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What is nociception?

Nociception is information transmitted about noxious stimuli (current or predicted tissue damage)


What is pain?

Pain is the brain’s perception of an adverse or unpleasant sensation
It is an unpleasant sensory and emotional experience associated with actual or potential tissue damage


What are nociceptors?

Are free nerve endings without specialised receptor cells


How do nociceptors receive stimuli?

Stimuli are received via noxious stimuli receptors that are built into C fibre endings at a molecular level. These noxious stimuli receptors are g-protien coupled receptors rather than specialised receptors e.g. merkle receptors or ruffini's corpuscles.


Do nociceptors have a specialised receptor?

No, they have a g protein receptor


Where do nociceptor free nerve endings terminate?

In the tissues


Where do nociceptor free nerve endings extend into?

The most superficial layers of the dermis


Where so nociceptor cell bodies sit?

In the dorsal root ganglion


What are the 2 fibre types of nociceptors?

A fibres or C fibres


What % of DRG cells are nociceptive?



What are the 4 different ways that we can classify nociceptor cells?

The type of noxious stimuli they respond preferentially to

Their degree of sensitivity and therefore the intensity of the stimuli they detect

Their fibre type

Their inflammatory capability


If we are to classify nociceptors by stimulus, what are the 3 classifications nociceptors can fall under? Briefly describe each of them.

Mechanical nociceptors: activated by strong mechanical forces on tissues and have a fairly high threshold, requiring a high input to fire. They are particularly sensitive to sharp stimuli

Thermal nociceptors: Either hot or cold, and can react to extremes in temperature.

Polymodal nociceptors: found through the skin and the deeper tissues. They can be activated by mechanical, thermal and chemical stimuli (esp acids).


If we are to classify nociceptors by degree of sensitivity, what can we say about them

Most nociceptors have a high threshold, meaning they require a must higher intensity of stimulus to evoke a neuronal response.

Some nociceptors have a very high threshold to mechanical stimuli and do not transmit mechanical information unless inflamed or sensitised, but do tend to be highly sensitive to chemical stimuli e.g. inflammatory mediators.


What % of DRG fibres are A beta?



What kind of information do A beta fibres transmit?

Mostly tactile and proprioceptive


What % of DRG fibres are A delta fibres? What % of these fibres transmit nociceptive information? What information does the remaining A delta fibres transmit?


50-70% of these fibres transmit nociceptive information. The rest transmit tactile information from hair cells


20% of DRG fibres are A beta, and 20% are A delta. What type of fibres is the remaining 60% and what kind of information do they transmit?

C fibres.

They transmit mostly nociceptive information.


Where do A fibres relay sensory information to in the cortex?

So S1 where they have localised or discriminant perception.


What fibres relay fast and slow pain to S2?

A and C fibres


What speed of information do C fibres transmit and where do they get relayed to? Why do they get relayed here?

C fibres relay poorly localised, indiscriminant pain to the cingulate cortex, a highly emotional area of the cortex which is thought to add emotional colouring and prior experience to our pain experience and drive motivation to act on pain and decide on behavioural responses.


What % of DRG cells are peptidergic? What does this mean?


This means that they produce neuropeptides (substance P and CGRP) and release them at their peripheral terminals to produce neurogenic inflammation.


What does peptidergic mean?

If a cell is peptidergic it means that they produce neuropeptides (substance P and CGRP) and release them at their peripheral terminals to produce neurogenic inflammation.


How large are nociceptor fields?

2-10mm in diameter


What does the overlap of nociceptor fields protect us from?

Hyposensitivity, but not hypersensitivity


Do primary afferents have a fixed receptive field?



General info on primary and secondary afferents and their receptive fields:

Much overlap which protects from hyposensitivity but not hypersensitivity
Primary afferents have a fixed receptive field
Primary afferents converge on the secondaries making their receptive field much larger

By the time we reach the thalamic neurons we start to see whole body receptive fields being generated by this convergence

This is also true of the somatosensory cortex

At a cortical level we’re then able to adjust the degree of sensitivity and discrimination by switching between neurons with differing receptive fields

You might consider that we have fast, generalised screening operations that are highly sensitised but poorly localised to allow us to detect changes to our environment or we have slower, more highly processed operational systems that allow for fine, discriminant examination of our environment

The switch between these is more like a dimmer switch than an on/off button and thought to be mediated by inhibitory interneurons


What does ALS stand for? Describe the ALS (terminations, decussation level, what info does it transmit?

Anterolateral system

Transmits crude touch, pain and temp

It decussates in the cord at the level it enters the cord at

It has brain stem terminations

It also has cortical and subcortical terminations


General pain information

Put simply the nervous system has mechanisms for amplification and attenuation of nociceptive transmissions

This allows for a heightened response to aid tissue repair and remove ourselves from threat; or a reduction in perceived pain while tissues heal from minor injury that poses minimal threat

Nociception is relayed via peripheral and central pathways and can be modulated at several points including at tissue, cord and cortical levels


List some of the inflammatory chemicals that chemoreceptors on nociceptors respond to

Histamine, prostaglandins and serotonin (mast cells)
ATP, glutamate and adenosine (tissue/ platelets)
Bradykinins, interleukins and nerve growth factors (various immune cells)


Describe the basis of nociceptor sensitisation

A positive feedback loop involving inflammatory mediators released upon tissue damage. This sensitises or activates local nociceptors (A 2nd messenger (G protein cascade sensitises their associated ion channel meaning they open in response to a lesser stimuli) . Activation causes substance P and CGRP to be released. This increases vascular permeability in order to accelerate healing.