Astrocytes found to have a direct role in brain plasticity.


Astrocytes are the most abundant glial cells in the central nervous system and are involved in many roles in the brain including composing the blood-brain barrier, provision of nutrients to neurons, maintenance of extracellular ion balance, and damage repair to name a few.  Even though many new roles for astrocytes have been identified recently they are still sometimes overlooked as active participants in intercellular communication and information processing in the central nervous system, 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 state that 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 that when a person is born, their brains have a great deal of flexibility, which allows the immature brain to adapt to new experiences and organize its  neural circuits; as the brain matures this quality, known as plasticity, lessens.  Recent studies from the group showed that astrocytes are important for the development of the brain; however, very little is known as to 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.

Th current study shows that astrocytes produce a signalling protein called Chrdl1, which increases the number and maturity of connections between nerve cells, enabling 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 that these mice had a level of plasticity in their brains that was much higher than normal. Data findings show that adult mice with the Chrdl1 mutation had brain plasticity that looked very much like that of young mice, whose brains are still in early stages of development.

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

The team surmise their study shows that 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 and look for potential ways to use astrocytes as therapy.

Source: Salk Institute

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