IC3- Touch and pain receptors Flashcards

1
Q

When the touch receptors (afferents Aβ) are stimulated, which pathway do the first order neurons travel through next?

A
  • Touch signals travel through the dorsal columns of the spinal cord
  • First-order neurons ascend the dorsal columns without crossing over immediately
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2
Q

Where does crossing over happen for the touch pathway? Elaborate

A
  1. In the dorsal column pathway, first order neurons synpase with the second order neurons in the medulla (haven’t crossover yet!!)
  2. Afterwards, second-order neurons then CROSS OVER to the contralateral side before ascending to the thalamus
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3
Q

In the dorsal column pathway, where does the second neuron synapse with the third neuron?

Where does it travel to after?

A

In the thalamus.

Then afterwards it travels to the somatosensory cortex

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4
Q

When the pain receptors (afferents Aδ and C) are stimulated, which pathway do the pain signals travel through?

Where does the first order neuron synapse with the second order neuron?

A

First-order neurons synapse with second-order neurons in the dorsal horn of the spinal cord

Crossing over happens in the spinal cord itself, and pain signals then travel through the ventrolateral/ anterolateral quadrant (spinothalamic tract) of the spinal cord.

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5
Q

In the anterolateral quadrant (spinothalamic tract) pathway, where does the second neuron synapse with the third neuron?

Where does it travel to after?

A

At the thalamus

Then afterwards it travels to the somatosensory cortex

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6
Q

Which pathway do the pain and touch receptors travel through?

A

Touch pathway = dorsal column pathway
Pain pathway = spinothalamic pathway

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7
Q

What are the 4 principles that underlie sensory processing?

A
  1. Action potential as signal to relay information
  2. Signal travels along topographic lines
  3. The signal travels along labeled line
  4. The signal along the relay encode for properties of the stimuli, such as –
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8
Q

Explain what it means for signals to travel along topographic lines

A

It means that different populations of afferent relay information to different regions in the somatosensory cortex.

There is regular organisation.

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9
Q
A
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10
Q

What is the significance of such regular organisation via topography lines?

A

This regular organisation makes it easy for the brain to interpret the signals

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11
Q

According to the somatosensory homunculus, which parts of the body are more medial and lateral?

A

Lower part of the body (feet, hands) are more medial.

The upper part of the body (face) is more lateral.

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12
Q

Explain the somatosensory processing principle of ‘the signal travels along labeled line’

A

There are different types of receptors to pick up only one type of specific stimuli, and the signals travel along separate pathways to the CNS.

Eg. Touch and pain pathways are separate.

Touch pathway = dorsal column pathway
Pain pathway = spinothalamic pathway

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13
Q

Labelling occurs via different receptors, where different signals travel through different pathways. What are some examples of specific receptors? (5)

A
  • Vision (photoreceptors)
  • Chemoreceptors
  • Osmoreceptors
  • Thermoreceptors
  • Nociceptors (stimulated by tissue damaging stimuli)
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14
Q

Increasing the rate of electrical stimulation of the same receptor (eg touch receptor) will evoke sensation of pain. T/F?

A

False.

According to the label line concept, increasing the rate of electrical stimulation will only increase magnitude of the same sensation which is touch!!!

Pain sensation is a different label line altogether.

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15
Q

In the principles of somatosensory processing, how does the signal along the relay encode for properties of the stimuli?

A

Eg. Intensity

The more intense the stimulus, the more the number of action potentials per unit time (frequency) and more intense will be the sensation

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16
Q

Define hyperalgesia

A

Increased pain to a given noxious stimulus

17
Q

Define allodynia

A

Pain to a normally non-painful stimulus (e.g. pain to a
stimulus normally sensed as touch)

18
Q

What are the possible mechanisms that can lead to touch allodynia? (3)

A
  1. Degeneration of inhibitory neuron
  2. The nature of the inhibition is affected such that the inhibitory neuron excites the spinothalamic neuron post-injury
  3. Sensitization of nociceptors due to the release of variety of chemicals at damaged site → lowers threshold to excite, no. of TRV1 receptors increase.

In turn, the excitable nociceptors affect 2nd order spinothalamic (ST) neuron by release of chemicals glutamate, Substance P and CGRP, making it more excitable.

Such a ST neuron might be more responsive to touch stimulus (hence non-painful stimulus might activate the nociceptors this time round)

19
Q

When there is injury, what are the chemicals released which can sensitize the nociceptors? (recognise, no need to memorise all)

A

CGRP, Substance P, histamine, bradykinin, 5-HT, PG

20
Q

With regards to touch allodynia, which medications can help in pain relief?

Include their MOAs

A
  • Aspirin (COX inhibitor → blocks PG synthesis)
  • Acetaminophen (reduction of the COX pathway in CNS and antagonism of TRPV receptors esp spinal cord)
  • Ubrogepant (migraine)
21
Q

Explain the general gist of the modulation of pain

A

Pain can be enhanced or suppressed according to the individual’s state

E.g. stress (about something else) can cause the pain to be suppressed

anxiety causes pain to be enhanced

22
Q

When the nociceptors are hyperexcitable, how do they lead to sensitization of the second order neuron?

A

They release glutamate which binds to the NMDAR and AMPAR receptors on the dendritic spines → ↑ in no. of AMPAR receptors on ST neuron + lower threshold to excite AMPAR receptors

This leads to sensitization of the second order neuron

23
Q

What are the 2 ways of pain modulation?

A
  • Segmental modulation (gate theory)
  • Descending (PAG)
24
Q

Elaborate on the segmental modulation (gate theory)

A

Stimulation of large diameter afferents (for touch) excite inhibitory interneuron that in turn decreases transmission of pain signal in spinal cord.

(more information: the theory suggests that when touch sensations are actively transmitted, they compete with and inhibit the transmission of pain signals, effectively closing the gate and dampening the pain experience.)

25
Q

Which part of the brain is involved in pain modulation (descending way)?

A

Midbrain PAG (periaqueductal gray)

26
Q

Explain the route of pain modulation through the periaqueductal gray

A

Stress/ morphine/ expectation → midbrain (PAG) → excites neurons in medulla (nucleus raphe magnus) → excites neurons in spinal cord (interneuron) → **inhibit transfer of signal to ST neuron → blocks sensation of pain

27
Q

Elaborate more on how during pain modulation, the transfer of signal from the first order neuron and second order ST neuron is inhibited (talk about the neurotransmitter involved

A

E (endogenous opioid peptides) releases enkephalin at the synapse which inhibits the transfer of signal

28
Q

What are the types of movements generated? (3)

A
  1. Reflexes
  2. Rhythmic motor patterns (require voluntary initiation and termination)
  3. Voluntary
29
Q

Which part of the brain controls voluntary movement?

A

Cortex

30
Q

Which part of the brain controls reflexes and rhythmic motor patterns?

A

Brain stem

31
Q

What happens if the efferent neurons are damaged?

A
  • Paralysis (no motor behaviour)
32
Q

For reflexes and rhythmic motor patterns, how is the signal transmitted to the motor efferent neurons?

A

Neurons in brainstem synapse with lower motor neurons in the ventral horn of the spinal cord

33
Q

For voluntary movement, how is the signal transmitted to the motor efferent neurons?

A

Signal travels form neuron in cortex down the corticospinal pathway to synapse with lower motor neurons in the ventral horn of the spinal cord

34
Q

Function of the cerebellum related to signalling?

A

Indirectly affects movement by adjusting the output of the efferent via cortex and brainstem → makes the movements more ‘smooth’

35
Q

Since the cerebellum helps to make our movements more ‘smooth’, what happens if there is a lesion in the cerebellum? (3)

A
  • Lesion disrupt coordination of limb and eye movement
  • Impair balance
  • Decrease muscle tone
36
Q

What are the 2 key roles of the basal ganglia?

A
  • Initiation
  • Selection of motor program
37
Q

What happens if there is degeneration of dopamine neurons in the basal ganglia? (ie. what disease?)

A

Parkinson’s disease (marked by tremor, rigidity and bradykinesia)

37
Q

What are the effects of damage to the basal ganglia? (2)

A
  1. Disorder of movement
    - Tremor at rest
    - Rapid flicking movements or chorea
    - Violent flailing movement or ballism
    - Slow writhing/ twisting
    movements (athetosis/dystonia)
    - Bradykinesia
  2. Disorder of posture
    - Rigidity

(parkinson’s disease marked by tremor, rigidity and bradykinesia)