Fear memories and neuronal disorders

Rapid gene expression and DSBs

In a research study, it was found that the neuronal activity induced DNA double strand breaks (DSBs) to cause a change in neuronal activity regulated genes, when an organism is exposed to new sensory experience due to change in organism's external environment. That is a process of quick access to store genetic instructions as store memories.

Neuronal damage

But Li-Huei Tsai, the Picower professor of neuroscience found in her lab studies that fear memories induced repeated DSBs causes severe neuronal damage results neurological diseases causing neurodegenerative disorders impacting learning and memories. As routinely repair process of breaks become flawed and fragile with age, as repair mechanism falters.

In a research article Aging brain initiative, Tsai says, "We wanted to understand exactly how widespread and extensive this natural activity is in the brain upon memory formation because that can give us insight into how genomic instability could undermine brain health down the road," "Clearly, memory formation is an urgent priority for healthy brain function, but these new results showing that several types of brain cells (including Glia called astrocytes), break their DNA in so many places to quickly express genes is still striking." It was found that Glia DSBs response to hormone glutocorticoids, secreted in response of stress in fear conditioning, shows robust transcriptional response of glia to stress through hormone.

Brain sites of fear memories 

Author in their study found that creation of fear memories doubled the number of DSBs in variety of cell types in prefrontal cortex and hippocampus regions essential for formation and storage of conditioned fear memories, affecting more than 300 genes in each region for making synaptic connections due increased transcriptionally induced loci, a phenomenon called 'synaptic plasticity'. So such new groups of neurons connected together cause formation of new memories, called engrams. 

 

Damages due to frequent DSBs

The researchers wrote, 'Overall we have identified sites of DSBs at genes important for neuronal and glial functions, suggesting that impaired DNA repair of these recurrent DNA breaks which are generated as part of brain activity could result in genomic instability that contribute to aging and disease in the brain'.

*This blog is inspired by the MIT news from Picower institute for learning and memory. Many more research paper links are also thankfully inserted in blog, from public domain publication for detail study if needs. Graphic is by blog author.