CNS sensory and motor (Lecture 4):
We will focus on the somatosensory system, then the visual and finally auditory systems.
Somatic (bodily) sensation is mediated by several types of receptors:
Temperature: Thermoreceptors are free nerve endings [in the skin] containing ion
channels that respond to different temperature ranges.
o Cold afferents: 0-35 C (activated by menthol) – afferents transmitting information
about cold stimuli. o
o Warm afferents: 30-50 C (activated by capsaicin and ethanol).
Extreme temperatures (< 0 C or >50 C) activate pain receptors.
o Pain receptors are activated when the sensory stimuli causes tissue damage.
The law of specific nerve energies applies here: we can activate a cold afferent with other
than temperature. Indeed, menthol activates cold afferents. Warm afferents can be
activated by other chemicals, like ethanol (in a shot of alcohol) and capsaicin (active
ingredient in hot chili pepper -> if too hot due to excess of capsaicin, pain receptors can
o Regardless of how we activate the afferents, despite that they were designed to
respond to temperature, if activated differently, the perception is still cold/warm.
Pain: Nociceptors are free nerve endings containing ion channels that open in response to
intense mechanical deformation, excessive temperature, or chemicals.
o Nociceptors become activate when the mechanical deformation of the skin or
excessive temperature starts causing (or even before it starts causing) tissue
Pain afferents are highly modulated (enhanced and suppressed).
Visceral pain receptors (inside organs): activated by inflammation.
o Overlap between visceral pain receptors and somatosensory pain receptors. This
confusion is important in clinical aspects.
Nociceptors are sensitized by many chemical mediators:
How pain is encoded and how this information is sent to the CNS?
How nociceptors are sensitized? How they increase their sensitivity to upregulate pain
Transduction process and how information is being communicated to CNS:
1. You cut your skin with something sharp. 2. Because tissue was damaged, there is an immediate activation of nociceptors,
which then send APs to spinal cord.
3. In the spinal cord, they release substance P (neurotransmitter) onto 2 order
4. These 2 order neurons send this information up to the brain and we feel the
o This is not where most nociceptors are sensitized however.
5. Sensitization of surrounding nociceptors by injured tissue & afferent feedback
onto mast cells: on the next day, we touch a surface with our previously
injured finger and it really hurts. The wound itself has become more sensitive.
Normally, a somatosensory stimulation to your finger wouldn’t cause any
pain, but now it does.
o This mechanism prevents you from using this part of the body until the
o This step is where most nociceptors are sensitized.
As these nociceptors send their APs to the spinal cord, they also
send APs back to mast cells located nearby. These mast cells
will release histamine.
Extracellular chemicals/substances from the damaged tissue
surrounding the nociceptors are also released, like serotonin,
Bradykinin, Prostaglandin (no need to know the names). This
also increases sensitivity of nociceptors.
6. APs are sent back to blood vessels; substance P is released and causes blood
vessels to dilate. This is the reason why there is a swelling around the wound.
o This also increases the sensitivity of the nociceptors.
o Dilation of nearby blood vessels brings in more blood to the area, thus
promoting the healing process, and because they swell around the nerve
endings, they make the latter more sensitive to mechanical deformation.
The next day, after all these processes have occurred (the 2 circled regions & #6),
nociceptors are extremely sensitive and their threshold for transmitting pain is reduced.
Normally, it requires tissue damage for APs to be released, they wouldn’t be activated by
simple reaching out and grabbing an object, but now they are.
Hyperalgesia = increased sensitivity to pain.
The process described above is a bottom-up modulation of pain, which increases the pain
input to the CNS without our involvement. Dorsal columns:
Understanding the circuitry that sends somatosensory information to the brain is
important to fully grasp the top-down regulation of pain.
E.g. You lightly stroke your finger with a feather activating Meissner’s corpuscles. This
causes afferents to be activated. These afferents will then send their APs along an axon
(nerve reaching the spinal cord).
o Recall that, on the diagram, we see only a spinal segment with a piece of spinal
cord with two corresponding nerves, each spinal nerve innervating a particular
strip section the body. Here, it’s a cervical segment.
o Cell bodies for the afferents are located outside of the CNS inside the dorsal root
o White matter contains
tracks going up and
down the spinal cord.
E.g.(cont’d): Axons come in
via the spinal nerve.
Dorsal root contains the
axons that enter the spinal
cord. The ventral root
contains the motor axons that
come out to innervate our
muscles. These axons come
in at the dorsal horn in the
gray matter, where cell bodies
are found. Axons quickly go over to the dorsal columns, containing track of axons going up and
down the spinal cord on the dorsal side in the back. There, the afferents from the finger at
the cervical segment (rather high) would join the other nerves coming from all the way
down our body (trunk, legs, toes, all coming up). These axons join up and so this
track/group of axons [dorsal columns] carry the same information (ipsilateral touch and
proprioception, from the same side of the body).
They go up to the medulla, the beginning of the brain stem and they synapse.
The axons or second order neurons then cross the midline.
o Ipsilateral: Same side relative to midline.
o Contralateral: Opposite side relative to midline.
As a neurosurgeon, if I cut the dorsal columns, the loss to the patient is
ipsilateral loss of touch and proprioception (+ temperature and pain) for
the cervical level (arm and hand all the way down one side of the body to
The 2 order neurons start going up the brain into the medial lemniscus, which is
carrying contralateral information regarding touch and proprioception. It’s a track of
axons travelling together whereas column is a specific name for axons travelling up and
down the spinal cord.
Then, this information about touch and proprioception synapses in the thalamus.
These neurons then project to the somatosensory cortex.
The cortex thus receives contralateral somatosensory information about touch and
proprioception via the dorsal columns.
Anterolateral pathway - Temperature and pain:
Instead of tickling your finger
with a feather, we now hold it
over a candle: ouch!
Nociceptors activate since the
temperature rises above 50 C
and send APs through the spinal
nerve, cell bodies in the dorsal
root ganglion and come into the
dorsal root. The synapse in the
dorsal horn of the gray matter
with 2 order neurons.
Substance P is released, since
it’s a nociceptor. If we do not
hold our finger so close to the
flame so that we do not feel
pain, then it’s the
thermoreceptors which are activated and we’re not releasing substance P.
The 2 order neurons cross the midline in this spinal segment and then form a track of
axons, called the anterolateral column (spinothalamic track), joining axons already
coming up from below. The secondary axons then travel up through the brain stem. Some synapses coming off
there (branching into the reticular formation), but most of the information goes to the
They synapse in the thalamus and go to the somatosensory cortex, which receives all
somatosensory information from the contralateral side of the body.
What happens if we create damage…
o In the case of damage to anterolateral column at the cervical level, the patient
experiences a contralateral loss of temperature and pain at the level of the lesion
and below (on the opposite side of the body).
Not only we have damaged axons entering from this cervical level, but all
other axons sending information from the anterolateral column are
damaged as well.
o If we damage the dorsal root instead, the patient experiences an ipsilateral loss of
touch, proprioception, temperature and pain, only at the cervical level, since the
tracks coming up from below in the dorsal column or anterolateral colum