CNS sensory and motor (Lecture 5):
Where’s that lesion?
o Bilateral loss of touch and proprioception from the
bellybutton down to the toes.
o Pain and temperature are intact.
Answer: Bilateral dorsal column lesion at the
lumbar region (both sides are damaged).
o Bilateral loss of pain and temperature in a thin strip
at the level of my lower chest.
o Touch and proprioception are intact.
Good Answer: In the middle (doesn’t impact
touch and proprioception).
Remember pain receptors synapse
with 2 order neurons and cross both
sides. So if there is a lesion in the
gray matter in the central canal for instance, then you lose pain and
temperature on both sides in the thin strip of the body
corresponding to this segment.
Wrong Answer: Taking out the dorsal roots would also affect touch and
o All somatosensory information on the LEFT side in a thin strip is lost. Numbness.
Loss of touch, proprioception, temperature and pain.
o Below that, on the LEFT, there is a loss of touch and proprioception (& motor)
o On the RIGHT side, there is a loss of temperature and pain going all the way up.
Answer: Brown-Sequard Lesions - Left hemisection of spinal cord at
lower thoracic level
(damaging of the dorsal
ipsilateral touch and
temperature and pain,
and the dorsal root
carrying all 4 from the
ipsilateral side of the
body – temperature and
pain haven’t crossed yet).
Common optical defects of the eye that require corrective vision (glasses, contacts, etc.): Nearsighted: the eye is myopic.
o Eyeball is too long for the
refraction of cornea and
lens, such that objects that
are far away tend to be
focused in front of the
retina (refraction is too
strong when you are
o Solution: We could squish
the eye to make it less long,
but this is hard to do, so we
use corrected lenses.
o Is there a correlation
between behaviour (e.g.
near work, sitting close to
the TV) and myopia?
more, read more for
more TV, played more video games and did less sports.
Farsighted: the eye is hyperopic
o Eyeball is too short. Close object is focused behind the retina (refraction is not
strong enough when you are farsighted), so corrective lenses are needed to bring
the focus point onto the retina.
Astigmatism: the lens or cornea are not spherical, so adjustments are needed.
Presbyopia: the lens gets stiff and is unable to accommodate for near vision. Starts
developing where you are over 40 years old.
Cataract: changes in lens color. Happens with age.
Organization of the retina:
Retina: lining at the back of the eye with photoreceptors and has a lot of circuitry.
Retina is part of the central nervous system (CNS) -> essentially part of your brain.
Vitreous humor is present in the eye. Light travels through the cornea, the lens, through
the vitreous humor and then strikes the retina. The lining behind it is the choroid.
The transduction process (where ion channels are opened/closed as light comes in)
occurs in the photoreceptors, which are the rods and cones of the retina.
Notice: rods and cones are in the back, and light has to travel through all this neural
circuitry to get to them.
Circuitry is formed in the front and there is not too much distortion produced by it ->
o Except in the central part of your vision: the circuitry gets pushed out of the way.
There is a layer of pigment epithelium sitting behind the photoreceptors that captures
scattered light (i.e. photons that do not interact with the transduction process get simply
absorbed). Nocturnal animals (e.g. cats): their eyes glow when you hit them with a flashlight or light
from your car, because their back of eyes are somewhat reflective.
o At night, there are so few photons that we do our best to capture each one, even if
it causes distortion.
So, light comes in and changes the neurotransmitter release from the photoreceptors to
this middle circuitry (we won’t talk about its functioning).
o 3 types of cells involved: bipolar cells, amacrine cells, and horizontal cells.
This middle circuitry processes light signals coming from the photoreceptors and allows
o The processing … … receptor field of output neurons called ganglion cells
o Convergence: ganglion cell = output of retina, its axons become the optic nerve.
We have about a 100 million photoreceptors (90M rods and 10M cones),
but we only have a million ganglion cells with their axons.
Many photoreceptors converge through the middle circuitry onto a single
Output of the retina = optic nerve.
The ganglion cells fire APs. All the processing in the retina is mainly by
graded potential releasing neurotransmitters and changing membrane
potential. Nobody tells the ganglion cells to send this info to the brain.
In fovea centralis (highest acuity where most of the cones are, which
control [colour] vision in bright light conditions), the retinal circuitry is
shifted out of the way to where the fovea is. There is little distortion of
that light striking the cones.
Recall: receptor fields in the fovea are very small.
Acuity in the periphery is not as good as in the fovea. When you move
your eyes away to the side from your target (e.g. text), you can still see the
image, but not distinguish single words.
Recall: receptor fields of the ganglion cells are large in the
periphery, since there is a relationship between acuity and RF size. Phototransduction:
o Light reduces
coming out from
in the dark.
How can you see light if
This is where the retina circuitry comes in, because it inverts this signal. It turns the
reduction in neurotransmitter release in an increase of ganglion cell activity.
Photoreceptors (2 kinds = cones & rods) have an inner segment with the cell body and
nucleus as well as an outer segment which contains stacked membranes, where
transduction occurs. Here we zoom into one of these membranes.
Each membrane contains specialized molecules that we will refer to OPSIN molecules.
o In these opsin molecules, there is a chromophore, related to vitamin A, which
causes the molecules to be sensitive to photons. When photons strike them, they
o Rhodopsin (visual pigment): opsin molecule found in rods. In this class, we will
simply refer to this as the opsin molecule (blue one on the diagram).
o There are in fact 4 different opsin molecules (3 others in the cones).
Normally, in the dark, there is a lot of cGMP (cyclic) in this outer segment and it
activates cGMP-gated channels, which allow sodium enter the outer segment. Opening
these channels, by the flow of ions, triggers the depolarization of the membrane in the
outer segment. This depolarization then causes the inner segment to depolarize, followed
by transmitter release in the dark.
Here comes light (a photon) => Phototransduction
1. Light activates opsin molecule: photons are so tiny but carry much energy and you
need all these outer segments to capture one. Each photoreceptor has about a
billion opsin molecules. When a photon happens to strike one of these opsin
molecules sitting in this disc inside the photoreceptor, it changes conformation.
2. G-protein cascade: this change in conformation activates the cascade. Sort of like
a motor running on its own.
3. cGMP to GMP: this cascade concerts cyclic GMP to GMP.
4. Na+ channels close: they start closing as you take away the cGMP floating around
in the outer segment. Takes 10s-100s milisec for sodium chann