Pain and analgesics first half of 2 2.0

Question 1

Where does peripheral sensitisaiton occur?

Answer 1

The primary nociceptive neurons (in the skin etc)

Question 2

Where in the spinal cord is the first synapse?

Answer 2

Most dorsal aspect (lamina 1 or lamina 2)

Question 3

Which NTs are released from the nociceptive neurons in the spinal cord?

Answer 3

Mostly glutamate, also some substance P and a little amount of CGRP

Question 4

What is CGRP?

Answer 4

Calcitonin gene related peptide

Question 5

Which receptors does glutamate activate?

Answer 5

AMPA and NMDA

Question 6

Which receptor does substance P activate?

Answer 6

NK-1 receptor

Question 7

What type of receptor is NK-1?

Answer 7

GPCR

Question 8

Why is a fast slow time course observed in glutamate transmission?

Answer 8

AMPA are fast and NMDA are slow

Question 9

Which second messenger does NK-1 release?

Answer 9

Gq

Question 10

What does Gq second messenger do regarding PIP2?

Answer 10

Breaks down PIP2 into Diacylglycerol (DAG) and inisitol triphosphate (IP3)

Question 11

What does inositol triphosphate do?

Answer 11

Activates calcium stores which leads to an increase in intracellular Ca2+ concentrations

Question 12

What does DAG do?

Answer 12

Activates protein kinase C

Question 13

What does Gq second messenger do regarding ion channels?

Answer 13

Activate Na+, Ca2+ entry ion channels and inhibit K+ exit ion channels–> more depolarisation

Question 14

What happens if there is a burst of activity from the presynaptic neuron in the spinal synapse part of the pain pathway?

Answer 14

The synapse increases in strength over time (i.e. after 11th AP the postsynaptic response is bigger than previous)

Question 15

What is synaptic plasticity?

Answer 15

The strength of a synapse changes over time

Question 16

Why does the spinal synapse become more sensitive over time?

Answer 16

NMDA receptors and NK-1 receptors

Question 17

How is it known that NMDA receptors affect synaptic plasticity?

Answer 17

Synaptic plasticity does not occur with AP5 (NMDA agonist) present

Question 18

How is it known that NK-1 receptors affect synaptic plasticity?

Answer 18

Synaptic plasticity does not occur with SP antagonist (NK-1 antagonist) present

Question 19

Where in the nociceptive pathway do inhibitory interneurons attach?

Answer 19

The dorsal horn projection neuron

Question 20

How are inhibitory interneurons activated in the pain pathway?

Answer 20

Offshoots of mechanoreceptors that are in the spinal cord can activate inhibitory interneurons

Question 21

What type of neurons activate inhibitory interneurons in the pain pathway?

Answer 21

Glutamatergic

Question 22

What is nursing the injury?

Answer 22

Touching an injured part of the body

Question 23

Why do we “nurse an injury”?

Answer 23

Touching it activates mechanoreceptors which can cause inhibitory interneurons to be activated, thus inhibiting the pain

Question 24

What is TENS?

Answer 24

Transcutaneous electrical nerve stimulation–>An electrical pack that stimulates touch receptors on the skin

Question 25

Why does TENS work?

Answer 25

Activates mechanoreceptors which can cause inhibition of pain

Question 26

Which two types of pathway can inhibit nociception?

Answer 26

Descending inhibitory pathway and ascending inhibitory pathway

Question 27

What is the ascending inhibitory pathway?

Answer 27

Mechanoreceptors causing inhibition

Question 28

What is the descending inhibitory pathway?

Answer 28

Parts of the brainstem, when stimulated, can inhibit pain

Question 29

Which parts of the brain can cause descending inhibitory input?

Answer 29

Periaqueductal grey and raphe nuclei

Question 30

Where does the periaqueductal grey project to in inhibitory input?

Answer 30

The raphe

Question 31

Where does the raphe project to in inhibitory input?

Answer 31

The first synapse in the spinal cord

Question 32

Where in the brain does the periaqueductal grey receive inputs from?

Answer 32

Hypothalamus, amygdala, cortex