Do you see what I see?

An enduring question in philosophy and neuroscience is whether any individual’s subjective perceptual experiences are the same as those of other people. Do you experience a particular shade of red the same way I do? We can both point to something in the outside world and agree that it’s red, based on our both having learned that things causing that perceptual experience are called “red”. But whether the internal subjective experience of that percept is really the same is almost impossible to tell.

There are some exceptions, of course, where there are clear differences between people’s perceptions. Colour blindness is the most obvious, where individuals clearly do not experience visual stimuli in the same way as non-colourblind people. This can be contrasted with the experience of people who are tetrachromatic – who can distinguish between a greater number of colours, due to expression of a fourth opsin gene variant. Conditions like face blindness and dyslexia may involve difficulties in higher-order processing of specific categories of visual inputs. And synaesthesia provides a striking example of a difference in subjective perceptual experience, where certain stimuli (such as sounds, musical notes, graphemes, odours or many other inducers) are accompanied by an extra visual percept (or percept or association in some other modality).

But what about more general experience? Do people without such striking conditions exhibit stable individual differences in how they see things? Geraint Rees and colleagues have done some fascinating work to show that they do and also linked such differences in subjective experience to differences in the size of the visual cortex.

They have used a number of visual illusions as tools to quantify individuals’ subjective experience. One of these is the well-known Ebbinghaus illusion, where a circle seems to differ in size when surrounded by either bigger or smaller circles. (Even though you know it’s the same size it’s almost impossible to see it that way). Rees and colleagues assayed how susceptible people were to this illusion by asking them to match the perceived size of the internal circle with one of a set of circles that really did vary in size.

They then used functional neuroimaging to map the spatial extent of the primary visual cortex (area V1) in these people. This is the first region of the cerebral cortex that receives visual information. This information is conveyed by direct connections from the dorsal lateral geniculate nucleus (dLGN), the visual part of the thalamus, which itself receives inputs from the retina. The important thing about the projections of nerve fibres from the retina to the dLGN and from there to area V1, is that they form an orderly map. Neurons that are next to each other in the retina project to target neurons that are next to each other in the dLGN and so on, up to V1. Since the visual world is itself mapped by the lens across the two-dimensional surface of the retina, this means that it is also mapped across the surface of V1.

Rees and colleagues took advantage of this feature to map the extent of V1 using functional magnetic resonance imaging (fMRI). By moving a stimulus across the visual field one gets an orderly response of neurons from different parts of V1, until a point is reached at which the responses reverse – this is the start of the second visual area, V2.

Remarkably, the strength of the visual illusion (and of another one called the Ponzo illusion) experienced by individuals correlated strongly (and negatively) with the size of their V1. That is, individuals with a smaller V1 experienced the illusion more strongly – they were the least accurate in judging the true size of the inner circle. Put another way, their perception of the inner circle was more affected by the nearby outer circles. This suggests a possible explanation for this effect.

Neurons in V1 receive inputs from the dLGN but also engage in lateral interactions with nearby V1 neurons. These integrate responses from neighbouring visual fields and help sharpen response to areas of higher contrast, such as edges of objects. If the visual world is projected across a physically smaller sheet of neurons, then the responses of neurons in one part may be more affected by neighbouring neurons responding to nearby visual stimuli (the outer circles in this example). Conversely, a larger V1 could mean that each neuron integrates across a smaller visual field, increasing visual resolution generally and reducing responsiveness to the Ebbinghaus illusion.

That makes a pretty neat explanation of that effect (probably too neat and simple, but a good working hypothesis), but leads us on to another question. How do differences in the size of V1 come about? What factors determine the spatial extent of the primary visual cortex determined? There is considerable variation in this parameter across individuals, as assessed by neuroimaging or by post mortem cytoarchitecture (as in the diagram, showing the extent of V1, labelled as 17 and of V2, labelled as 18, in eight individuals). Is the extent of V1 genetically determined or more dependent on experience?

The heritability of the extent of V1 itself has not been directly studied, to my knowledge, but the surface area of the occipital lobe (encompassing V1 and other visual areas) is moderately heritable (h2 between 0.31 and 0.64 in one study). This is supported by a more recent twin study, which used genetic correlations to parcellate the brain and also found that the surface area of the entire occipital lobe is heritable, largely independently of other regions of the brain. (Another reason to expect the extent of V1 to be heritable is that it is very highly correlated (r=0.63) with the peak gamma frequency of visual evoked potentials as measured by EEG or MEG. This electrophysiological parameter is a stable trait and has itself been shown to be extremely highly heritable (h2=91%!)). Size and shape of cortical areas also vary between inbred mouse strains, demonstrating strong genetic effects on these parameters.

Interestingly, cortical thickness and cortical surface area are independently heritable. This is consistent with the radial unit hypothesis of cortical development, which suggests that the surface area will depend on the number of columns produced while the thickness will depend on the number of cells per column. These parameters are likely affected by variation in distinct cellular processes.

What could these processes be? What kinds of genes might affect the surface area of V1? One class could be involved in early patterning of the cortical sheet. A kind of competition between molecular gradients from the front and back of the embryonic brain determines the relative extent of anterior versus more posterior cortical areas. Mutations affecting these genes in mice can lead to sometimes dramatic increases or decreases in the extent of V1 (and other areas). A negative correlation that has been observed between size of V1 and size of prefrontal cortex in humans might be consistent with such an antagonistic model of cortical patterning. This mechanism establishes the basic layout of the cortical areas, but is only the first step.

The full emergence of cortical areas depends on their being innervated by axons from the thalamus. For example, axons from the dLGN release an unidentified factor that affects cell division in V1, driving the expansion of this area. The size of the dLGN is thus ultimately correlated with that of V1. In addition, the maturation of V1, including the emergence of patterns of gene expression, the local cellular organisation and even the connectivity with other cortical areas all depend on it being appropriately innervated. Variation in genes controlling this innervation could thus indirectly affect V1 size.

Axons from the dLGN are specifically guided to V1 by molecular cues, though the identity of these cues remains largely mysterious. For example, my own lab has shown – in studies of a line of mice with a mutation in an axon guidance factor, Semaphorin-6A – that even if dLGN axons are initially misrouted to the amygdala, they eventually find their way specifically to V1 and are even able to evict interloping axons from somatosensory thalamus, which had invaded this vacant territory. Not all the misrouted axons make it to V1, however, and many that do not eventually die. The end result is that the dLGN is smaller than normal and V1 is also smaller. I am not suggesting that this specific scenario contributes to variation in V1 size in humans but it illustrates the general point that the number of dLGN axons reaching V1 is another factor that will affect its ultimate size.

Whatever the mechanisms, the studies by Rees and colleagues clearly demonstrate considerable variation in subjective visual experience across the population and provide a plausible explanation for this in a heritable variation in brain structure. So, the short answer to the question in the title is most probably “No”. (And the long answer is already way too long, so I’ll stop!)