Posts tagged prefrontal cortex

Posts tagged prefrontal cortex
First measurements made of key brain links
Until now, brain scientists have been almost completely in the dark about how most of the nonspecific thalamus interacts with the prefrontal cortex, a relationship believed to be key in such fundamental functions as maintaining consciousness and mental arousal. Brown University researchers performed a set of experiments, described in the Journal of Neuroscience, to explore and measure those circuits for the first time.

Research shows binge drinking inhibits brain development
Teenagers who binge drink risk inhibiting part of their brain’s development and many are laying the groundwork for alcoholism down the track a Queensland University of Technology (QUT) researcher has found.
Professor Selena Bartlett, from QUT’s Institute for Health and Biomedical Innovation (IHBI), studied the effect excessive binge drinking during adolescence had on a particular receptor in the brain and discovered teen bingeing altered it irreversibly, keeping the brain in an adolescent state.
"The human brain doesn’t fully develop until around age 25 and bingeing during adolescence modifies its circuits, preventing the brain from reaching maturity," she said.
"During adolescence, the brain undergoes massive changes in the prefrontal cortex and areas linked to drug reward but alcohol disrupts this.
"The research, which was carried out on rats, suggests that during ageing, the brain’s delta opioid peptide receptor (DOP-R) activity turns down, but binge drinking causes the receptors to stay on, keeping it in an adolescent stage.
"The younger a child or teenager starts binge drinking and the more they drink, the worse the possible outcome for them."
Professor Bartlett said recent trends to mix high-caffeine drinks such as Red Bull with alcohol were making the binge drinking problem worse.
Almost everyone knows the feeling: you see a delicious piece of chocolate cake on the table, but as you grab your fork, you think twice. The cake is too fattening and unhealthy, you tell yourself. Maybe you should skip dessert.
But the cake still beckons.
In order to make the healthy choice, we often have to engage in this kind of internal struggle. Now, scientists at the California Institute of Technology (Caltech) have identified the neural processes at work during such self-regulation—and what determines whether you eat the cake.
"We seem to have independent systems capable of guiding our decisions, and in situations like this one, these systems may compete for control of what we do," says Cendri Hutcherson, a Caltech postdoctoral scholar who is the lead author on a new paper about these competing brain systems, which will be published in the September 26 issue of The Journal of Neuroscience.

Unlocking a major secret of the brain
McGill researchers uncover crucial link between hippocampus and prefrontal cortex
A clue to understanding certain cognitive and mental disorders may involve two parts of the brain which were previously thought to have independent functions, according to a McGill University team of researchers led by Prof. Yogita Chudasama, of the Laboratory of Brain and Behavior, Department of Psychology. The McGill team discovered a critical interaction between two prominent brain areas: the hippocampus, a well-known memory structure made famous by Dr. Brenda Milner’s patient H.M., and the prefrontal cortex, which is involved in decision-making and inhibiting inappropriate behaviours.
“We had always thought that the hippocampus and the prefrontal cortex functioned independently,” says Prof. Chudasama. “Our latest study provides the first indication that that is not the case.”
The team’s finding, just published in the Journal of Neuroscience, reveals a critical interaction between these two brain areas and the control of behavior, and may advance the treatment of some cognitive and mental disorders including schizophrenia, and depression. The interaction between the hippocampus and the prefrontal cortex shows that brain circuits function not just as specific parts of the brain, but are linked together and work as a system.
“Although the prefrontal cortex has long been known to be the driving force that steers our behavior, pushing us to make good decisions and withhold improper actions, it turns out that it can’t do this unless it interacts with the hippocampus,” added Prof. Chudasama. “We found that when we prevented these two structures from communicating with each other, like humans with compulsive disorders, rats persisted with behaviours that were not good for them; they didn’t correct their errant behaviours and could not control their natural urges.
The ability to control impulsive urges or inhibit our actions allows us to interact normally in personal or social situations, and this type of behaviour depends on the normal interaction of the hippocampus and the prefrontal cortex. This result provides a means for understanding the neural basis for social and cognitive deficits in disorders of brain and behaviour, such as those with frontotemporal dementia”, concludes Prof. Chudasama.
12 August 2012
Certain brain regions in people with major depression are smaller and less dense than those of their healthy counterparts. Now, researchers have traced the genetic reasons for this shrinkage.
A series of genes linked to the function of synapses, or the gaps between brain cells crucial for cell-to-cell communication, can be controlled by a single genetic “switch” that appears to be overproduced in the brains of people with depression, a new study finds.
"We show that circuits normally involved in emotion, as well as cognition, are disrupted when this single transcription factor is activated," study researcher Ronald Duman, a professor of psychiatry at Yale University, said in a statement.

Shrinking brain
Brain-imaging studies, post-mortem examinations of human brains and animal studies have all found that in depression, a part of the brain called the dorsolateral prefrontal cortex shrinks. The neurons in this region, which is responsible for complex tasks from memory and sensory integration to the planning of actions, are also smaller and less dense in depressed people compared with healthy people.
Duman and his colleagues suspected that these neuronal abnormalities would include problems with the synapses, the points where brain cells “talk” to one another. At synapses, neurons release neurotransmitters that are picked up by their neighbors, carrying signals from cell to cell at rapid speed.
The researchers conducted gene profiling on the postmortem brain tissue of both depressed and mentally healthy subjects. They found a range of genes that were significantly less active in depressed people’s dorsolateral prefrontal cortexes, particularly five related to synaptic function: synapsin 1, Rab3A, calmodulin 2, Rab4B and TUBB4.
Synaptic damage
These genes are all involved in either the chemical signaling that occurs at synapses or the cellular recycling and regeneration processes that keep the synapse-system humming. All five are regulated by a single transcription factor called GATA1, which was overproduced in depressed brains.
The researchers activated GATA1 in the brains of rats and found that the factor decreased the complexity of the long, branchlike projections, or dendrites, of brain cells. These projections are the telephone lines that carry synaptic messages, integrating all the information a cell receives.
Extra GATA1 also increased depression-like behavior in the rats. For example, when given a swimming task, rats with extra GATA1 stayed immobile in the water longer, a signal of despair, than normal-GATA1 rats, the researchers report today (Aug. 12) in the journal Nature Medicine.
The researchers believe the damage could be a result of chronic stress, and they hope the findings lead to new depression treatments.
"We hope that by enhancing synaptic connections, either with novel medications or behavioral therapy, we can develop more effective antidepressant therapies," Duman said.
Source: Live Science