Studies have shown a correlation in animal models between learning and cell survival in the hippocampus. Research also provides evidence that there are sets of neurons in the brain that code the critical features of habits, and as a habit is acquired, brain circuits change their activity to recode the events and actions. Other findings suggest that the brain may be capable of self-repair after seizures, because it produces new nerve cells that naturally migrate to the place where damaged cells were located.
For decades, it was believed that the adult brain did not produce new neurons after birth. But that notion has been dispelled by research in the last ten years. It became clear by the mid- to late-1990?s that the brain does, in fact, produce new neurons throughout the lifespan.
This phenomenon, known as neurogenesis, occurs in most species, including humans, but the degree to which it occurs and the extent to which it occurs is still a matter of some controversy, says Tracey Shors, PhD, at Rutgers University.
However, there is no question that neurogenesis occurs in the hippocampus, a brain region involved in aspects of learning and memory. Thousands of new cells are produced there each day, although many die with weeks of their birth. Shors recent studies have shown a correlation in animal models between learning and cell survival in the hippocampus.
About 10 years ago, Shors lab and that of Elizabeth Gould, PhD, showed that new neurons can be prevented from dying if animals are trained to associate events across time or space. Most of the tasks that increase the survival of new neurons are dependent on the hippocampus for learning itself, providing indirect support for the idea that the new neurons are used in processes of learning, says Shors.
Shors has been training animals with a variety of tasks in a range of difficulty, requiring different responses and engaging different brain structures. If the animal learns, says Shors, more new cells survive and go on to become neurons. If the animal does not learn, the cells die. It is not an all or none phenomenon, she says, but rather a correlation such that the better an animal learns, the more cells that remain in the hippocampus. She adds that this phenomenon does not apply to all types of learning, but rather to those that are dependent on the hippocampus for learning itself.
Shors says that they dont yet know what the cells do once they are rescued from death by learning. We do know that the cells remain in the hippocampus for months after the learning has occurred. Thus, the cells have become incorporated into the existing brain circuitry, she says.
Also, the number of cells that remain in the hippocampus is directly related to how well the animal remembers what it learned, she says. These findings suggest that the new cells may be used somehow for retrieving memories, but do not prove that particular hypothesis, says Shors.
It is clear that learning can enhance the presence of new neurons in the adult brain, says Shors, implying a use it or lose it phenomenon. I want to stress that the cells that are rescued from death by learning were born before the learning experience. It is not the case, at least as far as we can tell, that learning produces more cells, she says. Rather, their data indicate that the cells that were already there at the time of the training experience are affected by learning and thereby rescued from death.
Shors says that these data may apply to patients with neurological or psychological disease, generally, rather than any specific disease. Indeed, she says, there are few diseases that are not impacted by learning. Interestingly enough, many diseases are accompanied by changes in the production of new cells in the brain, usually by decreases.
I am often asked whether learning and other cognitive activities will help prevent a decrease in neurogenesis or even the onset of diseases such as Alzheimers, she says. It seems prudent to assume so until we know different.
Other research provides evidence that there are sets of neurons in the brain that code the critical features of habits, and as a habit is acquired, brain circuits change their activity to recode the events and actions.
Habits free us to think and to react to new events in the environment, says Ann Graybiel, PhD, at the Massachusetts Institute of Technology. Her research explores what forms of neural representation are built up in cortico-basal ganglia networks as animals make and break habits, and how such learning and memory functions of the basal ganglia could illuminate clinical work on basal-ganglia-based disorders.
Recordings from the striatum, the largest input side of the basal ganglia, suggest remarkable plasticity in the response properties of striatal neurons as animals learn sequential procedures and also as they undergo bouts of learning, extinction and reacquisition training. New techniques permitting long-term recording of neural activity have yielded dramatic evidence that there are sets of neurons in the brain that code the critical features of habits, she says. These neurons appear to set the boundaries of habits, marking both the beginning and end of an habitual behavior. These neurons are found in the same brain sites affected in several neurologic and neuropsychiatric disorders, ranging from Parkinsons disease to obsessive-compulsive disorder and substance abuse.
What seems to happen when a habit is acquired is that brain circuits change their activity to recode the events and actions related to the habit in a very particular context, a particular place and time, says Graybiel. At the point when the habit has become ingrained and automatic, the representation of the whole habit takes shape.
Remarkably, she adds, the new representation can be suppressed, but it comes back when the original context is reentered. This may be related to the key problem in drug addiction, that a single dose may reinstate the original habit at its full strength. Computational studies are making important steps to model the change from pre-habit, goal-directed behavior to the semi-automatic behavior that comes when habits take hold, says Graybiel. Together, the findings suggest a new role for the release circuits of the basal ganglia, the nodal points in the habit system of the brain.
These circuits may release movements and thoughts normally, says Graybiel, but in disorders such as Huntingtons disease or OCD, they over-release packets of behavior without intention driving the release. And in disorders such as Parkinsons disease, they under-release behaviors, despite strong intention on the part of the person.
Plasticity-related genes related to habit formation and stereotypes are still being discovered, says Graybiel. There is great hope for finding common molecular mechanisms underlying the development of motor and cognitive habits and also the broad range of habit-related neurological and neuropsychiatric disorders.
While learning and habits may seem normal mechanisms, researchers are also using disorders to gain more insight into neurogenesis.
New findings suggest that the brain may be capable of self-repair after seizures, because it can produce new nerve cells that naturally migrate to the place where damaged cells were located. Data also points to seizures as extremely potent in their ability to increase neurogenesis.
One neurological disorder of particular relevance is epilepsy, specifically the type of epilepsy that involves seizures arising from the temporal lobe (temporal lobe epilepsy). This is because one of the areas of the adult brain where neurogenesis occurs throughout life is in the temporal lobe: the dentate gyrus. Damage in the dentate gyrus and adjacent structures has already been suggested as a contributing factor in temporal lobe epilepsy, says Helen Scharfman, PhD, at Columbia University. Studies of animal models of epilepsy have provided a greater understanding of the ways that seizures increase dentate gyrus neurogenesis, and how the new neurons influence the activity of the dentate gyrus.
Some of the new neurons appear to migrate into the hilus, a region where neurons are damaged in temporal lobe epilepsy, says Scharfman. Additional studies in animals that have had experimental seizures have shown that the issue is more complex, she says, because the new nerve cells develop in some ways that increase the likelihood of abnormal neuronal activity.
The majority of the data suggest that seizures are extremely potent in their ability to increase neurogenesis, she says, but the new nerve cells that are born may not be easily used to reverse the disease process, or the state of recurrent seizures that defines epilepsy. Although the new data may dampen enthusiasm that neurogenesis can be manipulated to treat epilepsy in the near future, it has supported the original idea that these cells may have clinical potential eventually, says Scharfman. They appear to be robust in their function, connectivity, and influence adult neurogenesis, and could possibly lead to clinical advances once it is better understood.
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