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Astrocytes found to have a direct role in brain plasticity.

Astrocytes are the most abundant glial cells in the central nervous system (CNS) known to be involved in many roles in the brain including the composition of the blood-brain barrier, provision of nutrients to neurons, maintenance of extracellular ion balance, and damage repair.  Even though many new roles for astrocytes have been identified they are still sometimes overlooked as active participants in intercellular communication and information processing in the CNS in part due to their lack of electrical excitability.  Now, a study from researchers the Salk Institute identifies a previously unknown role for astrocytes, namely helping to enable the brain’s plasticity, the ability of the brain to modify its connections, or re-wire itself.  The team states the findings could point to ways to restore connections that have been lost due to aging or trauma.  The study is published in the journal Neuron.

Previous studies show when a person is born, their brains have a great deal of flexibility, allowing the immature brain to adapt to new experiences and reorganize its neural circuits in a process known as brain plasticity.  As the brain matures plasticity lessens with more rigid neural circuits in place.  Recent studies from the group showed astrocytes are important for the development of the brain, however, very little is known about the role of astrocytes in the adult brain.  The current study investigates the role of astrocytes in the mature brain and identifies a signal made by astrocytes crucial for brain maturation.

The current study shows astrocytes produce a signaling protein called Chrdl1, responsible for increasing the number and maturity of connections between nerve cells to enable the stabilization of neural connections and circuits.  To further understand the role of Chrdl1, the team developed mouse models with the gene disabled by mutations. Results show these mice had a level of plasticity in their brains much higher than normal. Data findings show adult mice with the Chrdl1 mutation possessed levels of brain plasticity similar to young mice, whose brains are still in the early stages of development.

The lab explains in the developing brain immature synapses contain calcium-permeable AMPA glutamate receptors (AMPARs) subsequently replaced with GluA2-containing calcium-impermeable AMPARs as synapses stabilize and mature.  Results show this essential switch in AMPARs and neuronal synapse maturation is regulated by astrocytes.

The team surmises their study shows astrocytes, via the release of Chrdl1, are responsible for GluA2-dependent synapse maturation and thereby limit synaptic plasticity as the brain ages.  For the future, the researchers state they plan to dive deeper into the relationships between astrocytes, and neurons to look for potential ways to use astrocytes as therapy.

Source: Salk Institute

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