The Somatic Sensory System - Pain - Nociceptors and the transduction of painful stimuli

8 important questions on The Somatic Sensory System - Pain - Nociceptors and the transduction of painful stimuli

Where are nociceptors present? And where notably not?

Nociceptors are present in most body tissues, including skin, bone, muscle, most internal organs, blood vessels, and the heart.

They are notably absent in the brain itself, except for the meninges.

Where does the transduction of painful stimuli occur?

In the free nerve endings of unmyelinated C fibers and lightly myelinated A(sigma) fibers

Many nociceptors show selectivity in their responses to different stimuli. What kinds of nocireceptors are there?

Polymodal nociceptors -> respond to mechanical, thermal and chemical stimuli.
Mechanical ""
Thermal ""
Chemical "" -> show selective response to histamine and other chemicals
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Name three examples of released substances that cause ion channels on nociceptors to open:

- Proteases (enzymes that digest proteins, breaks down kininogen that bradykinin, bradykinin binds to receptor molecules that activate ionic conductances)

- ATP (binds to ATP-gated ion channel)

- K+ (elevation of K+ levels causes depolarization)

What is hyperalgesia? And what is the difference between Primary- and Secondary hyperalgesia?

Hyperalgesia can be a reduced threshold for pain, an increased intensity of painful stimuli, or even spontaneous pain.

Primary hyperalgesia occurs within the area of damaged tissue, but tissues surrounding the damaged area can get supersensitive as well, this is called secondary hyperalgesia.

What are prostaglandins and what kind of effect does aspirin have on them?

Prostaglandins are chemicals generated by the enzymatic breakdown of lipid membrane. They increase the sensitivity of nociceptors to other stimuli.

Aspirin is a useful drug for hyperalgesia because they inhibit the enzymes required for prostaglandin synthesis.

What is substance P and what is its function?

Substance P is a peptide synthesized by the nociceptors themselves.

Activitation of one branch of a nociceptor can lead to the secretion of substance P by the other branches of that axon in the neighbouring skin.  --> Secondary hyperalgesia.

Substance P causes vasodillation and the release of histamine by mast cells.

What kind of channels does Capsaicin open and what is the effect?
What is an paradoxal clinical application of capsaicin?

Capsaicin activates a particular ion channel, called TRPV1, which is also activated by >43 degrees C. TRPV1 is a member of the TRP (transient receptor potential) channel family.

Capsaicin mimics the effect of endogenous chemicals released by tissue damage. These chemicals (and capsaicin) cause the TRPV1 channel to open at lower temperatures.

Capsaicin applied in large quantities can cause analgesia, the absence of pain. The capsaicin desensitizes pain fibers and depletes the peptide substance P from their nerve terminals

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