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Blame it on the astrocytes
Date:7/11/2014

Rio de Janeiro, Brazil- In the brains of all vertebrates, information is transmitted through synapses, a mechanism that allows an electric or chemical signal to be passed from one brain cell to another. Chemical synapses, which are the most abundant type of synapse, can be either excitatory or inhibitory. Synapse formation is crucial for learning, memory, perception and cognition, and the balance between excitatory and inhibitory synapses critical for brain function. For instance, every time we learn something, the new information is transformed into memory through synaptic plasticity, a process in which synapses are strengthened and become more responsive to different stimuli or environmental cues. Synapses may change their shape or function in a matter of seconds or over an entire lifetime. In humans, a number of disorders are associated with dysfunctional synapses, including autism, epilepsy, substance abuse and depression.

Astrocytes, named for their star-like shape, are ubiquitous brain cells known for regulating excitatory synapse formation through cells. Recent studies have shown that astrocytes also play a role in forming inhibitory synapses, but the key players and underlying mechanisms have remained unknown until now.

A new study just published in the journal Glia and available online on July 11th, details the newly discovered mechanism by which astrocytes are involved in inhibitory synapse formation and presents strong evidence that Transforming Growth Factor Beta 1 (TGF β1), a protein produced by many cell types (including astrocytes) is a key player in this process. The team led by Flvia Gomes of the Rio de Janeiro Institute of Biomedical Sciences at the Federal University of Rio de Janeiro investigated the process in both mouse and human tissues, first in test tubes, then in living brain cells.

Previous evidence has shown that TGF β1, a molecule associated with essential functions in nervous system d
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Contact: Flávia Gomes
fgomes@icb.ufrj.br
55-219-980-22770
Publicase Comunicao Cientfica
Source:Eurekalert

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