secondary taste cortex?

A

Orbitofrontal cortex

(This is the same as the secondary olfactory cortex)

295
Q

What is this?

A

Nucleus of the solitary tract

296
Q

What does the nucleus of the solitary tract receive input from?

A

Cranial nerves VII, IX and X.

297
Q

Where does the orbitofrontal cortex output to that is relevant to taste?

A

It outputs to the lateral hypothalamus ‘feeding centre’.

298
Q

Describe how temperature affects taste.

[EXTRA]

A
299
Q

Describe some taste disorders.

[EXTRA]

A
300
Q

What is the mechanism of sensory transduction?

A

The mechanism generally relies on ionotropic receptors:

  • In mechanoreceptors, this is in the form of a stretch-mediated Na+ channel which, when opened by stretch of the skin to which they are tethered (in a process potentially aided by ridges), will allow for a depolarising influx of sodium cations that increases the rate of signal firing along the afferent pathway.
  • For free nerve endings, the channels are instead gated by the specific noxious or thermal stimulus as needed – for example, heat-sensitive domains in the TRPV1 channel will only lead to a conformational change and open the pore domain of these Na+ channels when the temperature of the overlying skin is within a certain range.
301
Q

What is the mechanism of sensory adaptation?

A
  • Pacinian and Meissner’s corpuscles both possess multilaminate discs which have been shown to make them responsive to on/off change in pressure only – thus adapting them for detection of vibration or changes in stimulation of the skin.
  • Between the laminae surrounding the nerve ending, there is lamellar fluid which is able to spread out and disperse the force so that the membranes do not stretch, and the gated channels remain closed after a constant pressure is applied.
  • This can be illustrated by the delamination of one of these corpuscles and measurement of the spike-train it produces; it starts to mirror that of a slow-adapting receptor instead.
302
Q

Summarise the body dermatomes.

A
303
Q

What is syringomyelia?

A

A CSF-filled cyst that forms within the spinal cord.

304
Q

What is an unexpected type of drug that can be used in the treatment of pain?

A

Anxiolytics

305
Q
A

YEAR 2 - The Nervous System (18 decks)

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