How brain learns new skills

The skills needed to perform any activities are stored in the brain as procedural memories. Researchers from the Gladstone Institutes uncovered how a special type of neuron improves the efficiency of this type of learning. The scientists wanted to show how the specialized brain cells, called fast-spiking interneurons, cause movement disorders, such as Tourette's syndrome, dystonia, and dyskinesia.

The team, led by Gladstone Senior Investigator Anatol C. Kreitzer, PhD, was trying to understand the basic mechanisms of the basal ganglia, which are a group of interconnected neurons in the brain that control movement and are associated with decision-making and action selection. Fast-spiking interneurons represent only about 1 percent of the neurons in that brain region, but are known to have an outsized role in organizing the circuit activity.

The leading hypothesis in the field was that these interneurons were involved in motor control, and that their loss might be related to movement disorders. They discovered that the interneurons are much more important for learning and memory, and potentially more closely related to psychiatric disease than movement disorders.

The team found that the interneurons play a fundamental role in brain plasticity, which is the brain's ability to strengthen or weaken connections between neurons. By doing so, the brain can store information and procedural memory.

The fast-spiking interneurons act like gatekeepers for plasticity. They restrict when plasticity can occur, meaning that they can prevent changes in the connection strength between neurons. This is crucial for learning and memory and, more specifically, for enabling the basal ganglia to remember how to perform tasks.

In other parts of the brain, these same neurons are known to be crucial for processing sensory input, such as vision or touch, and their dysfunction is associated with bipolar disorder and schizophrenia. Fast-spiking interneurons could be a key factor in controlling the efficiency of the learning process in those systems as well.
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Brain cells may prevent Parkinson's disease

A Norwegian study shows that impairment in mitochondria may actually protect the brain in Parkinson's disease. Mitochondria are microscopic power stations found inside human cells. They convert foodstuffs into fuel, providing the required energy. Studies in brain tissue from individuals with Parkinson's disease showed that an essential component of the mitochondrial energy generators, called respiratory complex-I, becomes impaired in an area of the brain called the "substantia nigra" .

A new study from the University of Bergen (UiB), in Norway, in collaboration with the University of Cambridge, shows that the function of mitochondria, the microscopic powerhouses of the cell, is altered throughout the entire brain of individuals with Parkinson's disease. This new study shows that complex I deficiency is a global phenomenon in the brain of people with Parkinson's disease, and is found indiscriminately in both affected and healthy brain regions.

 Intriguingly, brain cells (neurons) with decreased complex I levels are significantly less likely to contain Lewy bodies, the abnormal protein-aggregates that characterize Parkinson's disease. These discoveries suggest that, contrary to mainstream theory, mitochondrial complex I deficiency may not be entirely deleterious for the brain in Parkinson's disease. It is possible that complex I deficiency is part of a compensatory regulation attempting to protect the brain in Parkinson's disease.

Parkinson's disease is one of the most common brain disorders. It affects millions of people worldwide. It starts after the age of 50 and causes a combination of debilitating symptoms, including shaking and other abnormal movements, loss of balance, low blood pressure, bladder and intestinal problems, sleeping disorders and dementia. Presently, there is no cure and patients die prematurely due to increasing disability.
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Antidepressants medications increase the risk of death

Antidepressants are psychiatric medications given to patients with depressive disorders to alleviate symptoms. The medications may be used for social anxiety disorder and dysthymia.

Antidepressant medications increase the risk of death, brain serotonin affects mood, the most commonly used antidepressant treatment for depression blocks the absorption of serotonin by neurons. The major organs in the body - the heart, kidneys, lungs and liver use serotonin from the bloodstream.

Antidepressants block the absorption of serotonin in these organs, the medications increase the risk of death by preventing multiple organs from functioning properly. Antidepressant users also had higher risk of strokes and heart attacks.

The researchers discovered that antidepressants are not harmful for people with cardiovascular diseases such as heart disease and diabetes because antidepressants have blood-thinning effects that are useful in treating such disorders but it is harmful for people with healthy heart.
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Smoking causes anxiety and phobia

Smoking may make smokers more vulnerable to suffering from phobias and other types of chronic fear like post-traumatic stress disorder PTSD.

Scientists have discovered that smoking tobacco can impair the brain's ability to repress fear-related memories, making smokers unable to deal with fear and anxiety after a traumatic experience.

Dangerous chemicals in tobacco may interfere with neurotransmitter and neurons in the brain. Neurotransmitters are responsible for controlling fear.

Smoking is a common habit among people who suffer from post traumatic stress disorder PTSD. The more people smoke, the less they were able to inhibit fear response.

Smoking impairs the repression of fear related memories, when there is no danger. Long-term smoking leads to higher deficit in inhibiting fear responses.

Smoking changes neurotransmitter balances in the brain, which are necessary for successful safety learning.
Enhancing dopamine in the brain and putting an end to tobacco smoking can put an end to fear associated with smoking.
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Effects of sleep deprivation on memory formation

Nicolette Ognjanovski of the Department of Molecular, Cellular and Development Biology at Michigan and colleagues discovered that sleep deprivation interfere with the rhythm of neuronal firing in hippocampus part of the brain that is responsible for formation of long-term memories.

National Sleep Foundation recommend 7 to 9 hours of sleep per night for sound health.  Sleep deprivation prevents memory formation because it prevents brain from converting short-term memory to long-term memory.

The researchers examined the hippocampal of mice and discovered that those that had sufficient sleep displayed better sleep-related oscillations than sleep-deprived mice.

This discovery shows that memories are not stored in one cell, but distributed through the network. The dominant oscillatory activities for learning is being controlled by cells in hippocampus.