Section 0.1.2 Flashcards
What are the 3 distinct groups of nociceptors, based on modality?
- Mechanical nociceptors: respond to physical damage such as cutting or crushing.
- Thermal nociceptors: respond to temperature, especially heat.
- Chemical nociceptors: respond to noxious chemicals which are both external and internal to the
body.
What are nociceptors?
The specialized nerve endings of afferent nerve fibres, called pain fibres
Describe the difference between the fast and slow pain fibres.
Fast pain fibres are A-delta (δ) fibres. They are responsible for responding to temperature, and both chemical and mechanical stimuli. The perceived sensation associated with activation of these fibres includes acute, sharp, or stabbing pain
Slow pain fibres are C-fibres. They are unmyelinated, and similar to fast pain fibres, they are responsible for responding to both chemical and mechanical stimuli as well as temperature. However, unlike A-delta fibres, polymodal receptors* can
be activated. The perceived sensation associated with activation of these fibres includes burning, aching or throbbing.
what do you think contributes to rapid speed of conduction of fast pain fibres?
Myelination and diameter! These fibres have a larger diameter than slow pain fibres. They are also myelinated, which increases the conduction speed of these fibres to approximately 6-30 m/s as opposed to 1-2 m/s of slow pain fibres
Describe what bradykinin does in the slow pain pathway
Commonly associated with the slow pain pathway is bradykinin, a chemical that is activated by
enzymes that are released from damaged cells. Once activated, bradykinin can directly stimulate pain receptors. Because nociceptors do not adapt until the bradykinin is removed, they will continue to stimulate the nociceptor, which could explain long lasting, persistent pain.
What are polymodal receptors?
Receptors that can respond to more than one stimuli
How does the brain process pain?
When an action potential reaches the end of an afferent pain fibre axon, it triggers the release of
neurotransmitters. The most well studied are substance P and glutamate.
Substance P coexists with glutamate to activate the ascending pathways and transmit the pain signals to higher levels for further processing.
Understand which brain regions are influenced by substance P and glutamate
Hypothalamus/Limbic system:
Receives input from the thalamus and reticular formation, and allows for behavioural and emotional responses to the pain stimuli.
Cortex:
Cortical somatosensory processing localizes the pain to a discrete body region.
Thalamus:
Processing here allows for the perception of pain.
Reticular Formation:
Increases the level of alertness and awareness of a painful stimulus.
Describe glutamate in pain reception.
Glutamate is an amino acid that also functions as a neurotransmitter. It is released by nociceptive afferent nerve fibres to activate the postsynaptic glutamate receptors on neurons in the dorsal horn of
the spinal cord.
Glutamate has two actions, depending on which type of receptor on the dorsal horn neurons are activated; either AMPA or NMDA receptors.
Describe the different glutamate receptors in the spinal cord dorsal horn.
AMPA Receptors:
The activation of AMPA receptors leads to permeability changes that can generate action potentials in
the dorsal horn neuron and send the signal to higher brain centres. As sodium enters the AMPA
channel, depolarization occurs. Only when a certain level of depolarization is reached will the Mg2+ ion in the NMDA channel be dislodged, and the NMDA channel will be activated.
NMDA Receptors:
Once NMDA receptors are activated, they allow calcium to enter the neuron. This leads to the activation of a second messenger pathway that results in the neuron being more excitable than normal. This explains why injured areas are more sensitive to stimuli that would not normally cause pain. For example, the pain felt when clothing rubs against an area of skin with sunburn
How is a pain signal stopped?
After an initial painful stimulus there is a decrease in the perception of pain but it is
not caused by receptor adaptation. Instead, it is the result of the CNS’s built-in pain suppressing system.
One of the consequences of the central processing of pain is the activation of descending pathways
that in turn activate inhibitory neurons in the dorsal horn. The axons of these interneurons terminate on the afferent fibre nerve terminals. They release endogenous opiates* that act on opiate receptors and result in a suppression of neurotransmitters being released from the afferent pain fibres. Similarly, exogenous opioids* can activate the opioid receptors to decrease the perception of pain
Can afferent pain fibres adapt?
No
What are endogenous opiates?
Substances that are produced by the body and have painkilling effects (i.e. endorphins, enkephalins, dynorphins)
What are Exogenous opiates?
Substances that are not produced by the body and have painkilling effects (i.e.
morphine).
Describe in a few sentences what
would occur if you stepped on a particularly sharp piece of Lego. What kind of receptor would
be activated? How would you become consciously aware of this pain?
How might this perception of pain be different if you were taking an exogenous opioid such as
morphine?
Pain would first be perceived at the source and travel up A-delta fibres. As the action potential reaches the end of each A-Delta fibre, glutamate would be released. The signal would travel to the dorsal horn where AMPA receptors would be activated. The signal would travel to the reticular formation to increase alertness, to the thalamus to consciously perceive the pain, and to the cortex to localize the pain on your foot. The hypothalamus would allow for a behavioural and emotional response.
Morphine, an exogenous opioid, would activate the opioid receptors which would result in a suppression of neurotransmitter being released from the A-delta fibres. Morphine, therefore, would decrease the perception of pain.
