Chemical messenger in brain could point to better treatments for anxiety

I suppose your doctor could treat your anxiety this way rather than getting you 100% recovered but the best solution would be 100% recovery. 

Post stroke depression(33% chance), post stroke anxiety(20% chance), and posttraumatic stress disorder(23% chance) all part of the same inaction toward 100% recovery.  

 

When  this CRF antagonist was tested in mice in June 2016 did your doctor do ONE DAMN THING to get human testing done? Or did incompetence reign and NOTHING WAS DONE?

Hormone causes decline in cognition after social stress June 2016

The latest here:

Chemical messenger in brain could point to better treatments for anxiety

MedicalXpress Breaking News-and-Events|June 5, 2020

New research by a University of Alberta neuroscientist reveals more about how the mechanism the brain uses to regulate our response to stress could lead to better treatments for anxiety.

Bill Colmers and his team discovered that two chemical messengers—corticotropin-releasing factor (CRF) and neuropeptide Y (NPY)—work in a synchronized opposition to one another to remodel and rewire neurons in a part of the brain responsible for emotions, called the amygdala, as part of the body's natural response to stress.

The research not only shows the change is occurring in the amygdala, but also reveals the process can be manually reversed, said Colmers.

"Anxiety disorders represent a huge unmet medical need. Any new information we can gather in relation to understanding the mechanisms involved with anxiety provides new targets for possible drug development," said the U of A professor of pharmacology.

Where senses meet memories

The amygdala is a small, almond-shaped structure in the brain where information from our senses is combined with our memories and experiences.

"When you see a car, it's just a car—unless you were previously T-boned by a red convertible. Then, thanks to your amygdala, that red convertible will elicit negative feelings in you," explained Colmers.

"We see abnormal functioning in the amygdala in individuals who suffer from conditions such as anxiety, depression and post-traumatic stress disorder. It's an interesting part of the brain that's responsible for many essential processes, and it's where we see the NPY and CRF in action."

Better control

In previous research, Colmers' team showed that NPY reduced anxiety in rats. Repeated exposure to NPY made the animals more resilient to stress for weeks or even months, and the team was able to identify the exact mechanism that elicits this response.

Building on this research, Colmers' team observed that the body's ability to react to a stress or threat is the result of CRF increasing the number and length of dendrites (or branches) found in neurons located in the amygdala. The lengthening and expansion of the neural network allows the brain to increase its signaling power and trigger the rest of the body to get ready to respond.

But the longer and more often our brains are in hyperdrive, which makes us feel anxious, the more difficult it is to get back to a healthy state.

Because it's harmful for our bodies to be in this amped-up state for too long, NPY is normally released in our brains once the perceived threat has passed.

The NPY has the opposite effect of CRF and reduces or shrinks the number and length of the dendrites, effectively telling the brain to "stand down" from the alert and let the body relax.

Colmers' research also revealed that one of the first steps in getting back to this relaxed state begins when NPY binds with the Y5 receptor, which occurs on the surface of a neuron. This binding activates the pathway that reconfigures the dendrites. According to Colmers, understanding each step in the pathway is important because each represents a potential target for drug development.

"My research areas have varied throughout my career and included anxiety, obesity, cachexia and energy balance. However, the common thread that has run through all of it is my friend neuropeptide Y," said Colmers.

"While we definitely answered some of our questions with this latest study, it also revealed new questions, as the work was only conducted in male rats. The very important next question is whether this works the same in females."

Colmers, a member of the Neuroscience and Mental Health Institute, and his collaborator Janice Urban from the Rosalind Franklin University of Medicine and Science, published the study, "Contribution of NPY Y5 Receptors to the Reversible Structural Remodeling of Basolateral Amygdala Dendrites in Male Rats Associated With NPY-Mediated Stress Resilience," in the Journal of Neuroscience.

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Hormone causes decline in cognition after social stress

Your social stress is going to go thru the roof post-stroke after you lose most, if not all of your friends. What the hell is your doctor doing to combat that stress? I bet nothing, especially since nothing was done to stop the neuronal cascade of death.

Hormone causes decline in cognition after social stress

How does stress influence our cognitive performance? This is an issue scientists at the Max Planck Institute of Psychiatry in Munich have been dealing with. For the first time, they have identified a brain mechanism that explains why the cognitive performance of mice is reduced after being exposed to social stress. This finding will help to improve our understanding and treatment of disorders involving cognitive decline in humans.

The prefrontal cortex is a brain region responsible for mental activity, perception and recognition, in short for cognition. No matter whether we want to respond flexibly to certain situations, have to do several things simultaneously or make plans for the future – none of this would be possible without our prefrontal cortex. However, these processes are very susceptible to stress. Our anger resulting from being stuck in a traffic jam in the morning or trouble with the boss at lunchtime causes social stress. The so-called Corticotropin-releasing factor (CRF) controls our reaction in the prefrontal cortex; however, which exact role it plays was not clear previously.
Therefore, scientists at the Max Planck Institute of Psychiatry tested what exactly happens in the brain during such stressful periods in mice. They exposed mice to acute social stress and observed a cognitive decline in the rodents some hours later. The mice were not able to show cognitive flexibility in a test maze or remember the chronological sequence of events they had learned before.
In order to find out more about the role CRF plays in this process, the scientists blocked the action of the peptide using a drug, a so-called CRF antagonist. This time, the performance of the mice did not decrease several hours after the stressful event; they were able to perform the required tasks as successfully as they had done without stress.
"The crucial point is that we were able to identify the mechanism responsible for the reduction in performance after stress," Mathias Schmidt, research group leader and head of the study, summarizes. Understanding this mechanism is important in order to comprehend how stress affects our thinking, feeling and perceiving. Since the mechanisms underlying the flexibility in perception and memory performance are similar in mice and humans, it is very probable that the findings are transferable to humans. Many psychiatric diseases such as depression or schizophrenia are accompanied by impaired cognitive function. With their findings, the scientists hope to develop approaches for novel treatments and medications.

Explore further: Homer prevents stress-induced cognitive deficits: A lack of Homer-1 in the brain causes learning problems in mice

More information: Andrés Uribe-Mariño et al. Prefrontal cortex corticotropin-releasing hormone receptor 1 conveys acute stress-induced executive dysfunction, Biological Psychiatry (2016). DOI: 10.1016/j.biopsych.2016.03.2106

Journal reference: Biological Psychiatry