UCSF scientists report that they were able to prompt a new period of "plasticity," or capacity for change, in the neural circuitry of the visual cortex of juvenile mice. The approach, they say, might some day be used to create new periods of plasticity in the human brain that would allow for the repair of neural circuits following injury or disease.
The strategy which involved transplanting a specific type of immature neuron from embryonic mice into the visual cortex of young mice could be used to treat neural circuits disrupted in abnormal fetal or postnatal development, stroke, traumatic brain injury, psychiatric illness and aging.
Like all regions of the brain, the visual cortex undergoes a highly plastic period during early life. Cells respond strongly to visual signals, which they relay in a rapid, directed way from one appropriate cell to the next in a process known as synaptic transmission. The chemical connections created in this process produce neural circuitry that is crucial for the function of the visual system. In mice, this critical period of plasticity occurs around the end of the fourth week of life.
The catalyst for the so-called critical period plasticity in the visual cortex is the development of synaptic signaling by neurons that release the inhibitory neurotransmitter GABA. These neurons receive excitatory signals from other neurons, thus helping to maintain the balance of excitation and inhibition in the visual system.
In their study, published in the journal Science, (Vol. 327. no. 5969, 2010), the scientists wanted to see if the embryonic neurons, once they had matured into GABA-producing inhibitory neurons, could induce plasticity in mice after the normal critical period had closed.
The team first dissected the immature neurons from their origin in the embryonic medial ganglionic eminence (MGE) of the embryonic mice. Then they transplanted the MGE cells into the animals' visual
|Contact: Jennifer O'Brien|
University of California - San Francisco