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Med Student Stress
Fascinating new research reveals that the male human brain responds to severe stress by reducing our ability to switch attention. The study closely mirrors similar findings in the brains of rats.
Working with male med students who were soon to take their boards (i.e., stressed), the researchers compared their ability to switch task focus with that of young men who were not under particular stress. The med students performed significantly less well at attention shifting.
In rats, the same kind of research had shown shriveled brain cells in the medial prefrontal cortex (a region controlling executive function in humans). An alarming concept. But once the stress was removed, the brain cells rebounded and attention shifting returned to normal.
The same proved true for the med students. A month after boards, their ability to shift attention had returned to normal.
The researchers also want to look at whether the brain’s of women respond differently to stress.
(Now, tell me why the medical profession has developed a system of putting incredible amounts of stress on young doctors and then setting them loose on patients?)

Henry Gustav Molaison
In 1953, in a procedure never tried before and never repeated since doctors removed both medial temporal lobes of Henry Gustav Molaison, then aged 27, in an attempt to control his severe epilepsy and seizures. The surgery helped reduce Molaison’s symptoms but from that point on he was incapable of forming new and lasting memories. Molaison died last month, his body 82 and his mind and personality stuck at 27.
Scientist Nelson Spruston, professor of neurobiology and physiology in the Weinberg College of Arts and Sciences at Northwestern, has begun to unravel a theory of memory formation that may explain the odd and sad case of Henry Gustav Molaison and tell us more about how the healthy brain forms new memories.
Spruston and his colleagues have found that in the process of memory formation two brain operators (called neuronal metabotropic receptors) work together to change the way a neuron fires, increasing the neuron’s electrical output and strengthening the signals it sends to other brain regions, including those involved in reward and decision making.
It appears that the two types of metabotropic receptors collaborate in creating a “coincidence detection” system, triggered when two things happen at the same time and forming an association between the separate neural events. (Associating a smell with a specific memory, for instance.)
Spruston’s work promises to lead to a rich new field of investigation.

Norman Doidge: The Brain That Changes Itself
The fourth and sixth chapters of Norman Doidge’s “The Brain That Changes Itself” deal with the subject of compulsion, inclination, and habit from different perspectives. In some parts of these chapters Doidge lose some of his objectivity and lets his personal judgments and beliefs creep into the text. In most cases these subjective moments don’t detract from the point being made and are easily enough ignored. But overall they tend to cloud the central argument that Doidge is making: Our psychology is written through plastic change and can be rewritten through plastic change.
As an example from his psychology practice Doidge uses sexual compulsion and addiction to make the case that such things as addiction to pornography result from plastic change that gradually desensitizes the subject, leading to the desire for more gratification. The most interesting thing about Doidge’s reflections on this kind of addictive behavior is the information that being aware of this kind of plastic change can help us to rewrite it, reversing the behavior pattern.
With alcohol and narcotics, however, the problem is amplified by the chemical trigger.
Doidge: “By hijacking our dopamine system, addictive substances give us pleasure without our having to work for it.”
And later, refering to a study by Eric Nestler of the University of Texas: “A single dose of many addictive drugs will produce a protein, called delta-FosB, that accummulates in the neurons. Each time the drug is used more delta-FosB accummulates, until it throws a genetic switch, affecting which genes are turned on or off.”
But then there’s an example of Doidge’s overreaching. He draws the conclusion that once flipped the damage is irreversible. But he makes no argument to substantiate this conclusion. In several places Doidge refers to “harmful” or “unpleasant” plastic change as permanent in a way that seems to reveal a certain personal distaste or bias.
Doidge makes the point that learning a new association involves a different process and a different chemical change from unlearning.
Whereas children learn during a critical period of plastic change — absorbing new information like sponges — through the action of BDNF (brain derived neurotrophic factor) critical periods of unlearning are associated with the release of oxytocin.
Massive unlearning happens when we fall in love and when we begin parenting. It’s also released in smaller quantities during orgasm.

Neurogenesis and memory
It’s an interesting question. Could the process of neurogenesis, the formation of new neural nerve cells in the hippocampus, lead to the loss of memories already formed in the brain.
If so, then new neural growth would be a double-edged sword, leading to the formation of more gray matter at the expense of old gray matter. Scientists from Seoul National University, Korea, have taken a big step toward answering this question. The team conducted an ingenious experiment showing that neurogenesis may not lead to the destruction of existing memories.
The team showed that mice with a contextual fear memory retain that fear memory whether neurogenesis has been stopped or not.
So, in and of itself, it seems that new brain cell growth doesn’t destroy existing neural connections.
While this conclusion may seem like common sense. It’s an important finding from a philosophical and scientific perspective. And will doubtless lead have practical implications for the concept of promoting neurogenesis.
It also means that pruning of old memories isn’t simply a matter of making space for new neurons. Again, a fairly common sense idea, but one that it is important to have confirmed scientifically.
Robert Vassar of Northwestern University has found that a key brain protein changes when the brain’s supply of energy drops. EIF2alpha, the altered protein, increases the production of an enzyme that stimulates the production of the sticky protein clumps symptomatic of Alzheimer’s.
What to do?
“[This finding] suggests that improving blood flow to the brain might be an effective therapeutic approach to prevent or treat Alzheimer’s,” said Vassar.
- Reduce cholesterol intake, manage high blood pressure, and exercise, especially entering mid-life.
“If people start early enough, maybe they can dodge the bullet,” Vassar said.
The study is published in the Dec. 26 issue of the journal Neuron.
Neuroscientists from Johns Hopkins University School of Medicine have identified one of the mechanisms at work in the process of new brain cell generation. They found that cell growth involves a change in gene expression (an epigenetic change).

Adult Neural Stem Cell Neurogenesis
Since an epigenetic change persists through cell division, the scientists believe that further unravelling of this mechanism may shed light on the processes by which memories are formed and behaviors and skills are learned.
“How is it that when you see someone you met ten years ago, you still recognize them? How do these transient events become long lasting in the brain, and what potential role does the birth of new neurons play in making these memories?” says Hongjun Song, Ph.D., an associate professor of neurology and member of the Johns Hopkins Institute of Cell Engineering’s NeuroICE. “We really want to understand how daily life experiences trigger the birth and growth of new neurons, and make long-lasting changes in the brain.”
It seems amazing but really when one reflects on the growing depth of knowledge about the way the brain works, this was bound to be achieved at some point.

Brain Imaging - Reading Your Mind
Using fMRI scanning scientists have been able to decode and recognize patterns of brain activity that reveal “intent.”
The diagram to the left shows how the impressions of thoughts precede those of execution in different areas of the brain.
Columbia researchers have found a link between high blood-sugar levels and brain aging. The immediately obvious remedy for this is regular exercise to help lower blood sugar levels.
Scientists have been discovering the process by which we learn as we observe. By monitoring the firing of neurons as an animal watches an activity, they find that the neurons fire in the same pattern as they do when the animal performs the same activity.
That we learn by watching doesn’t seem so surprising. But the mechanism itself is intriguing.
I’m reading Norman Doidge’s book — The Brain That Changes Itself — in which he describes the parallels between doing and thinking of doing. Subjects imagining that they are stressing a muscle for a set period each day actually increase muscle strength. Likewise mental practice of a piece of music results in improved proficiency at playing the music.
As Doidge points out, the brain responds to our being in the physical world, but can also operate and send messages without direct stimulation from from the physical world.
With this in mind, visualization and imagination become powerful tools in learning and practicing skills and proficiencies.
Scientists at the University of British Columbia have discovered the mechanism that controls and suppresses neural sprouting and brain plasticity in adults. The adult brain is less plastic than a child’s brain, which helps to maintain the (presumably helpful) connections that have been formed over the years. But in cases of injury or disease this process inhibits healing and regrowth.
The team found that a protein called calpain inhibits the plasticity of neural connections. In animal models, when they reduced the impact of calpain, the neural connections became plastic again.
The trick to devising a drug therapy from this finding will be to stimulate plasticity for healing without risking the good connections that have been so long in the making.
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