• European Marine Science
• 10. No inequality close
• eLife close

eLife digest Every task that an animal performs, even a simple one, typically requires numerous signals to pass across complex networks of cells called neurons. These networks develop early in an animal’s life, beginning when progenitor cells called neural stem cells divide over and over to produce new cells. Specific molecular signals then induce these new cells to become different types of neurons. However, in many animals, it is poorly understood what these critical molecular signals are and how they work. Fruit flies, for example, have a network of neurons that control how they navigate when flying. The same type of progenitor cell gives rise to at least four types of neurons in this network; these progenitor cells make an increasing amount of a protein called Eyeless as they age. Sullivan et al. have now specifically disrupted production of the Eyeless protein in the progenitor cells, and found that this altered the relative numbers of navigation neurons. The fruit flies had too many of some types of navigation neurons and too few of others. Fruit flies normally navigate in a variety of directions relative to the sun, which may allow them to disperse and find food. This was not the case in experiments where the production of Eyeless was briefly disrupted when the flies were larvae. In these experiments, the adult flies tended to head towards a bright light (that represented the sun) much more often than normal, which would presumably keep them from dispersing effectively. This was true even if the disruption of Eyeless was not long enough to change the numbers of neuron types, showing the protein is important in determining both how these navigation neurons form networks, and whether they are born at all. A better understanding of the complexities of how healthy networks of neurons develop may give scientists more insight into what goes wrong during human developmental disorders that affect the brain. In theory, it may also someday lead to tools that can help to repair the brain if it is damaged. The insect central complex (CX) is a conserved brain region containing 60 + neuronal subtypes, several of which contribute to navigation. It is not known how CX neuronal diversity is generated or how developmental origin of subtypes relates to function. We mapped the developmental origin of four key CX subtypes and found that neurons with similar origin have similar axon/dendrite targeting. Moreover, we found that the temporal transcription factor (TTF) Eyeless/Pax6 regulates the development of two recurrently-connected CX subtypes: Eyeless loss simultaneously produces ectopic P-EN neurons with normal axon/dendrite projections, and reduces the number of E-PG neurons. Furthermore, transient loss of Eyeless during development impairs adult flies’ capacity to perform celestial navigation. We conclude that neurons with similar developmental origin have similar connectivity, that Eyeless maintains equal E-PG and P-EN neuron number, and that Eyeless is required for the development of circuits that control adult navigation.

eLife digest The world around us changes all the time, and the brain must adapt to these changes. This process, known as neuroplasticity, peaks during development. Abnormal sensory input early in life can therefore cause lasting changes to the structure of the brain. One example of this is amblyopia or ‘lazy eye’. Infants who receive insufficient input to one eye – for example, because of cataracts – can lose their sight in that eye, even if the cataracts are later removed. This is because the brain reorganizes itself to ignore messages from the affected eye. Does the adult visual system also show neuroplasticity? To explore this question, Binda, Kurzawski et al. asked healthy adult volunteers to lie inside a high-resolution brain scanner with a patch covering one eye. At the start of the experiment, roughly half of the brain’s primary visual cortex responded to sensory input from each eye. But when the volunteers removed the patch two hours later, this was no longer the case. Some areas of the visual cortex that had previously responded to stimuli presented to the non-patched eye now responded to stimuli presented to the patched eye instead. The patched eye had also become more sensitive to visual stimuli. Indeed, these changes in visual sensitivity correlated with changes in brain activity in a pathway called the ventral visual stream. This pathway processes the fine details of images. Groups of neurons within this pathway that responded to stimuli presented to the patched eye were more sensitive to fine details after patching than before. Visual regions of the adult brain thus retain a high degree of neuroplasticity. They adapt rapidly to changes in the environment, in this case by increasing their activity to compensate for a lack of input. Notably, these changes are in the opposite direction to those that occur as a result of visual deprivation during development. This has important implications because lazy eye syndrome is currently considered untreatable in adulthood. Sensory deprivation during the post-natal ‘critical period’ leads to structural reorganization of the developing visual cortex. In adulthood, the visual cortex retains some flexibility and adapts to sensory deprivation. Here we show that short-term (2 hr) monocular deprivation in adult humans boosts the BOLD response to the deprived eye, changing ocular dominance of V1 vertices, consistent with homeostatic plasticity. The boost is strongest in V1, present in V2, V3 and V4 but absent in V3a and hMT+. Assessment of spatial frequency tuning in V1 by a population Receptive-Field technique shows that deprivation primarily boosts high spatial frequencies, consistent with a primary involvement of the parvocellular pathway. Crucially, the V1 deprivation effect correlates across participants with the perceptual increase of the deprived eye dominance assessed with binocular rivalry, suggesting a common origin. Our results demonstrate that visual cortex, particularly the ventral pathway, retains a high potential for homeostatic plasticity in the human adult.