TEXTBOOK – Chapter 9
Retina: net-like, thin film of cells lining inside back wall of eye.
Image is projected on outer margins of retina, where there are photoreceptors.
Photoreceptors: light-absorbing elements. They are the transducers – convert light energy into signals. Those
signals are then processed by other neurons in the retina.
Pigment epithelium. Photoreceptors nestled in this layer of cells. These cells absorb stray light that
photoreceptors don’t catch. If stray light isn’t absorbed it can interfere with normal processing of vision.
Albinos usually lack this.
Two types of PHOTORECEPTORS:
- Rods: much more numerous. 120 million rods. Look like rods. Night vision.
- Cones: not as many. 6 million cones. Look like cones. Day vision.
Fovea: small pit in center of retina.
Optic disk: point in retina where nerve fibres converge to exit eyeball. Blind spot, it does not contain
Cones are low in peripheral parts. Reaches maximum amount at center of fovea. Opposite with rods: more
numerous in periphery and less so in centre. Absolutely no rods in fovea.
Large concentration of cones in fovea is dedicated to processing image detail (in light conditions)
In dim light, periphery is better. More rods.
Phototransduction: transduction of visual stuff.
Photopigment: captures light photons, found in photoreceptors. The photopigment is called rhodopsin.
Photopigments concentrated in outer segment of photoreceptors (embedded within fibrous matrix)
Dark current: inward flow of sodium (that bind to cGMP) in rhodopsin in the absence of light.
- Balanced out by outward flow of K ions in inner segment.
- Sodium potassium pump reverses this so there isn’t excess buildup
Photons have to pass through inner segment before reaching outer segment with rhodopsin molecules.
Ohh, so when rhodopsin is activated it interacts with G protein in the discs. G protein activates an enzyme that
converts cGMP to GMP. Removal of cGMP makes it impossible for sodium to bind and therefore abolishes
It takes a bit for the potassium to stop being ejected to balance sodium intake, so it may be hyperpolarized for
a bit. In dark conditions rods and cones steadily release glutamate (neurotransmitter). Light absorption auses
photoreceptors to release less glutamate, and somehow this is interpreted as “photoreceptor activation has
Spectrophotometry: experimenting with rhodopsin in test tube to see how much it absorbs and how much
emerges out of other side of test tube (which can be measured) graphed as “absorption spectrum”
Rhodopsin is said to be ‘bleached’ when it is temporarily unable to absorb any more photons until it is
Cone receptors can also be bleached – at super intense light conditions like looking at the sun – but they
recover much faster than rod receptors.
-axons leave the eye
-first site within retina where action potentials are generated (in other retinal neurons it occurs by
-parallel visual streams? 2 separate types of ganglion cells.
Photoreceptor -> bipolar cell -> ganglion cell (closest to lens)
It’s actually backwards, so light passes through ganglion cell-bipolar cell then reaches photoreceptor, then has
to go back the opposite direction to reach ganglion cell which will then transmit message.
Spontaneous activity among ganglion cells in darkness, and this persists in uniform illumination too. Which is
weird. Solution to this is that ganglion cells aren’t set up to signal overall light levels, but to detect differences
in light stimulation in adjacent parts of retina.
Receptive field: area in retina that influences a ganglion cell/neuron by excitation/inhibition.
Ganglion cell: either ON(center)/OFF or OFF(center)/ON. Roughly equal numbers of each in retina.
OK SO. When light only shines on ON part = burst of action potentials.
When light shines on ON part and a bit of OFF part = a little less action potentials because light on OFF region
has an inhibitory influence.
When light shines on both ON and OFF regions = only spontaneous firing left, because excitatory and
inhibitory signals balance each other out