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The Bridge that could not..

16 Dec

 

 

nobridge

 

I have heard it said “if you want friends, do not build walls, build bridges”. But if you have ever felt depressed or under stress, you may have noticed that you did not really feel very sociable.  In fact, you may remember that you avoided being around people. You may even recall how stress impaired your thinking and planning. We tend to become myopic, or near sighted and any task undertaken can seem very energy demanding.

I have been reading an article recently that explains how this experience is actually a part of a neurobiological process ; one that is common not only for times of stress and depression, but it also appears to have a common involvement in most dementias.

You see, the bridgework of social engagement is much like the bridgework that can be found between neurons of our brains.  This bridgework aligns neurons across the a signalling gap between downstream neurons.  The terminal end of one firing neuron (presynapse) communicates with the dendrite (postsynapse)  of the next neuron through a gap known as a synapse.

synapse

synbridge

The alignment of neurons is an important feature for effective communication downstream.  Researchers discovered a structure protein known as Nectin-3 that maintains this alignment to secure connections in place.  Now, what has been found is that when mice were placed in a stressful environment, there was a significant reduction in Nectin-3 in their brains.  This also correlated with the avoidance behaviour observed in these mice from the stress induced.  In order to be certain of this relationship, other experiments were designed to restore  fibronectin-3, which resulted in increased cognitive function and improved  socialization in mice.

When the scientist explored the mechanism behind nectin-3 reduction, an enzyme known as MMP-9 was identified.  During times of stress, high glutamate levels prompt the release of this enzyme which degrades  nectin-3 protein. I think of this as Military Police (MP) that lose their role as peacekeepers, causing mass chaos.

mpshadow

Normally, this enzyme has an important role, probably in modifying memory like fine tuning a piano to the right tone.  However, stress clearly permits a runaway mechanism to hinder our social interaction and capacity to think clearly.

 

I invite you to read this article below.


Stress Management Makes Us Antisocial Due To Severed Synapses: New Finding Opens Window For Disorder Treatment

grouchy
If you find yourself avoiding human interaction when you’re stressed, be sure to thank an enzyme in your brain. greg westfall, CC BY 2.0

The people who can carry on amiable conversation while also fighting a war inside their heads are few and far between. When we get stressed, we shut down.We recede from the social sphere, if only to count to 10, before rejoining the group with a clearer frame of mind. But what, exactly, is going on between our ears when all this is happening?

New research from the Brain Mind Institute at École polytechnique fédérale de Lausanne (EPFL), in Switzerland, suggests the neural mechanism that makes stress a precursor to antisocial behavior happens at the synaptic level. Specifically, there is a disruption between a key enzyme and a set of proteinsnecessary for sociability. Keeping that relationship intact could open important doors for the treatment of psychiatric disorders.

There’s a type of protein whose main function in the brain is to keep neurons stuck together. They’re called adhesion proteins, and one in particular, the nectin-3 adhesion protein, has been found in prior research to play a vital role in the preservation of cognitive functions. In rats with chronic stress, researchers recently found nectin-3 levels were substantially lower.

In looking for possible causes of the decrease, the researchers ended up at the enzyme MMP-9, known for its role in protein degradation. What they found when they looked at MMP-9 activity in the brain was that during episodes of chronic stress, when the neurotransmitter glutamate is released, the receptors responsible for memory and synaptic plasticity activated MMP-9. Literally like scissors, the enzyme cut the nectin-3 proteins.

“When this happens, nectin-3 becomes unable to perform its role as a modulator of synaptic plasticity” explained lead author and Brain Mind Institute professor Carmen Sandi in a statement. The end result for the rats was decreased sociability, avoidant behavior, and impaired memory and understanding.

By contrast, when EPFL researchers and a team of Polish scientists tried to reverse the effect — in other words, boost sociability through nectin-3 restoration — they found in in vitro and in vivo models that these external treatments yielded positive effects. Cognitive skills improved and memory returned. “The identification of this mechanism is important because it suggests potential treatments for neuropsychiatric disorders related to chronic stress, particularly depression,” Sandi said.

The research is admittedly early for any clinical application. So far, no drugs have been developed using nectin-3 as their primary target. Sandi and her team hope the findings can be repeated in future studies. Given the success with MMP-9, they also hope to exploit its benefits for other neurological diseases, like amyotrophic lateral sclerosis or epilepsy.

“This result opens new research avenues on the still unknown consequences of chronic stress,” Sandi said.

Source: Sandi C, et al. Nature Communications. 2014.

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