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Notes

CNS physiology - Vision

Niamh McLoughlin Central Nervous System English 6 pages

Content of the notes (6)

Page 1

Eye anatomy

CNS physiology - Vision

CNS physiology - Vision

Iris

Pigmented smooth muscle

More pigment = darker eye colour (Brown, black)

Less pigment = lighter eye colour (Blue, green)

Blue = least pigmented

What is gluacoma?

Build up of excessive aqueous humour

Fluid becomes trapped in anterior eye compartment - drainage system blocked (can be due to Iris/Corneal junction being too narrow)

Use anticholinesterase drugs to treat (link pharma lecture Cholinergic drugs pg. 3 section iv)

Vitreous humour

Nutrients to retina

Structural support - maintains shape of eyeball

Choroid

Melanin-containing region

Absorbs light

Absent in albinism (lack of melanin) - causes poor eyesight due to light 'ping-ponging' around retina but not actually being absorbed (See vision anatomy)

i) Lens accommodation

Focuses light onto retina

Unaccommodated:

Cillary muscles contracted

Zonule fibres relaxed

Lens becomes thick & round

Allows us to see things close-by

Accommodated:

​​​​​​​Cillary muscles relaxed

Zonule fibres contracted

Lens becomes thin & flat

Allows us to see things far away

CNS physiology - Vision

CNS physiology - Vision

Light is focused by cornea & lens onto fovea in retina

Remember image projecting onto retina is inverted (Link vision anatomy lecture)

Emmetropia = 20:20 vision

What is the fovea?

Centre of the macula

Point where cone density is highest -approx 30'000 (only cones found in fovea!)

Acute vision (sharpest & most detailed images) arises from here

Macular degeneration can lead to damage to fovea

Link to vision anatomy lecture

Disorders of lens accommodation

Myopia:

Short-sightedness

Light rays converge before reach retina

Results in fuzzy image when viewing long distance

Treated using concave lenses

Hypermetropia:

Long-sightedness

Light rays converge 'after' retina

Results in fuzzy image when viewing close up

Treated using convex lenses

Presyopia:

Long-sightedness that occurs as we age

CNS physiology - Vision

CNS physiology - Vision

Page 2

Rods & cones

i) GF of rods & cones

Rods

Responsible for night vision

Very light sensitive (low threshold)

Contain high levels of photopigment

Low accuracy - more focused on general details, not specifics

High signal amplification - which converges & summates at bipolar cells in retina

Slow adapting

Cones

Responsible for day vision

Light insensitive (high threshold)

High accuracy - focused on fine details

Concentrated in fovea

Low signal amplification - little convergence

Fast adapting

3 types of cones:

Red (H)

Green (M)

Blue (L)

Light stimulation causes rods & cones to hyperpolarise!

ii) Rhodopsin

Pigment contained in retina

Opsin + retinal (a.k.a. retinaldehyde)

How does rhodopsin work?

11-cis retinal (unactivated rhodopsin) is floating about when no light is striking retina

When light hits, 11-cis retinal is converted into trans retinal (any kind) - it is now activated

This causes opsin & retinal to split

Metarhodopsin II (activated rhodopsin) is formed!

The metarho excites electrical change in photoreceptors (in our case, rods & cones)

Hyperpolarisation in Rs & Cs occurs & a signal is transduced!

Rods & cones contain diff isoforms of opsin (but both contain rhodopsin!)

Rods = Scotopsins

Cones = Photopsins

CNS physiology - Vision

CNS physiology - Vision

iii) Dark current vs light current

In the dark...

Sodium ion influx into outer rod segment

cGMP splints sodium channels open

K+ efflux from inner rod segment

Creates MP of -40mV

In the light...

Sodium ion influx stopped

cGMP levels drop - due to metarhodopsin II activating cGMP phosphodiesterase

K+ efflux remains

Creates hyperpolarisation

CNS physiology - Vision

iv) Glutamate release

Glutamate = neurotransmitter used by rods & cones

Released in the dark!

Not released in the light!

Glutamate receptors located on bipolar cells

Page 3

Bipolar & ganglion cells

i) Bipolar cells

2 types of glutamate receptors on bipolar cells - Ionotropic & Metabotropic

Ionotropic

AMPA & kainate

Glutamate binding activates ligand gated sodium channels

Bipolar cell is depolarised

Signal is sent to off-centre ganglion cells

Metabotropic

mGluR6

Glutamate binding leads to closure of cGMP-gated sodium channels

Bipolar cell is hyperpolarised

Signal is sent to on-centre ganglion cells

Equal & opposite responses to the light signal

ii) On vs off centre

Contrast of visual info

Allows us to detect stimuli against a background

How does it work?

Half of the cells check for stimuli brighter than the background

Other half check for stimuli darker than the background

http://www.sumanasinc.com/webcontent/animations/content/receptivefields.html - video explaining on-centre off-centre vision

CNS physiology - Vision

iii) Ganglion cells & parallel pathways

Bipolar cells synapse with ionotropic receptors on ganglion cells (AMPA, Kainate & NMDA)

Glutamate = neurotransmitter used

Depolarisation in ganglion cells & AP generated

3 types of ganglion cell:

P cells

M cells

K ganglion cells

CNS physiology - Vision

Page 4

Visual pathway beyond the retina

i) Image transmission from retina to cortex

Optic chiasm

Fibres from nasal half each eye decussate

Allows depth perception

(See Visual anatomy lecture)

Pretectum

Blinking response

Superior colliculus

Head & eye movements

Suprachiasmatic NHypo

Circadian rythms (Melanin secretion, sleepiness due to darkness falling)

Lateral geniculate nucleus

90% ganglion fibres head here

Cerebral cortex

Perception of vision

CNS physiology - Vision

CNS physiology - Vision

Page 5

Lateral geniculate nucleus

90% of retinal axons synapse here

50% foveal representation

Sends signal on to cerebral cortex

Composed of 6 cell layers of cell bodies separated by intralaminar layers:

Layers 1+2 = Magnocellular layer - M cells input

Layers 3+6 = Parvocellular layer - P cells input

Layers 1,4+6 = Contralateral nasal hemiretina

Layers 2,3+5 = Ipsilateral temporal hemiretina

CNS physiology - Vision

CNS physiology - Vision

Page 6

Primary visual cortex

Primary visual cortex comprised 6 layers of cells

LGN inputs enter in Layer 4 (Internal granular layer) + layers 2 & 3

Comprised of 4 sublayers:

4A

4B

4C alpha

4C beta

Axons M cells terminate 4C aplha - Motion information

Axons P cells terminate AC beta - Detail information

Axons intralaminar region LGN terminate layers 2 & 3 (Blobs) - Colour information

What are blobs?

Structures within visual cortex that 'put the colour on the picture'

Resemble K ganglion cells (they are specifically targeted by K-ganglion cells!)

Used in colour perception, colour discrimination + the learning & memory of the colour of objects

How do they work?

Each pink circle below represents a 'pixel' coming from the retina

The blob combines these 'pixels' together to create an image - to which it adds colour

CNS physiology - Vision

i) Visual cortical pathways

These pathways form the basis of 'learning from & reacting emotionally to what we see'

Magnocellular pathway - Motion & change

V1 - V2 -V3 -MT

Dorsal pathway

Connects with posterior parietal cortex

V3 = orientation

MT = object movement

What does Magnocellular pathway transmit?

Processes P-channel info about object location & M-channel info about object movement

Gives us our sense of:

Spatial orientation

Binocular fusion/depth perception

Location, movement, direction & velocity of objects in space

Concerned with the 'WHERE' of the stimulus!!

Parvocellular pathway - Form & detail

V1 - V2 - V4

Ventral pathway

Connects with inferior temporal cortex

V4 = colour & form

What does Parvocellular pathway transmit?

P-channel info about object colour & form

Allows us to:

Recognise objects & colours

Read text

Learn & remember visual objects (words & their meanings)

Concerned with the 'WHAT' of the stimulus!!

Information

Description
Central Nervous System (CNS Physiology) Note on CNS physiology - Vision , created by Niamh McLoughlin on 05/11/2017.
Created by
Niamh McLoughlin · Nov 2017
Updated
Nov 9, 2017
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