Sensory systems Flashcards

1
Q

Name the 5 different types of sensory receptors there are

A
mechanoreceptors
chemoreceptors
thermoreceptors
nociceptors
proprioceptors
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2
Q

Which types of receptor have free nerve endings?

A

Nociceptors (pain receptors - can’t call them this though)

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3
Q

What is the area called that a sensory receptor responds to?

A

receptive field

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4
Q

What does Meissner’s corpuscle detect?

A

Light touch

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5
Q

What does Merkle’s corpuscle detect?

A

touch

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6
Q

Pacinian corpuscle detects what?

A

deep pressure

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7
Q

Ruffini corpuscle detects what?

A

warmth

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8
Q

What is the potential called that sensory receptors produce?

A

receptor (generator) potential

this is local, graded, decremental - depends on the strength of the stimulus

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9
Q

What is a local, graded potential?

A

it doesn’t travel very far but travels enough to the trigger zone - where APs begin to fire

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10
Q

The frequency of APs is proportional to ____?

A

The stimulus intensity

More APs = bigger potential = more neurotransmitters are released

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11
Q

What determines acuity? (2) (acuity = how accurately a stimulus can be located on body)

A

Density of innervation and size of receptive fields

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12
Q

How are action potentials transmitted to the CNS?

A

by axons

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13
Q

What are the 3 types of primary afferent fibres?

A



C

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14
Q

Describe C fibres

A
unmyelinated fibres (0.5-2m/s) 
warmth, “slow” pain
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15
Q

Describe Aβ fibres and what modality they carry?

A
Large myelinated (30-70m/s) 
Touch, pressure, vibration
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16
Q

Describe Aδ fibres and what modality they carry?

A

Small myelinated (5-30m/s)

Touch and pressure
‘Fast pain’
Cold - thermoreceptors

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17
Q

Which 2 types of primary afferent fibres mediate proprioception?

A

Aβ - secondary receptors of muscle spindles

Aα - golgi tendon organ and proprioception

18
Q

Where do all primary afferent fibres enter the spinal cord

A

dorsal horn

19
Q

Describe the route of mechanoreceptive (Aα & Aβ) fibres (touch, pressure, proprioception, vibration)

A

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

20
Q

Describe the route of thermoreceptive & nociceptive (Aδ & C) fibres

A

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

21
Q

What can damage to dorsal columns cause? (3)

A

loss of touch
loss of vibration
loss of proprioception

below lesion on ipsilateral side

22
Q

What can damage to anterolateral quadrant cause? (3)

A

Loss of nociceptive and temperature sensation below lesion on contralateral side

23
Q

Where is the ultimate termination of sensory afferent fibres?

A

in the somatosensory cortex (S1) of the postcentral gyrus

primary somatosensory cortex is the main sensory receptive area for the sense of touch

24
Q

What are the endings of the fibres grouped according to?

A

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

25
Q

What does the term rapidly adapting receptor mean?

A

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

26
Q

What is convergence?

A

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

27
Q

What is lateral inhibition?

A

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

28
Q

How does the body prevent every piece of information from making it into the brain?

A

Descending inhibition prevents all the info coming in - this is when you can sense something but you aren’t aware of it

29
Q

What is the difference between fast and slow pain?

A

fast (initial) short, stabbing pain that is highly localised but then get a delayed throbbing pain (harder to pinpoint where this is)

30
Q

Why can’t you call nociceptors pain receptors?

A

Becomes pain in the brain

‘Damaging stimuli’ until it reaches there

31
Q

How is the signal transduced to begin with in nociceptors? Mention ASIC, TRPV1 and G proteins

A

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

32
Q

Nociceptive fibres travel up which tract to the brain?

A

anterolateral spinothalamic tract

33
Q

What is the gate control theory of pain?

A

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

34
Q

What are the 2 ways in which nociceptive fibres can be inhibited?

A

Descending controls

Inhibitory interneuron releasing opioid peptide-

35
Q

Describe the inhibitory interneuron releasing opioid peptide method of inhibition

A

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

36
Q

Describe the descending control inhibition method

A

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

37
Q

How do non-steroidal anti-inflammatory drugs (NSAIDs) act as anasthesia?

A

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

38
Q

How do local anaesthetics work?

A

block Na+ action potential and therefore all axonal transmission

39
Q

How do Trans cutaneous electric nerve stimulation (TENS) work as analgesia?

A

Electrical patch put onto skin - electrical wave activating same segmental control – activates A beta fibres but not the others so these ‘close the gate’

40
Q

How do Opiates (eg morphine) work?

A

reduce sensitivity of nociceptors

block transmitter release in dorsal horn (hence epidural administration - injection in the back)

activates descending inhibitory pathways