Previously, most of these cells, known as subplate neurons, were thought to die off shortly after development, leaving behind 10 to 20 percent of the original fleet as nonfunctional remnants. Several tests conducted by a pair of researchers at the Baylor College of Medicine in Houston, however, revealed that the leftover neurons are not just vestiges but electrically active messengers that can send and receive signals to and from any of the six layers of the cerebral cortex (the brain's outermost layer, which is essentially the brain's central processing unit).
The function of subplate neurons have yet to be determined, but the study's senior author, Michael Friedlander, chair of Baylor's department of neuroscience, speculates that it is possible they can be coaxed to reprise their fetal role of developing proper circuits between neurons to possibly rewire and repair the cortex after a brain injury.
During development, subplate neurons serve as bridges and scaffolding while connections are established between neurons in the cortex and other cell populations in the thalamus, a midbrain structure responsible for sensory processing, motor control and consciousness. When subplate cells are damaged, the normal pattern of developmental activity in the cortex is disrupted and there are multiple visual processing deficits. According to Friedlander, binocular vision (the ability to see a single image with two eyes) is blocked as is the ability to discern the orientation of visual stimuli.
In the rat brain, during normal development these cells begin to disappear shortly after birth and the trend continues for about three weeks at which point their levels plateau. The remaining subplate neurons live in a narrow band of space in the cortex between the six-sublayers of gray matter (made up mostly of cell bodies) and the white matter (neuronal projections and support cells that connect to other cells in structures deeper in the brain). "You have to go find them," Friedlander says, about their hard-to-access residence.
After Friedlander's former student Juan Torres-Reveron, now a neurosurgical resident at Yale University, tracked down a few of the neurons in a slice of rat brain, the team set out to determine whether they were still functional. The answer: "Yes," Friedlander says, adding that the cells still showed electrical activity. "They are very healthy, card-carrying neurons."
A few more tests proved that the cells maintained the structure of normal neurons with their internal processes intact. Following their axons (the fingerlike protrusions that send signals away from the cell body), the researchers could see that these neurons communicate with cells throughout the cortex. "They are in circuit in the cortex; they are not just sitting there by themselves," Friedlander says. "At least theoretically, they are strategically positioned to talk to all the layers of the cortex." Further, the cells showed that they could engage in synaptic plasticity in the synapses between each of their axons and a cortical cell. (A synapse is the space between neurons through which information is exchanged. Synaptic plasticity is a strengthening or weakening of communication between two neurons and is thought to underlie learning and memory.)
"In my mind, the most interesting possibility is that they continue to play a role in regulating plasticity in the adult cortex," says Anirvan Ghosh, a professor of biology at the University of California, San Diego. He notes that the neurons could facilitate the exchange of information between the hippocampus (the seat of short-term memory formation) and the cortex, where long-term memory is believed to be stored.
The researchers speculate that the hippocampus is the source of inputs for subplate cells in the human brain but are not certain, because they only examined cortical slices from rat brains.
But, given their strong link to cortical cells, Friedlander is optimistic it will one day be possible to manipulate them to reverse cortex damage. "Perhaps we could get these cells to recapitulate their role in setting up connections in a brain where that might be useful," he says. "However, it may be that even if we could reprogram these cells…, the sheer number is not sufficient" to repair any sustained damage.
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