Fitzakerely – Skin & Muscle Receptors – NS Exam 2
1. Define somatosensation, be able to distinguish it from proprioception.
SOMATOSENSATION refers to the process that conveys information regarding the body surface and its
interaction with the environment. It can be subdivided according to modality: 1. thermosensation, 2.
mechanoreception and 3. nociception. Even among these modalities, receptors are specialized to
transduce specific stimuli, and have very different receptive field sizes and speeds of adaptation.
PROPRIOCEPTION is the awareness of body movement and position – mediated both by generalized
receptors found in the joints (and elsewhere) as well as vestibular system. Includes several types of
sensation but excludes special senses.
2. Compare and contrast the characteristics of thermo-, mechano- and noci-ceptors (stimuli, receptor
types, location, receptive field size, adaptation), including what is known about the gating of the
channels involved. In particular, be able to identify the adequate stimuli for nociceptors. Describe the
nature of the currents that flow through TRP channels.
In many sensory systems, the transduction channel is a member of the transient receptor potential
superfamily of ion channels. Transduction couples a stimulus detector (receptor protein) to an ion
channel  receptor potential is generated.
Thermoreceptors adapt rapidly to changes in temperature, as well as specific chemical stimuli.
 Cold – respond to temps between 5-35 C & above 45 (‘paradoxical cold’)
 Warm – respond to temps bxt 30-35 C.
 Can also respond to specific chemical stimuli – menthol / capsaicin.
Mechanoreceptors respond to deformation of the cell membrane, but why this causes opening is
unknown but may be b/c of:
 Direct activation d/t lipid tension
 Direct linkage via intracellular & extracellular proteins
 Indirect activation via a 2nd messenger system that activates the channel
Nociceptors respond to heat (>45⁰C), protons, and vanillinoids (esp. capsacin),
 responses can be sensitized by several compounds, including prostaglandins
o blocking PG activation of nociceptors is a key mechanism of action of some analgesic
drugs – especially NSAIDs
 Sensitation lowers the activation threshold for the channel (for example, channel will open at
body temp) and also leads to hyperalgesia & allodynia (characteristics of inflammatory pain)
TRP
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TRP channels : taste, smell, hearing, mechanoreception, thermosensation and nociception
7 subfamilies; 18 genes
all TRP channels have 6 transmembrane domains - structurally similar to voltage-gated ion
channels
o TRP channels incorporate the receptor protein with the channel structure (i.e., there is no
need for 2nd messengers)
TRP channels are permeable to cations, however, many of them are relatively non-selective
i.e., they admit K+, Na+ or Ca2+
o the direction and nature of ion flow therefore depends on the concentration gradients for
the various ions (see the discussion of the hair cell transduction current) - in most cases,
most of the transduction current will be carried by Na+
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3. Compare and contrast the transmission of touch and nociceptive information (pathways and
conduction velocities).
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there are 2 primary somatosensory pathways:
1. DORSAL COLUMN-MEDIAL LEMNISCUS (mechano- and proprioception)
2. SPINOTHALAMIC TRACT (thermoreception and nociception)
from a physiology perspective, there are 3 key points:
1. the inputs from the body and head that form the medial and trigeminal lemnisci coalesce in the
thalamus to form a single body map, which projects to the somatosensory cortex to form the
humunculus
2. both pathways are crossed (although they cross at different anatomical levels) - this means that
somatosensory stimuli from one side are perceived in the contralateral cortex
3. the spinothalamic tract projects to more diffuse areas of cortex, directly activating non-sensory
regions – divergence
Somatosensory nerve fibers can be divided into several subcategories based on their conduction velocity
(which is determined by their diameter and degree of myelination). This classification system is
important for understanding pain and the mechanism of action of local anesthetics.)
4. Explain the perception of temperature.
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Modulate information from receptors
Illusions happen in every sensory system
In brain  all about contrast. Water cups example.
5. Contrast the three types of pain. Define referred pain, and explain why it is perceived.
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pain is a perception that represents the interpretation of the sensations that arise from nociceptors
nociceptors can activate several pathways in addition to the main spinothalamic pathway (i.e., this is an
example of parallel processing)
o activation results in autonomic (increased heart rate, dilation of pupils, etc.), and emotional (fear)
responses, as well as initiation of protective (withdrawal) reflexes
pain perception varies widely among individuals, and can be significantly affected by emotions and past
experience
o modulation of pain can serve either to magnify or to suppress the experience --- or to alter other
processes such as localization (for example, referred pain
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ex: MI pt w/ arm pain – activation of nociceptors in heart – signals converge in SC onto
same cells that get information from skin – brain perceives signal as skin b/c of labeled
line processing (usually that signal means ‘skin’)
3 types of pain:
o Acute nociceptive
 Fast (sharp, pricking) – well localized, transmitted by A delta fibers
 Slow (dull, aching) – poorly localized, transmitted by C fibers
o Inflammatory: caused by damage or sensitization of peripheral receptors – PGs
o Neuropathic: a complex pain state, changes in transmission system (not receptors) – CNS damage
or remodeling of synapses
o Inflammatory & neuropathic pain  Chronic pain syndromes
 ex: hyperalgesia, when a normally innocuous stimulus causes pain
6. Diagram the gate theory of pain, and explain how it accounts for the success of TENS.
Perception of pain is not simply due to activation of nociceptors, but is the outcome of modulation of
both nociceptive and non-nociceptive inputs.
According to the gate theory of pain, inhibitory interneurons regulate the transmission of ascending
nociceptive information at the level of the second order neuron, allowing modulation of the signal (both
increases and decreases in activity are possible). This modulation can explain phantom limb pain, as well
as the success of TENS treatment and the actions of opioid analgesics.
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Normally – inhibitory interneurons suppress 2nd order neurons
 pathway is inactive
Activation of C fibers  release glutamate  + on 2nd order
neuron / - on interneuron
o Inhibition of the inhibitory interneuron  Gate OPENS
Reactivate gate by activating mechanoreceptors  CLOSE gate
o TENS – transcutaneous electrical nerve stimulation 
suppresses pain
Endogenous analgesic system – releases endorphins, helps
decrease pain perception
o endogenous opioids (endorphins, enkephalins) act on
both the presynaptic (primary afferent) nerve terminal
and the postsynaptic (2nd order neuron) to decrease
nociceptive neurotransmission
o presynaptic actions include  in Ca conductance   neurotransmitter release
o postsynaptically, activation of opiod mu receptors causes and increase in K+ conductance  IPSP
7. List the sequence of events that occurs during the stretch reflex, and outline the role of co-activation of
alpha and gamma motoneurons in maintaining the sensitivity of spindle afferents. Explain the role of
gamma motorneurons in maintaining muscle tone.
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muscle spindles are stretch receptors
when the muscle is at rest, the spindle has a low level of tonic activity
o this tonic activity maintains a basal level of tension in the muscle, due to the same mechanism
described below for the stretch reflex
muscle stretch deforms the nerve endings, causing depolarization (mechanoreception)
o primary endings are dynamic (they respond to the velocity of the change)
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o secondary endings are static (they signal the amplitude of the change)
STRETCH REFLEX: increased activity in the spindle afferents causes depolarization of alpha motor neurons
(monosynaptic reflex), contracting the extrafusal muscle fibres
o the sequence is:
1. muscle stretch
2. depolarization and generation of action potentials in the spindle afferent
3. activation of alpha and gamma motor neurons
4. muscle contraction
5. hyperpolarization of spindle afferent (negative feedback)
co-activation of both the alpha and gamma motor neurons prevents the spindle afferents from becoming
completely silent (i.e., what the gap in firing shown in the diagram doesn't happen in real life!)
 activation of the gamma motor neurons contracts the intrafusal fibres and lengthens the
central region of the spindle, maintaining the stretch on the sensory nerve endings, keeping
the receptor in the middle of its dynamic range
resistance of a muscle to stretch is called TONE (or TONUS)
o severing the motor nerve to a muscle eliminates resistance à FLACCID
 also occurs when gamma efferent discharge is low
o high resistance to stretch occurs when the spindles are overactive (usually due to high rate of
gamma motor neuron discharge) à HYPERTONIC (SPASTIC)
 removing inhibitory inputs to the gamma motor neurons, increases their discharge rate, and
increases spindle output
8. Describe the role of Golgi tendon organs in the inverse stretch reflex. Define the lengthening reaction,
and the physiology of the circuit that explains why it is typically observed clinically under hypertonic
conditions.
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Mechanoreceptors – stretch  depolarization
Inverse stretch reflex (autogenic inhibition)
GTO afferent  excites inhibitory interneuron  decreasing activity of alpha motoneurons  relaxation
Stretch reflex & inverse stretch reflex work to keep muscle at correct tension
Under hypertonic conditions   in δ activation
o Moderate stretch  contraction (muscle spindles)
o Strong stretch  relaxation
 Sudden collapse  clasp knife effect
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