Sensory system and pain Flashcards
mechanoreceptors
tough, auction vesitbular
touch
pacinain corpuslce
audition
hair cell
vesitbular
hair cell
photoreceptors
vision
vision
rods and cones
chemoreceptors
olfaction, taste, arterial pO2, pH of CSF
thermoreceptors
temp
olfaction
olfactory receptors
taste
taste budsy
temperature
warm/ cold receptors
nocicpetors
extreme pain and temp
extreme pain and temps
- thermal nociceptors
- polmodal nocicpetors
when are arterial Po2 found
carotid and aortic bodies
where are vestibular hair cells found
macula, semicircular canal
where are audition hair cells found
organ of Corti
where are pH of CSH receptors found
ventrolateral medulla
where are nociceptor and thermal receptors found
the skin
neurophathic
’ pain which originates from the pathology of the NS)pain caused by damage or disease affecting the somatosensensory NS
somatosensor NS
part of the sensory system concerned with conscious perception of touch, pressure, pain, temp, position, movement and vibration
- arising from muscles, joints skin and fascia
sensitisation
typically results form a cellular receptors becoming more likely to respond to a stimulus e.g. repetition of a painful stimuli makes one more responsive to a loud noise
an enhancement in response to a stimuli
sensitisation
mechanism of peripheral sensistiasation
sensory neurone expression of alpha-adrenoreceptors causes over expression of voltage gated Na+ channels
- afferent neurones start expressing adrenooreceptors
adrenoreceptors are not usually expressed
in afferent nerves-but in chronic pain states, they become over epxressed
in chronic pain states, any kind of stress that stimulates sympathetic nervous system can lead to
more pain- thats how perception of pain can be changed
where nerves no longer listen to stimulus of nociepection-
sensitisation
and increase in voltage gates sodium channels
more sensitive- smaller stimuli will evoke a large response
neuropathic pain can also occur in
afferent synapses in reflect arc
- peripheral nerve at the spinal cord goes up into the brain
- pain then goes to the thalamus and cortex
cortex
where emotion and reasoning happens- therefore neuropathic pain can change emotions
fear and pain are interlinked
because peripheral nerves relaying a painful stimuli goes up into the brain and into the cortex where emotion and reasoning occur
Pain is all in
the CNS
inflammatory mediators are released
at sites of injury
inflammatory mediators
released in response to injury from leaky blood vessels and damaged tissues: ATP, histamine, prostaglandin, substance P, protons, 5-HT, bradykinin
pain pathway
1) nociceptive stimuli
2) impulse foes to the CBS via afferent neurone to the spine
3) synapse in dorsal horne of the spin- releases main eciatory NT- glutamate and ATP
4) binds to receptors (AMDA and NMDA)
5) impulse carried up to the hypothalamus which simulates the cortex- where we perceive pain
AMPA
fast
NMDA
slow due to prolonged membrane depolarisation being needed to remove magnesium block
- long term processes
- LTP (chronic pain states)
summary of sensitisation
Adrenoceptors are not usually expressed in afferent nerves- but in chronic pain states, they can become over expressed
Any kind of stress that stimulates sympathetic nervous system can lead to even more pain- that’s how perception of pain can be changed e.g. phantom limb injury
Peripheral sensitization- where nerves no longer listen to stimulus of nociception from the stump, also responding to the sympathetic nervous system e.g. levels of stress and fear
Also increase in expression of voltage gated sodium channels- more sensitive- smaller stimuli will evoke a large response
phantom limb
the perception of pain in absent body parts
-experienced by most amputee patients
perisperhal mechanisms involved in phantom limb
these pains are attributed to abnormal growth of injured nerve fares coming neuromas, which fire abnormal APs at the stump
spinal mechanism involved in phantom limb
peripheral nerve injury can lead to the degeneration of C fibres in the dorsal horn of the spinal cord, therefore A fibres may branch into some limning
- A fibre input could be reported as noxious
- expressing substance P
simple explanation for phantom limb
phantom pains can be attributed to abnormal goeth of injured nerve fibres at the stump site
capsaicin
the active compound in chillies acts on vanillin receptors and causes released of Substance P from the nociceptors, which is what causes the pain
-TRPV1
vanilliod receptors
trance noxious that stimuli
two types of pain conductance
fast response (Aδ fibres) and slow response (C fibres)
fast response Aδ fibres
- large
- myelinated
- up to 10m.sec
- sharpe stabbing pain
slow response C fibres
- small
- unmyelinated
- up o 1.2 m/sec
- acing budning
receptors for fast response Aδ fibres
Thermal or mechanical: Mechanically gated TRPV1- temp gated >42 degrees, pH<5.5 (gated by protons) Also vanilloids- e..g capsaicin TRPM8- cold and menthol
receptors for slow response C fibres
Polymodal High intensity Mechanical Chemical Hot/cold
inflammatory mediators can cause
hyperalgesia
hyperlgesia
is an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves.
inflammatory mediators and hyperalgesia
directly excited nociceptors making them more sensitive to other agents
inflammatory mediators
increase rate of opening of TRP channels
thermoreceptors are made up of
fast response Aδ fibres and slow response C fibres
each TRp has
a unique thrshold
TRPV2
extreme hot
TRPA1
extreme cold
thermal nociceptors sue
C fibres and response to extreme col/hot
withdrawal reflex
1) stimulus (pain) detected by receptors in the skin
2) impulse sent via sensory neurone to synapse with the relay neurone in the dorsal horn
3) relay neurone synapses with motor neurone which sends an impulse to the effectors
4) muscle moves limb away from noxious stimuli
recycling of ACH at the NMJ
ACH i converted by to choline and acetate by acetylcholinesterase
-co transported with sodium back to the pre-synaptic bouton
Each is made by
acetylcholinesterase
ionotropic
transmembran
- binding site and channel combines
- channels opena nd close letting ions in and out
- post synaptic in general
- rapid response
Metabotropic
- no channels
- linked to G proteins
- wen a ligand binds G proteins ar euactivated
- once activated 2nd messengers tole beings
- slow
- pre and post syanptic
long term potentiation definiton
-an increasee in efficacy of a synapse with repetitive stimulation
LTP - a repeated depolarisation of the post synaptic men results in
alterations in the NMDA glutamate receptor- allowing ore calcium to enter
LTP involves changes in
both the pre and post synaptic membrane
- a given response to any stimuli will increase
- can also cause new neurones to form from existing ones
calcium and LTp
-causes AMPA receptors in post synaptic vesicles to come to the surface- therefore depolarisation of pst synaptic neurone is increased for any given stimuli
memory
the ability to recall knowledge and skills learned in the past
- how info is encoded, stored and retrieved
two categories of meory
declarative and procedural
declarative
- the recall of new facts
- recall of events
- verbal reasoning
- personal experience
- short and long term (Hippocampus)
procedural
- applies memory to motor skills
- learning new motor skills
- once learned, rarely forgotten
- cerebellum has key role
