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Fall 2010 | Return to issue home
How Dendritic Arbors Stay in Shape
By Kristy Brady
In the nervous system, form plays a critical role in function. By looking at the shape of a neuron, you can intuit to a certain extent what that neuron does. But cells, including neurons, are not static. They are living units that experience wear and tear and morphological changes that accompany growth and development.
For example, you are born with a complete set of retinal ganglion cells, the neurons responsible for receiving visual information from your eyes’ photoreceptors and transmitting it to the appropriate regions of your brain. You do not grow more retinal ganglion cells as you age, so they need to last you your entire life. Furthermore, your eyes grow along with the rest of your body, so your retinal ganglion cells need to expand at exactly the right rate to keep pace with your growing eyes or your vision would suffer.
To do this, neurons undergo continual maintenance to keep the right shape while expanding and aging. Because form is so important, it makes sense that maintaining a neuron’s shape would be crucial. But what does this maintenance look like? Although we know a great deal about how shape corresponds to function, we know very little about how neurons establish and maintain their shape or “dendritic arbor”. That is the focus of Biology assistant professor Jay Parrish’s research.
Parrish uses the model organism Drosophila to study the genetic basis for dendrite morphogenesis. That is, how dendritic arbors initially develop and then maintain their functionally important pattern. Drosophila sensory neurons are ideal for this research because they have archetypal dendritic arbors that innervate the fly’s surface tissue. This is important because it means Parrish can use a confocal microscope to easily visualize the effects that different genetic variables have on dendritic arbors without sacrificing the fly. Thus he can look at the same neuron, in the same fly, over the entire lifespan of the fly.
A host of finer-scale questions follow the overarching dendrite morphogenesis question, such as: How, exactly, do neurons maintain an appropriate size and shape as their surroundings grow and change (as in the retinal ganglion cell example)? Do the same genes regulate maintenance during different developmental stages or do different genes regulate the different stages of a neuron’s life? Similarly, do different types of neurons use similar mechanisms to maintain their dendritic arbors, or are maintenance mechanisms specific to the type of neuron? And perhaps most intriguingly, can dendritic arbors be regenerated?
The obvious connection this research has to humans is how it might inform studies of neurological diseases, like Alzheimer’s disease and Parkinson’s disease, or disorders that can cause cognitive impairment, such as Down’s syndrome, or brain injuries due to severe traumatic events or repeated low-level trauma experienced in contact sports like football. For many neurological diseases, cognitive impairment stems not because dendritic arbors haven’t formed properly, but because they are not maintained properly over time. So if we understand how neuronal structure is maintained, it could be possible to develop the means of jump-starting malfunctioning maintenance machinery or augmenting the regulatory products produced by that machinery. In either case, the first step involves the basic research questions Parrish is addressing in his lab.
Fall 2010 | Return to issue home