There are times in an organism’s development when parts of the forming nervous system are particularly sensitive to changing inputs. Disrupting these critical periods can have lifelong effects on neuronal connectivity and brain function. For example, there is a critical period during childhood for language acquisition. And altered critical periods have been suggested to play a part in neurodevelopmental disorders, including autism spectrum disorder and schizophrenia. Critical periods have been extensively described in the visual system, but, until now, there has been less focus on non-sensory systems. Writing in Nature, Ackerman et al.close this gap. The authors identify a critical period for motor-circuit development in the fruit fly Drosophila melanogaster, and establish the cellular and molecular underpinnings of critical-period closure in this system.

During a critical period, neuronal connections can be reshaped in several ways. Ackerman et al. mainly address homeostatic plasticity, in which changes occur across an entire neuron — including in the size of structures called dendrites, which receive synaptic connections from other neurons, in synapse numbers and in the strength of electrical impulses transmitted by synapses.

These findings indicate that astrocytes regulate the timing of critical-period closure for the aCC/RP2 system, but not the potential for plasticity during this time. This is a key distinction, because it suggests that different mechanisms underlie the two phenomena.

The authors provide compelling evidence for the prominent role of astrocytes in regulating closure of a critical period. Astrocytes regulate aspects of critical-period plasticity in the mammalian visual system, including through the actions of the secreted proteins chordin-like 1 and hevin. 

The work also shows that the role of astrocytes in regulating critical periods extends to invertebrates, thus highlighting the centrality of these cells to nervous system development and maturation. It is becoming apparent that astrocytes and related cell types (collectively called glia) are master regulators of neuronal plasticity, particularly in the context of homeostatic and circuit changes. 


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