Lectere 3

Question 1

How do we measure single hehe responses to temperate 7

Answer 1

Electrode in medial never place had indiffrenttemp.

Question 2

Why does mental feel cool on the skin, whereas chillies feel not?

Answer 2

Activates trpm8 → menthol
Which senses 8-28
Activates trpv1 → caption
Senalse able 43°C

Question 3

When is 9-HODE generated? What is it metabolised from?

Answer 3

When the skin is hated abve 43°C, linolo il acid

Question 4

Does 9-HODE and capcacin bind at the cytoplasmicor extracellular region of TRPV1?

Answer 4

The both bind to the intracellular region

Question 5

What does PLA2 do to membrane lipids?

Answer 5

Hydrosies phospholipids to linoleum acicd

Question 6

How does heat lead to pain in the nerve endings of C fibres ?

Answer 6

Heat damages alls relating CA2+ this causes an increase in cPLA2 activity hydrosing phospholipids into linoleic acid, which then is converted into (
9-HODE, which opens TRPV1 causing deplasration of the neurone opting VGNC and causing an action-potential.

Question 7

What fibers convey first pain ?

Answer 7

A delta fibres

Question 8

Why does first pain have a high intensity and a direct small area of pain?

Answer 8

First order pain is carried by a Delta fibers which have a small receptive field and so produce a sharp short pain.

Question 9

Why does second pain have a wide dull ache?

Answer 9

The pain is traduced by C fibres which has a large receptive field so produces a large area of dull pain

Question 10

What do we mean when we say that nociceptors are polymodal?

Answer 10

It refers to the fact that they have a wide range of receptors, mechanical chemi thermo .

Question 11

How is prostaglandin (PGE2) synthesised?

Answer 11

In a similar manner to 9-HODE tissue damage relates Caw2+ activating cPLA2 which hydrolyses membrian phospholipids but this time into arachidonic acid, which is then metabolised into PGG2 by cycoloxgenases and finally into PGE2

Question 12

How does PGE2 cause hyperaglgesia?

Answer 12

binds to the GPCR EP4, which activates AC (Gs) and produces cAMP, this in turn opens HCN2 which depolises the cell, and hence lowers the the threshold potential of the cell allowing for AP at lower stimulus.

Question 13

How can we prove using a behavioural modle that HCN2 is important in sensitisation to inflammatory 2nd pain? What should we see

Answer 13

Inject irratant such as formalin into mouse paw for both WT and HCN2 KO and measured time spend in pain related behaviour, we should see the same same to early pain (no inflammation yet) then KO should be less sensitive to secondary pain.

Question 14

What sensations do the TRP channels help to transmit?

Answer 14

Temperature and pain

Question 15

What channel cause the sensitisation of C-fibers?

Answer 15

HCN channels

Question 16

What is the gate control theory of pain?

Answer 16

If C and A beta fibers are activated (same dermatologist are activated simultanusly the A beta fibre activation of the internueone will inhibit the projection (noiciative) of the spinothalmic tract.

Question 17

What would happen if there was no interneurone between the pro toon neurone and A a or A beta (touch neurones) to the sensation they transmit and why

Answer 17

Would be painful as there is a excitory synapse on the projection neurone from A beta neurone, and no inithibitory synapse from the intern our one, there is also an exciting synapse from the A beta neurone to the inhibitory neurone which causes the inhibiton of the projection neurone.