Proper maturation of the visual cortex in mice, and possibly humans, depends on a maternal gene

החלק היותר גדול של מוחנו, מוקדש לעיבוד של אותות הראייה.
עכשיו מתברר שגן מסוים, שאותו אנו יורשים מאימותינו בלבד,
הוא האחראי להתפתחות התקינה של האיזור הזה במוח.
אמא יש רק אחת, והיא קובעת את הדרך שבה אנו רואים את

The copy of the gene Ube3a inherited from the mother—not the father—is
crucial to proper wiring of the visual cortex in mice after birth, a RIKEN
researcher and his American co-worker have found In human babies,
a defective maternal Ube3a gene causes a developmental condition
known as Angelman syndrome that leads to mental retardation, speech
impairment and brain seizures, and affects behavior. The researchers therefore
suggest that stimulating the silenced paternal gene at the right time of
development might be worth exploring as therapy for this syndrome.
Nerve cell wiring of the visual cortex of the brain occurs after birth, and is
then refined by experience. Typically, images are constructed
using signals from nerve cells that receive more input from one eye than
the other, an occurrence known as ocular dominance (OD). The balance
of OD displays plasticity; it can be altered, for instance, by temporarily blinding
one eye during the critical period of development when the interconnections
of nerve cells in the brain are susceptible to experience.
Masaaki Sato from the RIKEN Brain Science Institute, Wako, and Michael Stryker from
the University of California, San Francisco, confirmed in mice that by about four weeks
of age—their critical period of development—the presence of the Ube3a protein is mainly
restricted to the nucleus of nerve cells in the visual cortex of the brain; and it is dependent
on the maternal gene.
The researchers then investigated how the interconnections of the nerve cells could be
changed before, during and after the critical period. They tested these changes using
optical imaging, a technique that can provide information on activity in the brain. They
found that both maternal and paternal copies of the gene contributed to normal development
until the critical period. From this stage on, however, the maternal copy alone was active
and required for maturation of the cortical circuits. Without the maternal gene the visual
system did not rapidly adjust OD to the experience of having one eye briefly blinded during
the critical period. And afterwards, there was impairment of the ability to make the minor
wiring adjustments as the system matured.
“We now want to investigate how Ube3a participates in the maturation process of cortical
neuronal circuits,” Sato says. “The other direction [of our work] will be to screen genes or
compounds which have potential to restore the impaired plasticity of
Ube3a maternal-deficient mice.”