Pain sensing nerves help fight skin infection

A recent discovery revealed that pain-sensing nerves help fight skin infections and prevent its spread, suggesting a new type of immunity. "These pain-sensing nerves can detect pathogens, and for the first time, we've shown that they activate an immune response and also signal protective immunity in sites adjacent to the infection. This demonstrates that the immune and nervous systems work synergistically for host defence. These findings also could have important implications for developing more specific therapies for autoimmune skin diseases like psoriasis," said the senior author of the study.

Until about a decade ago, the pain was thought to have evolved as a way for your body to tell you to stay away from a particular stimulus or to signal a problem with its function, like an injury. More recently, however, researchers have shown that it may play an important role in immunity against some pathogens.

In the study, the first author collaborated with neurobiology professors and pain experts, to develop an optogenetic mouse model where pain-sensing neurons in the skin could be activated by shining blue light.

They first showed that just activating these neurons released a small protein called CGRP, which recruited different types of immune cells to the site. This suggested that neurons detecting skin pathogens on their own kickstart an immune response even before sentry immune cells could.

Then in the same mouse model, they infected the animals with either Candida albicans, a fungus that causes candidiasis, commonly known as thrush, or Staphylococcus aureus, a common bacterium that can turn deadly under certain conditions.

Using optogenetics and chemical nerve blockers, the researchers showed through a series of elegant experiments that when the fungus infected the skin at one location, the nerves not only detected and initiated an immune response to fight the infection but also sent a signal toward the spinal cord.
The researchers called this new nerve-driven protective mechanism "anticipatory immunity."

"The advantage of involving the nervous system is that it can communicate information across space in a span of milliseconds, compared to hours or days for the immune cells to do the same function. It's the difference between sending Paul Revere to warn of the British advance and sending a telegram to do the same," said the first author of the study.

He said that while it remains to be seen how the findings translate to humans, they have interesting implications for autoimmune diseases of barrier tissues like the skin or gut.

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Scientists Identify The Physical Source of Anxiety in The Brain

We're not wired to feel safe all the time, but maybe one day we could be.

A 2018 study investigating the neurological basis of anxiety in the brain has identified 'anxiety cells' located in the hippocampus – which not only regulate anxious behaviour but can be controlled by a beam of light.

The findings, so far demonstrated in experiments with lab mice, could offer a ray of hope for the millions of people worldwide who experience anxiety disorders (including almost one in five adults  in the US), by leading to new drugs that silence these anxiety-controlling neurons.

"We wanted to understand where the emotional information that goes into the feeling of anxiety is encoded within the brain," says one of the researchers,a neuroscientist.

To find out, the team used a technique called calcium imaging, inserting miniature microscopes into the brains of lab mice to record the activity of cells in the hippocampus as the animals made their way around their enclosures.

These weren't just any ordinary cages, either.

The team built special mazes where some paths led to open spaces and elevated platforms – exposed environments known to induce anxiety in mice, due to increased vulnerability to predators.

Away from the safety of walls, something went off in the mice's heads – with the researchers observing cells in a part of the hippocampus called ventral CA1 (vCA1) firing up, and the more anxious the mice behaved, the greater the neuron activity became.

"We call these anxiety cells because they only fire when the animals are in places that are innately frightening to them," explains senior researcher.

The output of these cells was traced to the hypothalamus, a region of the brain that – among other things – regulates the hormones that controls emotions.

Because this same regulation process operates in people, too – not just lab mice exposed to anxiety-inducing labyrinths – the researchers hypothesis that the anxiety neurons themselves could be a part of human biology, too.

"Now that we've found these cells in the hippocampus, it opens up new areas for exploring treatment ideas that we didn't know existed before," says one of the researcher.

Even more exciting is that we've already figured out a way of controlling these anxiety cells – in mice at least – to the extent it actually changes the animals' observable behaviour.

Using a technique called optogenetics to shine a beam of light onto the cells in the vCA1 region, the researchers were able to effectively silence the anxiety cells and prompt confident, anxiety-free activity in the mice.

"If we turn down this activity, will the animals become less anxious?" the author said.

"What we found was that they did become less anxious. They actually tended to want to explore the open arms of the maze even more."

This control switch didn't just work one way.

By changing the light settings, the researchers were also able to enhance the activity of the anxiety cells, making the animals quiver even when safely ensconced in enclosed, walled surroundings – not that the team necessarily thinks vCA1 is the only brain region involved here.

"These cells are probably just one part of an extended circuit by which the animal learns about anxiety-related information," the author told,  highlighting other neural cells justify additional study too.

In any case, the next steps will be to find out whether the same control switch is what regulates human anxiety – and based on what we know about the brain similarities with mice, it seems plausible.

If that pans out, these results could open a big new research lead into ways to treat various anxiety conditions.

And that's something we should all be grateful for.

"We have a target," the neurosceintist explained . "A very early way to think about new drugs."

The findings were reported in a medical journal.



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Researchers discover 'anxiety cells' in brain

The neuroscientists have identified "anxiety cells" in the brains of mice, paving way for a potential treatment for humans suffering from anxiety disorders.

They found the cells inside a structure called the hippocampus.The hippocampus plays a well-known role in the brain's ability to form new memories and to help animals - from mice to humans - navigate through complex environments.

"We call these anxiety cells because they only fire when the animals are in places that are innately frightening to them," the researcher said.

"For a mouse, that's an open area where they are more exposed to predators, or an elevated platform," the researcher said.

The firing of the anxiety cells sends messages to other parts of the brain that turn on anxious behaviours, in mice, those include avoiding the dangerous area or fleeing to a safe zone, according to a study.

Though many other cells in the brain have been identified as playing a role in anxiety, the cells found in this study are the first known to represent the state of anxiety, regardless of the type of environment that provokes the emotion.

By turning the anxiety cells off and on using a technique called optogenetics that allows scientists to control the activity of neurons using beams of light, the researchers found that the anxiety cells control anxiety behaviours.

When the cells were silenced, the mice stopped producing fear-related behaviours, wandering onto elevated platforms and away from protective walls.

When the anxiety cells were stimulated, the mice exhibited more fear behaviours even when they were in "safe" surroundings.

"This is exciting because it represents a direct, rapid pathway in the brain that lets animals respond to anxiety- provoking places without needing to go through higher-order brain regions," said a researcher.

"Now that we have found these cells in the hippocampus, it opens up new areas for exploring treatment ideas that we didn't know existed before," said the researcher.

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Gene therapy in brain may stop binge drinking

Researchers at the University at Buffalo have found a way to change alcohol drinking behaviour in rodents, using the emerging technique of optogenetics - using light to stimulate neurons.

In the experiments, rats were trained to drink alcohol in a way that mimics human binge-drinking behaviour.

"By stimulating certain dopamine neurons in a precise pattern, resulting in low but prolonged levels of dopamine release, we could prevent the rats from binging. The rats just flat out stopped drinking," said Caroline E. Bass, assistant professor of pharmacology and toxicology in UB School of Medicine and Biomedical Sciences.

Interestingly, the rodents continued to avoid alcohol even after the stimulation of neurons ended, Bass added.

Researchers activated the dopamine neurons through a type of deep brain stimulation using a new technique called optogenetics.

"Optogenetics allows you to stimulate only one type of neuron at a time," said the study published in the journal Frontiers in Neuroscience.

"The results have application not only in understanding and treating alcohol-drinking behaviours in humans, but also in many devastating mental illnesses and neurological diseases that have a dopamine component," said Bass.

The findings are the first to demonstrate a causal relationship between the release of dopamine in the brain and drinking behaviours of animals.

"Research like this, which makes it possible to map the neuronal circuits responsible for specific behaviours, is a major focus of President Obama's Brain Research for Advancing Innovative Neurotechnologies initiative, known as BRAIN," concluded the study.

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