Our eyes give us the amazing ability to see the world around us, to appreciate its beauty and alert us to its dangers. But how exactly does light entering our eyes, get converted into a visual image that we perceive?
The eye essentially acts like a camera. The amount of light entering the eye is regulated by the size of the pupil, like an aperture, which can be made larger or smaller by the action of muscles in the iris.
Light is refracted, mainly by the cornea and also by the lens, as it passes through different mediums, starting with air in the atmosphere, to aqueous humor in the anterior chamber of the eyeball and finally through vitreous humour in the posterior compartment of the eyeball. Refraction allows the focusing of light rays on the retina, the light sensitive surface of the eye that acts like the film of a camera. Muscles that control the shape of the lens can alter the degree of light refraction, which can influence how well we focus on nearby and distant objects.
An overview of the visual pathway
The retina is the light sensitive surface of the eye and consists of a complex arrangement of cells. Light rays have to pass through many cells before they reach the light-sensitive pigments in photoreceptor cells. Only in the fovea, the central part of the retina known as the macula, do light rays directly hit photoreceptor cells. For this reason, the fovea is responsible for the highest visual acuity.
As light activates photochemicals in photoreceptor cells, it can influence the release of neurotransmitters from them. This can influence the subsequent activation of a chain of cells in the retinal layer, from the bipolar cells to ganglion cells. Cells of the retina are specialised neurons, so transmit incoming electrical messages via dendrites and transmit outgoing electrical messages via axons. Axons of the ganglion cells converge to form the optic nerve. The optic nerve from each eye crosses over at the optic chiasm and electrical messages continue to be transmitted to the brain via optic tracts. These signals are then interpreted by specialised areas of the brain. We will now discuss each of these steps in more detail.
Photoreceptor cells consist of rods and cones, which both contain light-sensitive pigments. Rods are associated with the detection of light and dark, whilst cones are associated with colour vision. First, we will look at the function of rod cells.
A rod cell consists of an outer segment that contains the light sensitive pigment rhodopsin, an inner segment which contains the cell’s organelles, a nucleus, and a synaptic body which releases neurotransmitters to nearby cells.
Rhodopsin is a transmembrane protein, formed by the conjugation of the protein scotopsin with the carotenoid pigment 11-cis-retinal. When light hits the surface of a rod cell, rhodopsin absorbs photons of light which activates electrons in 11-cis retinal. This causes retinal to change its structure, from the cis form, to a trans form. As a result, the all-trans retinal no longer “fits” with scotopsin, causing the pigment to decompose.
As scotopsin and all-trans retinal split, rhodopsin becomes incredibly unstable and quickly decays, forming bathorhodopsin initially, followed by lumirhodopsin, metarhodopsin I, metarhodopsin II and finally the completely split products scotopsin and all-trans retinal. Metarhodopsin II is known as activated rhodopsin, because it is this compound which activates rod cells.
Before moving on to the activation of rod cells, it is important to note that rhodopsin can be re-formed from its two separate constituents. All-trans retinal is converted into 11-cis-retinal by the enzyme retinal isomerase, which can then be conjugated with scotopsin to rhodopsin again, until it once again absorbs another photon of light.
Activation of the rod cell
So how does activated rhodopsin activate a rod cell? First let’s look at what’s going in the rod cell itself.
The inner segment of the rod cell contains sodium/potassium ATPases and potassium selective ion channels, which help to pump out sodium and potassium ions respectively, creating a negative potential inside the cell. This helps to maintain the cell in a hyperpolarised state, in which no neurotransmitters are released at the synaptic body.
The outer segment however, contains cGMP-gated ion channels which are permeable to both sodium and calcium. The level of cGMP inside the cell is influenced by the absorption of light by rhodopsin.
When it is dark, and rhodopsin has not been activated by light, levels of cGMP in the cell are high. cGMP opens up cGMP-gated ion channels, enabling sodium and calcium ions to flood inside the cell. The influx of positively charged ions depolarises the cell as it reduces the electronegativity of the cell which is normally maintained by the inner segment.
When it is light and rhodopsin has been converted to metarhodopsin II, this active pigment activates an enzyme called cGMP phosphodiesterase. This breaks cGMP down and its reduction in the cell closes cGMP-gated channels. This prevents the influx of sodium and calcium channels into the cell, thereby maintaining the electronegativity of the cell that is achieved by the inner segment. Therefore in the light, rod cells are hyperpolarised.
So, in the dark, rod cells are depolarised. The influx of calcium channels into the cell causes the fusion of neurotransmitter vesicles with the cell membrane and the subsequent release of glutamate to neighbouring cells. In the light however, no neurotransmitters are released by the rods.
The next cell in the retinal layer is the bipolar cell and its activity is influenced by glutamate released by the rod cells.
Bipolar cells can be classified as on-centre, or off-centre, depending whether they are depolarised or hyperpolarised when light is shone in the centre of their receptive field. Each cell in the retina has a receptive field, and this is an area of the retina, which, if light is shone upon it, it is responsive to. As each cell has its own receptive field, this means that signals from these cells to the brain accurately portray where light is shining on the retina, resulting in an accurate visual image.
On-centre bipolar cells are depolarised when light is shone in the centre of their receptive field, so they are in effect, activated by light. When a rod cell in its receptive field is hit by light, the rod is hyperpolarised as discussed earlier, and releases less glutamate. There is less glutamate to bind to metabotropic glutamate receptors on the on-centre bipolar cell, so the bipolar cell is depolarised and releases glutamate to the next cell in the retinal layer. And conversely, if these bipolar cells are in the dark, rod cells release more glutamate, which binds to receptors on the bipolar cell causing it to hyperpolarise and release less glutamate.
Off-centre bipolar cells are depolarised when the centre of their receptive field is in darkness, so they are in effect, activated by darkness, or the absence of light. When a rod in its receptive field is in darkness, it is depolarised and releases more glutamate. Glutamate binds to ionotropic glutamate receptors on the bipolar cell, causing it to depolarise and release more glutamate itself. Conversely, when off-centre bipolar cells have light shone in the centre of their receptive field, rod cells are hyperpolarised and release less glutamate, causing the bi-polar cell to become hyperpolarised and release less glutamate.
The receptive fields themselves are effectively created by the action of another cell in the retina, the horizontal cells. These inhibit the depolarisation, or activation, of bipolar cells through the release of the inhibitory neurotransmitter GABA. Horizontal cells prevent the activation of bipolar cells that surround a receptive field. This means, that only specific cells in the retina that are directly struck by light are activated, preventing the spread of excitatory signals across the retina, which would lead to widespread signalling to the brain and imprecise visual images
So imagine the retina, with lots of different receptive fields, each responding either to light or darkness. This influences whether cells in these receptive fields become depolarised and release glutamate to activate the next cell in the retinal “chain”.
The next and final cell in the retinal chain is the ganglion cell. Again, these cells can be split into on-centre cells which are activated by glutamate from on-centre bipolar cells, and off-centre cells which are activated by glutamate from off-centre bipolar cells, maintaining the control over the level of signalling from different areas of the retina.
Different ganglion cells respond to different stimuli and can also be classified as magnocellular (M), or parvocellular (P) cells. M cells are indirectly activated by rod cells. They have large receptive fields and are sensitive to black and white stimuli. We will discuss P cells shortly when we discuss the role of cone cells in colour vision.
When ganglion cells are depolarised, their axons converge to form optic nerves, which communicate signals to the brain. Before we look at this more closely, let’s first recap what we have covered and mention some important concepts.
Recap – Important Concepts
So far we have seen how light rays striking the retina trigger a chain of cells in the retina to become activated, starting with the photoreceptor rod cell, which activates a bipolar cell, which activates a ganglion cell which sends signals via the optic nerve to the brain.
The degree of activation of these cells is sensitive to the degree of light stimulation, which is determined by the amount of light striking the retina. As more light hits the retina, rod cells become more hyperpolarised, so rather than an “on” “off” state, rod cells are always releasing glutamate, but at varying amounts depending on how much light they are exposed to.
One final important concept to mention at this point is how these signals are transmitted across each cell in the retinal chain. As a cell becomes depolarised or hyperpolarised, it transmits these signals via electrotonic conduction, rather than action potentials as occurs with other neurons in our central nervous system. Action potentials are generally all or nothing and require a particular threshold of activation in order to generate them. In electrotonic conduction however, the same degree of hyperpolarisation or depolarisation, that is, the flow of ions through the cell, is kept constant, from the dendrite of the cell all the way through to its synaptic body. This allows for graded conduction of signals from one cell to the next. To put it simply, a little light shining on a rod will cause it to hyperpolarise a little, and this small signal will be conferred to the subsequent cell in the chain. If a lot of light is shone on a rod, it will hyperpolarise a lot, and this larger signal will be transmitted to the next cell in the chain. Again, this enables us to discriminate between the intensity of the light entering our eyes, which is important for conveying accurate messages about the visual stimuli we are exposed to.
So now we know how we see in black and white, let’s explore colour vision.
Photoreceptors responsible for colour vision are known as cones. Their colour sensitive pigments are similar to rhodopsin in rods, except the protein portion is slightly different to scotopsin. There are three types of colour sensitive pigment, blue sensitive pigment, green-sensitive pigment and red-sensitive pigment and each cone possesses just one of these.
Each colour pigment absorbs a particular frequency of light:
– Blue sensitive pigment: 445nm
– Green sensitive pigment: 535nm
– Red sensitive pigment: 570nm
As varying wavelengths of light hit the retina, this activates different proportions of each type of cone and the resultant neural activity determines the colour that we see as a result. So the colours that we see are determined by a ratio of cone activation. For example, when light is shone into the eye at a wavelength of 580nm, it stimulates red cones to 99%, green cones to 42% and doesn’t stimulate blue cones at all. This ratio of 99:42:0 is interpreted by our brain as the colour orange. An even stimulation of all three cone types gives the sensation of seeing white. It is also important to note that the fovea only contains green and red cones, which limits its colour discrimination but improves vision of fine spatial detail.
As with the rod cells, activation of the light-sensitive pigment in cones results in hyperpolarisation of the cell membrane and a reduction in the release of glutamate. This determines the activation of the subsequent ganglion cells, as we discussed earlier. Each ganglion cell may be stimulated by several or just a few cone cells. Generally, P ganglion cells are stimulated by cones as they are sensitive to colours.
Ganglion cells that can be stimulated by all three cone types may transmit signals for “white”, however some ganglion cells are only excited by one cone type and inhibited by another. This is the case for red and green cones, where red cones can excite a particular ganglion cell but green cones inhibit them and vice versa. Red cones will activate a depolarising bipolar cell which can activate the ganglion cell, whilst the green cone will activate a hyperpolarising bipolar cell which will inactivate the ganglion cell. Just think of this as a series of “on/off” switches. This control is important for colour-contrast in the visual image.
Cone cells thereby enable us to appreciate the many myriad of colours we see on a daily basis, which all helps improve the clarity of the world around us. Once they have stimulated ganglion cells, signals are sent along ganglion cell axons, the optic nerves, where they travel all the way to the visual cortex.
From the Eye to the Brain
So far we have seen how rod and cone cells affect the activity of bipolar cells, which then determine the degree of stimulation of ganglion cells through the release of glutamate. Let’s now consider how visual signals are conveyed to the brain.
As ganglion cells are depolarised by glutamate, signals are sent along their axons which converge to form an optic nerve. Each optic nerve is far too long for electrotonic conduction to convey signals across them, so instead ganglion cells transmit their signals by repetitive action potentials.
It is worth considering the visual fields and how different portions of these fields activate different portions of the retina. The visual field for each eye can be split into four quadrants. As light passes through the eye, light from the left upper quadrant of the visual field will affect the right lower quadrant of the retina, whilst light from the right lower quadrant of the visual field will affect the left upper quadrant of the retina. So basically light in any part of the visual field will strike the opposite side of the retina, due to the way in which light rays are refracted by the cornea and lens. The two medial quadrants of the retina make up the nasal half of the retina, whilst the two more lateral quadrants make up the temporal half of the retina.
Why is this important to know? Well, as the optic nerves form from the convergence of ganglion cell dendrites, both nerves then converge at the optic chiasm. Here, nerve fibres from the nasal halves of the retina cross to the opposite side (contralaterally) to join nerve fibres from the opposite temporal retinas, so fibres from the temporal retinas do not cross and continue ipsilaterally. When these nerve fibres converge they form the optic tracts, as they are technically no longer the optic nerves.
Nerve fibres in each optic tract synapse in the dorsal lateral geniculate nucleus of the thalamus. The thalamus is essentially a relay station in the brain, processing incoming information and deciding where to relay the signals to in the cortex and a nucleus within the brain is an area of grey matter consisting of cell bodies that communicate with one another via synapses. Within the lateral geniculate nucleus there are 6 layers which receive different incoming information. The visual signals from both eyes are kept apart within this nucleus, with layers II, III and V receiving signals from the ipsilateral retina and layers I, IV and VI receiving signals from the contralateral retina.
The lateral geniculate nucleus controls how much of the incoming visual signals are relayed to the visual cortex and inhibitory signals from the primary visual cortex and the reticular area of the midbrain help it to do this. This is yet another way of improving the resulting visual image that we see.
From the lateral geniculate nucleus, axons pass along optic radiations, also known as the geniculocalcarine tracts. Each optic radiation can be divided further into an upper and lower optic radiation. The upper optic radiation transmits nerve fibres from the superior retinal quadrants through the parietal lobe, whilst the lower optic radiation transmits nerve fibres from the inferior retinal quadrants through the temporal lobe. All the optic radiations eventually reach the visual cortex but just take a slightly different route through the brain as they do so. Some axons can travel elsewhere in the brain too, such as the suprachiasmatic nucleus of the hypothalamus (involved in circadian rhythms), the pretectal nuclei in the midbrain (involved in the pupillary light reflex) and the superior colliculus (involved in rapid directional movements of the brain). These pathways are much “older” areas of the brain but serve important functions nonetheless.
So to recap, once the optic nerves form they meet up at the optic chiasm, where nerves from the medial quadrants of the retina overlap. There, they travel to the lateral geniculate nucleus which continues to transmit this information through to the visual cortex, separated into optic radiations.
The Visual Cortex
The visual cortex is located mainly on the medial part of the occipital lobe and is divided into a primary visual cortex and secondary visual area. It acts as a kind of sieve, filtering information down its many columns of neurons. The visual cortex consists of millions of vertical columns of neurons that, like the lateral geniculate nucleus, are split into layers numbered I to VI. Most of the incoming visual information from the optic radiations are transmitted initially into layer IV. From here, information is transmitted through the visual cortex which then deciphers the incoming information.
Deciphering the Information
Different neurons are “activated” by particular types of incoming signals, for instance, particular colours or orientations of lines in the visual image. Neurons that have similar “triggers” are arranged in columns, so that each column is specific to a particular feature of a visual image.
Colour blobs contain neurons which are colour sensitive and determine colour in the visual image. Colour contrast helps to determine colours in the visual image, as certain colours excite one type of neuron but inhibit another, as we mentioned earlier. Simple cells decipher basic details of colour contrast, whilst complex and hypercomplex cells are stimulated by more subtle degrees of colour contrast to fine tune the resulting image we perceive.
Signals regarding contrast in the visual image can excite specific neurons too. Great sharpness of contrast along borders in the visual image, or between areas of light and dark can greatly stimulate neuronal activity.
As mentioned above, some neurons are selective for certain orientations of lines in the visual image. For example, a completely horizontal line may excite one kind of neuron, whilst vertical lines will excite another type. Simple cells can be activated by simple orientations, whilst complex cells are stimulated by lines at varying angles and are more difficult to excite.
Neurons are arranged in each column so that each responds to a different aspect of a visual image and the degree of stimulation of each column therefore determines how we view the image in our minds. The neuronal columns act like sieves, so that as information passes down them, different varieties of neurons are stimulated in the process, from simple cells that are stimulated by simple aspects of the image, to complex cells which are stimulated by complex features of the visual image.
Once neurons in the visual cortex have filtered and deciphered the incoming visual information, further signals are transmitted to the visual association area. This is very important, as whilst the visual cortex allows us to perceive the image in front of us, it cannot tell us anything about what it is or what it means to us. Therefore the visual association area helps us to understand the incoming visual information.
The Visual Association Area
Signals from the visual cortex can take one of two pathways known as the dorsal and ventral pathway, depending which direction they take.
The dorsal pathway transmits information through the superior occipital lobe and posterior parietal lobe. This is important for interpreting where objects are and whether they are moving.
The ventral pathway transmits information through the anteroventral occipital lobe and posterior temporal lobe. This is important for interpreting colour and detail in the visual image, such as letters, words and textures.
Information will also be sent to other areas within the brain too, such as the hippocampus so that we can form memories, or the limbic system so that we can feel emotions when we see certain things.
There is literally a lot more to our sense of vision that meets the eye. To make it simple, just think of the whole process in a more condensed way. Light enters our eye where it is bent so that it hits the retina, the light sensitive surface of the eye. Here it activates a chain of cells, which communicate the information from one cell to the next in order to pass on the information to the optic nerves. The optic nerves converge and split into optic tracts where they pass to the thalamus which relays the information onward to the visual cortex. Here, the information filters down through millions of neurons, exciting different types depending on the visual image being interpreted. This allows us to see what is around us, but signals are then sent elsewhere in the brain where we can understand where and what is around us.
It is also easy to appreciate how diseases of vision may arise, due to the complexity of the whole process. Lesions to parts of the optic nerves, tracts or optic radiations can wipe out signals from large parts of the retinas leading to a lack of vision in areas of the visual field. Likewise, diseases of the retina itself can lead to conditions such as macular degeneration in which degeneration of the highly sensitive macular leads to large scotomas, or blind spots in the vision which can progressively worsen and result in blindness. Whilst many of us take our vision for granted, it is an incredibly important sense and although we can live without it, understanding the physiology behind this and the diseases that can affect it can prove incredibly important to the many people who suffer from conditions affecting their sight.