Sensory Systems Flashcards

1
Q

Sensory receptors may be simple free nerve endings or complex structures, give some examples of both?

A

Nociceptors & cold receptors are free nerve endings

Pacinian Corpuscles (vibration) and Meissner’s Corpuscles (Touch) are more complex structures

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2
Q

How is tactile acuity determined?

A

Larger number of smaller receptive fields (i.e. nerve ending density) allows greater acuity as you can isolate a signal to a smaller area.

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3
Q

What is a receptive field?

A

The area of which a receptor will detect a stimulus

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4
Q

What does an “adequate Stimulus” mean?

A

The specific mode of stimulus the receptor responds to

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5
Q

Signal transduction occurs differently for mechanoreceptors and nociceptors, how do mechanoreceptors transduce a signal?

A

The receptor transduces the adequate stimulus into a depolarisation called the receptor or generator potential which then evokes an AP

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6
Q

How is the intensity of a stimulus encoded by mechanoreceptors?

A

In the size of the receptor or generator potential

Then in the frequency of the APs

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7
Q

What are the various types of sensory primary afferent fibres?

A

Aalpha & Abeta:

  • Large myelinated fibres
  • Touch, pressure, vibration (all the innocuous mechanoreceptive modalities)
  • Also carry proprioception from muscle spindles & GTOs

Adelta:

  • Small myelinated fibres
  • Carry cold and “fast” pain

C:

  • Small Unmyelinated fibres (slowest)
  • Carries Warmth & “slow” pain
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8
Q

Describe the pathway of mechanoreceptive fibres (Aalpha & Abeta)

A

They all enter through the dorsal root via the DRG

  • 1st order neuron projects striaght up through the ipsilateral dorsal column
  • 2nd order neuron decussates in the brainstem
  • Projects up to reticular formation –> Thalamus –> Cortex
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9
Q

Describe the pathway of thermoreceptive & nociceptive fibres (Adelta & C)

A

Enters through dorsal root via DRG

  • 1st order neuron synapses in the dorsal horn
  • 2nd order decussates in spinal cord
  • Then projects up the contralateral spinothalamic (anterolateral) tract to the reticular formation –> Thalamus –> Cortex
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10
Q

What happens if you damage the dorsal column?

A

You lose ipsilateral mechanoreception (Touch, vibration, proprioception)

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11
Q

What happens if you damage the spinothalamic tract?

A

You lose contralateral thermoreception & nociception

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12
Q

Define adaptation?

A

Receptors can be divided into slow and fast adapting.

Fast adapting receptors such as pressure receptors adapt to a sustained stimulus, only telling you when the stimulus changes

Slow adapting receptors such as muscle spindles maintain the signal until the stimulus is removed

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13
Q

Define Convergance?

A

Multiple receptive fields synapsing onto one neuron, this saves on neurons but reduces acuity

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14
Q

What is the difference between a specific and non-specific pathway per convergence?

A

A specific pathway has receptors of the same modality converging on one neuron

A non-specific pathway has receptors of different modalities converging on one neuron, usually pain and touch. These can’t be distinguished

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15
Q

Explain the concept of lateral inhibition?

A

The neuron closest to the stimulus inhibits the synapses of the neighbouring neurons.

This cleans up sensory info giving you a better definition of the stimulus boundary

(So the central neuron has a higher than tonic frequency of APs and the neighbouring ones have a lower than tonic level)

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16
Q

What are the different types of pain?

A

Fast (initial) pain - Sharp & Stabbing - Uses Adelta fibres

Slow (Delayed) pain - Diffuse & Throbbing - Uses C fibres

17
Q

What is a possible explanation for referred pain?

A

Convergence of neurons from the viscera and other tissues e.g. the skin

18
Q

How are nociceptors activated?

A
  • Low pH activates an ASIC receptor
  • Heat activates a TRPV1 receptor
  • Also by local chemical mediators such as prostaglandins and bradykinin (B2 Braykinin receptor) released on tissue injury
19
Q

How do prostoglandins affect pain?

A

They stimulate nociceptors themselves but more importantly sensitize nociceptors to bradykinin

20
Q

What is the Gate control theory?

A

The ability to “gate” pain signals, preventing them from crossing the 1st-2nd order synapse

21
Q

How is pain gated by segmental control?

A

Mechanoreceptive fibres (Aalpha/beta) activity in the same region

  • -> Activates an inhibitory internueron
  • -> Releases opioid peptides (endorphins)
  • -> Inhibit the nociceptive synapse

(Probably the basis for TENS & rubbing it better)

22
Q

How is pain gated by Descending Control?

A

Peri-aqueductal grey (PAG) matter in cortex gives off a descending fibre

  • > Synapses in Nucleus Raphe Magnus (NRM)
  • > Travels down to the spinal level of nociceptive fibres
  • > Activates the inhibitory interneuron
  • > Releases opioid peptides (endorphins) that inhibit the nociceptive synapse`
23
Q

What does TENS stand for and what does it do?

A

Transcutaneous Electrical Nerve Stimulation

Analgesic – It activates innocuous mechanoreceptors and so inhibits the nociceptive synapse. (Segmental Gate control)

24
Q

How do NSAIDs work as analgesics?

A

Remember prostaglandins sensitize nociceptors to bradykinin

So NSAIDs prevent the formation of prostaglandins by inhibiting the cyclo-oxygenase enzyme (Arachidonic acid –> Prostaglandins)

Therefore they work best with inflammation associated pain

25
Q

How do local anaesthetics work as analgesics?

A

The block Na+ channels preventing AP transmission

26
Q

How do opiates work as analgesics?

A
  • Directly reduce nociceptor sensitivity
  • Block neurotransmitter release at the 1st-2nd order synapse in the dorsal horn (Pain Gate Control)
  • Activate descending pathways in the peri-acqueductal Grey (PAG) matter (Descending Gate control) to inhibit the 1st-2nd order synapse