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Posts tagged ‘optogenetics’

SPEAK OUT! NewsBit . . . . . . . . . . . Depression Reversed in Mice

Depression Reversed in Mice

presented by

Donna O’Donnell Figurski

newsboy-thNOTE: This news is especially important for young brain-injury survivors because clinical application may take 10-20 years.

In a major advance in basic research of the brain, neuroscientists were able to reverse depression in mice by activating neurons storing a positive memory. The work was done by a team of brain scientists headed by Massachusetts Institute of Technology (MIT) Professor and Nobel Laureate, Dr. Susumu Tonegawa. This work on depression extended Dr. Tonegawa’s earlier work, on which I reported previously. The current research was done at the RIKEN-MIT Center for Neural Circuit Genetics.

The experiments were done on mice. (I have previously written why mice are good first models for humans.) Dr. Tonegawa’s team was able to use light to activate cells of the dentate gyrus, a part of the hippocampus – the area of the brain where memories are stored. They also showed that tagging a memory with a positive or negative feeling involved a pathway composed not only of neurons of the dentate gyrus, but also of neurons in two other areas of the brain: the nucleus accumbens and the basolateral amygdala.mouse-clipart-5

(The use of light to activate specific neurons is a powerful and relatively recent method called “optogenetics.” The mice are genetically engineered to allow the neurons that made new memories to be turned on by light. The light is supplied by implanting optical fibers near the desired neurons, in this case in the dentate gyrus of the mouse brain, and shining light from a laser through the fibers.)

When neurons storing a positive memory were light-activated in mice that showed the symptoms of depression, the mice no longer acted depressed. The depression had been reversed by turning on those neurons. Briefly activating the neurons storing a positive memory for five days and then stopping the trigger of activation (light) was also effective in reversing depression. This shows that the positive-memory neurons do not need to be continuously activated.

Current therapeutic drugs for the treatment of depression in humans act on all neurons of the brain. It is hoped that eventually drugs will be designed for specific neurons. Another approach to stimulate specific neurons is to use a kind of “pacemaker” that could be implanted in the brain. Such treatments would have fewer side effects. (Full story)

(Clip Art compliments of Bing.)

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SPEAK OUT! NewsBit . . . . . . . . Changing a Negative Feeling About a Memory

Changing a Negative Feeling About a Memory

newsboy-thThis is exciting, but complicated, basic research. Here I simplify the main experiments. Neuroscientists at the Massachusetts Institute of Technology (MIT) have identified a neuronal circuit in mice that associates a positive or negative feeling with a memory. In a tour de force of molecular studies of the brain, the researchers conducted experiments that provide considerable hope for future therapy in humans with syndromes like PTSD (post-traumatic stress disorder), anxiety, and depression. The scientists were able to turn a memory associated with a negative feeling into a memory that has a more positive feeling and vice versa.

(How relevant are studies done in mice? The mouse is an accepted animal model for humans. You might not expect it, but mice and humans are very similar genetically. The DNA sequences of the mouse and human chromosomes are known. Many mouse genes have sequences similar to human genes. They both code for proteins that have similar structures and do the same things. Because mouse and human genes are so similar, much of the underlying biology of mice and humans is also similar. Still there are differences. So until something has been shown to be true in humans, a scientist’s conclusions must be conservative. Most of the time, however, much is learned about humans from the mouse. It has become a convenient initial model for humans.)

The researchers at MIT engineered a virus that infects the mouse brain. They specifically infected either the hippocampus, the part of the brain that contains neurons that store contextual information about a memory (for example, the place), or the amygdala, the part of the brain that contains neurons that put a positive or negative emotional tag onto the memory. The engineered virus is essentially a dead-end. It doesn’t reproduce or harm the cell, but it does have an ability to cause infected neurons to make a light-sensitive protein – but only when the neuron is actively making a new memory. In this way, the researchers were able to make neurons involved in making a new memory sensitive to light. By implanting an optical fiber in the part of the brain that contained the light-sensitive neurons (i.e., in the hippocampus or in the amygdala), the scientists could use light to turn on these memory-making neurons at will. The general technique of using a light-sensitive protein to activate a cell is called “optogenetics.” When the light-sensitive neurons are activated by the researcher, the mice recall that memory with its associated positive or negative feeling. To make a memory with a positive feeling, male mice were allowed to mix with female mice. To make a memory having an associated negative feeling, mice were put into a special cage and given a mild electrical shock. For both kinds of memories, the neurons involved could be turned on by light.

The researchers then took the mice and put them into a cage with two compartments. When a mouse with a negative memory explored a particular compartment, the researchers turned on its bad-memory neurons by shining a laser into the optical fiber to activate those neurons. The mice “remembered” the bad feeling and avoided that compartment. When the experiment was done with the mice having a good memory, the mice preferred that compartment. These results were seen only when neurons of the hippocampus were activated. No change in mouse behavior was seen when amygdala neurons were activated. Whereas the amygdala is needed to add the positive or negative feeling to a memory, the researchers concluded that a memory with its associated feeling is stored in the hippocampus.

The researchers then asked if they could change a negative memory into a positive memory and vice versa. They took the male mice with the negative memory and mixed them with females to make a positive memory. When they used light to activate the bad-memory neurons, the positive feeling from mixing them with females dominated. Unexpectedly, those mice did not suddenly avoid the females when the researchers activated the bad-memory neurons. When the mice were put back into the cage with two compartments, they went randomly into both compartments, even when the researchers activated the bad-memory neurons with light. The bad memory was no longer causing them to avoid one of the compartments. The negative tag had been supplanted by the positive feeling. What happened to the first (negative) tag? Was it removed? Was it changed? This question is being investigated. When the experiment was reversed, the scientists found that the positive feeling became more negative.

This new research gives a molecular explanation for why emotion associated with a memory can be changed – the basis of current therapy. Dr. Susumu Tonegawa, who directed the research, believes that the amygdala has two kinds of neurons: neurons that can tag a memory with a positive feeling and other neurons that can tag a memory with a negative feeling. He wants to identify those two populations of cells and understand how they work at the molecular level. Such information will be valuable for the development of new therapies and drugs. (Full story)

(Clip Art compliments of Bing.)

SPEAK OUT! NewsBit . . . . . . Scientists Search for Therapies for Brain Injury

Stimulation of Specific Neurons Enhances Recovery

Research at Stanford newsboy-thUniversity examined recovery from stroke in mice, but its significance will affect future therapy for brain injuries in humans. The scientists were the first to use a relatively new technique, called “optogenetics,” for studies of the brain. They engineered mice to make a light-sensitive protein in the motor cortex of the brain. They also implanted an optical fiber so they could use light to stimulate that protein, and therefore those neurons specifically.

Stroke-impaired mice (stroke mice) that were stimulated with light recovered significantly more in tests of coordination, balance, and muscle mass than did stroke mice that were not stimulated. Unlike the only drug currently used for strokes, which works to dissolve a clot and must be given within a few hours of a clot-induced stroke, the neural stimulation was effective even five days after a stroke. There were no side effects from stimulating the brains of healthy mice in the same way.

The scientists also found that stimulated stroke mice showed better weight gain than did unstimulated stroke mice. Also, the brains of stimulated stroke mice showed enhanced blood flow, produced more natural neural growth factors, and made more of a protein that strengthens neural circuits during therapy, when compared to the brains of unstimulated stroke mice.

This research is just beginning. The objective is to identify specific neural circuits that have roles in the recovery of the brain to injury. Once the circuits are known, implants that stimulate specific neurons in humans (as is being done now to control epilepsy) and/or new therapies will enhance recovery from brain injury. (Full story)

(Clip Art compliments of Bing.)

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