Sensory systems Flashcards
Name the 5 different types of sensory receptors there are
mechanoreceptors chemoreceptors thermoreceptors nociceptors proprioceptors
Which types of receptor have free nerve endings?
Nociceptors (pain receptors - can’t call them this though)
What is the area called that a sensory receptor responds to?
receptive field
What does Meissner’s corpuscle detect?
Light touch
What does Merkle’s corpuscle detect?
touch
Pacinian corpuscle detects what?
deep pressure
Ruffini corpuscle detects what?
warmth
What is the potential called that sensory receptors produce?
receptor (generator) potential
this is local, graded, decremental - depends on the strength of the stimulus
What is a local, graded potential?
it doesn’t travel very far but travels enough to the trigger zone - where APs begin to fire
The frequency of APs is proportional to ____?
The stimulus intensity
More APs = bigger potential = more neurotransmitters are released
What determines acuity? (2) (acuity = how accurately a stimulus can be located on body)
Density of innervation and size of receptive fields
How are action potentials transmitted to the CNS?
by axons
What are the 3 types of primary afferent fibres?
Aβ
Aδ
C
Describe C fibres
unmyelinated fibres (0.5-2m/s) warmth, “slow” pain
Describe Aβ fibres and what modality they carry?
Large myelinated (30-70m/s) Touch, pressure, vibration
Describe Aδ fibres and what modality they carry?
Small myelinated (5-30m/s)
Touch and pressure
‘Fast pain’
Cold - thermoreceptors
Which 2 types of primary afferent fibres mediate proprioception?
Aβ - secondary receptors of muscle spindles
Aα - golgi tendon organ and proprioception
Where do all primary afferent fibres enter the spinal cord
dorsal horn
Describe the route of mechanoreceptive (Aα & Aβ) fibres (touch, pressure, proprioception, vibration)
Comes into dorsal horn of spinal cord, same axon goes up to brain via dorsal column (same side of spinal cord) synapse in cuneate & gracile nuclei (dorsal column nuclei that lie at junction between spinal cord and medulla)
The 2nd order fibres cross over midline (decussate) at level of medulla and now you call it the medial leminiscal tract. It will now project to reticular formation, thalamus and cortex
Describe the route of thermoreceptive & nociceptive (Aδ & C) fibres
Rest of info (thermo and nociceptive) comes into dorsal horn and synapses almost immediately on the same level it comes in at.
Cross over midline almost immediately and travels up contralateral side (spinothalamic or anterolateral tract)
Synapses in the somatosensory cortex
What can damage to dorsal columns cause? (3)
loss of touch
loss of vibration
loss of proprioception
below lesion on ipsilateral side
What can damage to anterolateral quadrant cause? (3)
Loss of nociceptive and temperature sensation below lesion on contralateral side
Where is the ultimate termination of sensory afferent fibres?
in the somatosensory cortex (S1) of the postcentral gyrus
primary somatosensory cortex is the main sensory receptive area for the sense of touch
What are the endings of the fibres grouped according to?
the location of their receptors
and the extent of representation is related to the density of receptors in each location - this creates the sensory homunculus
What does the term rapidly adapting receptor mean?
Receptor gets used to stimulus. Ie wearing a hat, you feel it at first then forget you’re wearing it until you take it off really.
When you stop the stimulus you get a little burst again.
Different neurones show different levels of adaptation
What is convergence?
2 or more primary afferent receptors synapses on a common cell body or group of cells
This reduces acuity as can cover a large area and not be able to specify area of pain etc
This also underlies reason for referred pain
What is lateral inhibition?
activation of one sensory input causes synaptic inhibition of its neighbours - by dampening the action of some sensory input and enhancing the action of others, lateral inhibition helps to sharpen our sense perception
gives better definition of boundaries
Example - a pin goes into your skin. The primary neuron is proportional to the stimulus strength (pin). The nearby/neighbouring neurons are inhibited so that the perception of the primary neuron is enhanced
How does the body prevent every piece of information from making it into the brain?
Descending inhibition prevents all the info coming in - this is when you can sense something but you aren’t aware of it
What is the difference between fast and slow pain?
fast (initial) short, stabbing pain that is highly localised but then get a delayed throbbing pain (harder to pinpoint where this is)
Why can’t you call nociceptors pain receptors?
Becomes pain in the brain
‘Damaging stimuli’ until it reaches there
How is the signal transduced to begin with in nociceptors? Mention ASIC, TRPV1 and G proteins
Need nociceptors nerve endings
Acid sensing ion channel – detects low pH – when that happens it opens channel - depolarises cell - activates APs
TRPV1 – activated by heat of skin and capsaicin (active ingredient in chili peppers)
G protein coupled receptors – respond to local chemical mediators released by damaged tissue (eg bradykinin, histamine, prostaglandins) – these activate G proteins that act on different channels – depolarise cell – start firing AP’s
Nociceptive fibres travel up which tract to the brain?
anterolateral spinothalamic tract
What is the gate control theory of pain?
If you can inhibit the gate (nociceptive neuron synapsing in dorsal horn) you can stop nociceptive information from getting into the spinal cord and up to the brain
This is how anesthesia works to reduce pain
What are the 2 ways in which nociceptive fibres can be inhibited?
Descending controls
Inhibitory interneuron releasing opioid peptide-
Describe the inhibitory interneuron releasing opioid peptide method of inhibition
Controls the gate by segmental controls – info coming in from same body segment but coming from innocuous (non-harmful) mechanoreceptive fibres (so if skin A beta fibres).
Info from these fibres modulate activity at gate. They activate inhibitory interneurons which release opioid peptide - inhibits transmitter release from Adelta and C fibres - therefore closing the gate
Describe the descending control inhibition method
Descending controls – these come from Peri-aqueductal grey matter (PAG).
Neurons from here activate neurons in Nucleus raphe magnus (NRM).
These travel all the way down the spinal cord and release transmitter that activates inhibitory interneurons and therefore closes gate.
These usually occur during horrific injuries like battle field injuries etc because they are heavily activating endogenous descending system
How do non-steroidal anti-inflammatory drugs (NSAIDs) act as anasthesia?
When a tissue is damaged it first forms phospholipids then arachidonic acid.
NSAIDs inhibit cyclo-oxygenase so stops it from converting arachidonic acid to prostaglandins
prostaglandins act on G protein coupled receptors which in turn make nociceptors more sensitive to bradykinin (linked to production of pain and hyperalgesia - increased pain sensitivity)
so NSAIDs work well against pain associated with inflammation
How do local anaesthetics work?
block Na+ action potential and therefore all axonal transmission
How do Trans cutaneous electric nerve stimulation (TENS) work as analgesia?
Electrical patch put onto skin - electrical wave activating same segmental control – activates A beta fibres but not the others so these ‘close the gate’
How do Opiates (eg morphine) work?
reduce sensitivity of nociceptors
block transmitter release in dorsal horn (hence epidural administration - injection in the back)
activates descending inhibitory pathways
