Are Crows Mind Readers … Or Just Stressed Out?

Are crows mind readers? Recent studies have suggested that the birds hide food because they think others will steal it — a complex intuition that has been seen in only a select few creatures. Some critics have suggested that the birds might simply be stressed out, but new research reveals that crows may be gifted after all.

Cracks first began forming in the crow mind-reading hypothesis last year. One member of a research team from the University of Groningen in the Netherlands spent 7 months in bird cognition expert Nicola Clayton’s University of Cambridge lab in the United Kingdom studying Western scrub jays, a member of the crow family that is often used for these studies. The Groningen team then developed a computer model in which "virtual jays" cached food under various conditions. In PLOS ONE, they argued that the model showed the jays’ might be moving their food—or recaching it—not because they were reading the minds of their competitors, but simply because of the stress of having another bird present (especially a more dominant one) and of losing food to thieves. The result contradicted previous work by Clayton’s group suggesting that crows might have a humanlike awareness of other creatures’ mental states—a cognitive ability known as theory of mind that has been claimed in dogs, chimps, and even rats.

In the new study, Clayton and her Cambridge graduate student James Thom decided to test the stress hypothesis. First, they replicated earlier work on scrub jays by letting the birds hide peanuts in trays of ground corn cobs—either unobserved or with another bird watching—and later giving them a chance to rebury them. As in previous studies, the jays recached a much higher proportion of the peanuts if another bird could see them: nearly twice as much as in private, the team reports online today in PLOS ONE.

Dopamine regulates the motivation to act

The widespread belief that dopamine regulates pleasure could go down in history with the latest research results on the role of this neurotransmitter. Researchers have proved that it regulates motivation, causing individuals to initiate and persevere to obtain something either positive or negative.

The neuroscience journal Neuron publishes an article by researchers at the Universitat Jaume I of Castellón that reviews the prevailing theory on dopamine and poses a major paradigm shift with applications in diseases related to lack of motivation and mental fatigue and depression, Parkinson’s, multiple sclerosis, fibromyalgia, etc. and diseases where there is excessive motivation and persistence as in the case of addictions.

"It was believed that dopamine regulated pleasure and reward and that we release it when we obtain something that satisfies us, but in fact the latest scientific evidence shows that this neurotransmitter acts before that, it actually encourages us to act. In other words, dopamine is released in order to achieve something good or to avoid something evil", explains Mercè Correa.

Studies had shown that dopamine is released by pleasurable sensations but also by stress, pain or loss. These research results however had been skewed to only highlight the positive influence, according to Correa. The new article is a review of the paradigm based on the data from several investigations, including those conducted over the past two decades by the Castellón group in collaboration with the John Salamone of the University of Connecticut (USA), on the role of dopamine in the motivated behaviour in animals.

The level of dopamine depends on individuals, so some people are more persistent than others to achieve a goal. “Dopamine leads to maintain the level of activity to achieve what is intended. This in principle is positive, however, it will always depend on the stimuli that are sought: whether the goal is to be a good student or to abuse of drugs” says Correa. High levels of dopamine could also explain the behaviour of the so-called sensation seekers as they are more motivated to act.

Application for depression and addiction

To know the neurobiological parameters that make people be motivated by something is important to many areas such as work, education or health. Dopamine is now seen as a core neurotransmitter to address symptoms such as the lack of energy that occurs in diseases such as depression. “Depressed people do not feel like doing anything and that’s because of low dopamine levels,” explains Correa. Lack of energy and motivation is also related to other syndromes with mental fatigue such as Parkinson’s, multiple sclerosis or fibromyalgia, among others.

In the opposite case, dopamine may be involved in addictive behaviour problems, leading to an attitude of compulsive perseverance. In this sense, Correa indicates that dopamine antagonists which have been applied so far in addiction problems probably have not worked because of inadequate treatments based on a misunderstanding of the function of dopamine.

Is There a Period of Increased Vulnerability for Repeat Traumatic Brain Injury?

Repeat traumatic brain injury affects a subgroup of the 3.5 million people who suffer head trauma each year. Even a mild repeat TBI that occurs when the brain is still recovering from an initial injury can result in poorer outcomes, especially in children and young adults. A metabolic marker that could serve as the basis for new mild TBI vulnerability guidelines is described in an article in Journal of Neurotrauma, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available on the Journal of Neurotrauma website.

In an Editorial, “The Window of Risk in Repeated Head Injury,” accompanying this article, John T. Povlishock, PhD, Editor-in-Chief of Journal of Neurotrauma and Professor, VCU Neuroscience Center, Medical College of Virginia, Richmond, states that recent studies of TBI in animal models have shown that while repeat injury can exacerbate structural, functional, metabolic, and behavioral responses, “these responses only occur when the injury is repeated within a specific time frame post-injury.”

"Specifically, this window of risk is greatest when the interval between injuries is short, hours to days, while any risk for increased damage is obviated when the intervals between injuries are elongated over days to weeks," says Dr. Povlishock. It is not yet clear if these time periods of increased risk are age- or gender-specific or depend on the intensity of the initial injury.

A consistent finding following TBI in both humans and animal models is a decrease in glucose uptake by the brain. Mayumi Prins, Daya Alexander, Christopher Giza, and David Hovda, The UCLA Brain Injury Research Center, Los Angeles, CA, simulated single and repeat (after 1 or 5 days) mild TBI in rats and measured cerebral glucose metabolism. They tested the hypothesis that the rats’ brains would be more vulnerable to the damaging effects of repeat TBI at 1 day post-injury, when glucose metabolism was still decreased, than at 5 days, when it had returned to normal levels.

In the article, “Repeat Mild Traumatic Brain Injury: Mechanisms of Cerebral Vulnerability,” the authors propose that the duration of metabolic slowdown in the brain could serve as a valuable biomarker for how long a child might be at increased risk of repeat TBI.

Researchers Find Causality in the Eye of the Beholder

We rely on our visual system more heavily than previously thought in determining the causality of events. A team of researchers has shown that, in making judgments about causality, we don’t always need to use cognitive reasoning. In some cases, our visual brain—the brain areas that process what the eyes sense—can make these judgments rapidly and automatically.

The study appears in the latest issue of the journal Current Biology.

“Our study reveals that causality can be computed at an early level in the visual system,” said Martin Rolfs, who conducted much of the research as a post-doctoral fellow in NYU’s Department of Psychology. “This finding ends a long-standing debate over how some visual events are processed: we show that our eyes can quickly make assessments about cause-and-effect—without the help of our cognitive systems.”

Rolfs is currently a research group leader at the Bernstein Center for Computational Neuroscience and the Department of Psychology of Berlin’s Humboldt University. The study’s other co-authors were Michael Dambacher, post-doctoral researcher at the universities of Potsdam and Konstanz, and Patrick Cavanagh, professor at Université Paris Descartes.

We frequently make rapid judgments of causality (“The ball knocked the glass off the table”), animacy (“Look out, that thing is alive!”), or intention (“He meant to help her”). These judgments are complex enough that many believe that substantial cognitive reasoning is required—we need our brains to tell us what our eyes have seen. However, some judgments are so rapid and effortless that they “feel” perceptual – we can make them using only our visual systems, with no thinking required.

It is not yet clear which judgments require significant cognitive processing and which may be mediated solely by our visual system. In the Current Biology study, the researchers investigated one of these—causality judgments—in an effort to better understand the division of labor between visual and cognitive processes.

Potential Drug Target to Block Cell Death in Parkinson’s Disease

Oxidative stress is a primary villain in a host of diseases that range from cancer and heart failure to Alzheimer’s disease, Amyotrophic Lateral Sclerosis and Parkinson’s disease. Now, scientists from the Florida campus of The Scripps Research Institute (TSRI) have found that blocking the interaction of a critical enzyme may counteract the destruction of neurons associated with these neurodegenerative diseases, suggesting a potential new target for drug development.

These findings appear in the January 11, 2013 edition of The Journal of Biological Chemistry.

During periods of cellular stress, such as exposure to UV radiation, the number of highly reactive oxygen-containing molecules can increase in cells, resulting in serious damage. However, relatively little is known about the role played in this process by a number of stress-related enzymes.

In the new study, the TSRI team led by Professor Philip LoGrasso focused on an enzyme known as c-jun-N-terminal kinase (JNK). Under stress, JNK migrates to the mitochondria, the part of the cell that generates chemical energy and is involved in cell growth and death. That migration, coupled with JNK activation, is associated with a number of serious health issues, including mitochondrial dysfunction, which has long been known to contribute to neuronal death in Parkinson’s disease. 

The new study showed for the first time that the interaction of JNK with a protein known as Sab is responsible for the initial JNK localization to the mitochondria in neurons. The scientists also found blocking JNK mitochondrial signaling by inhibiting JNK interaction with Sab can protect against neuronal damage in both cell culture and in the brain.

In addition, by treating JNK with a peptide inhibitor derived from a mitochondrial membrane protein, the team was able to induce a two-fold level of protection of neurons in the substantia nigra pars compacta, the brain region devastated by Parkinson’s disease.

The study noted that this inhibition leaves all other cell signaling intact, which could mean potentially fewer side effects in any future therapies.

“This may be a novel way to prevent neuron degeneration,” said LoGrasso. “Now we can try to make compounds that block that translocation and see if they’re therapeutically viable.”

Study: Model for Brain Signaling Flawed

A new study out today in the journal Science turns two decades of understanding about how brain cells communicate on its head. The study demonstrates that the tripartite synapse – a model long accepted by the scientific community and one in which multiple cells collaborate to move signals in the central nervous system – does not exist in the adult brain. 

“Our findings demonstrate that the tripartite synaptic model is incorrect,” said Maiken Nedergaard, M.D., D.M.Sc., lead author of the study and co-director of the University of Rochester Medical Center (URMC) Center for Translational Neuromedicine. “This concept does not represent the process for transmitting signals between neurons in the brain beyond the developmental stage.”

The central nervous system is home to many different cells. While neurons tend to garner the most attention, it is only recently that the function of the brain’s other cells have been fully appreciated. Glial cells known as astrocytes, for example, had long been considered mainly the “glue” that helps hold all the other cells in the central nervous system in place. Scientists now understand that that these cells are essential to maintaining a healthy environment in the brain by helping carry out functions such as removing waste.

“Neurons are like a racing car,” said Nedergaard. “While the driver gets all the credit, there are often 20 people behind the scenes that are optimizing his or her success.”

However, when it comes to moving signals between neurons in the brain it turns out that the scientists may have vastly exaggerated the role of the astrocyte.   

Neurons are connected to each other via axons or “arms” that extend from the cell’s main body. Communication between neighboring neurons takes place where axons meet other nerve cells – called a synaptic juncture – when an electrical charge causes chemicals called neurotransmitters or glutamate to be released by one cell and “read” by receptors on the surface of the opposite. The two cells do not actually touch, so the chemicals messages must pass through a gap in the synaptic juncture. The space around this gap is insulated by astrocytes.   

Under the tripartite synapse model, both astrocytes and neurons were believed to play a role in the “conversation” between cells. This understanding was largely based on animal models which showed active receptors and neurotransmission between not only the nerve cells but also the nearby astrocytes.  

Specifically, a key neurotransmission receptor called metabotropic glutamate receptor 5 (mGluR5) was observed to be present and active in astrocytes at the synaptic juncture. It was also observed that when the mGluR5 receptor was activated, the astrocytes would release chemical transmitters that were in turn read by the nerve cells. These findings led to the conclusion that astrocytes must in some manner modulate the signaling process between brain cells. 

While this model has held sway for decades, scientists have long been frustrated by their inability to influence this process by targeting it with drugs.

“If this concept was correct, it should have given rise to a clinical trial by now,” said Nedergaard. “It has not, which tells us that with so many labs work on this for 20 years that there must be something wrong.”

One of the barriers to understanding precise mechanics of passing signals from one neuron to another has been the inability to observe this process in the adult brain. The tripartite synapse model was based – in part – by examining the activity in the brains of very young rodents. Adult rodents could not be similarly studied because the synapses in the brain would die before they could be fully analyzed. This ultimately led to the presumption that the signaling process that was witnessed in the young brain carried over to adulthood. 

Collaborating with researchers at the University of Rochester’s Institute of Optics, Nedergaard and her team developed a new 2-photon microscope that enables researchers to observe glia activity in the living brain. Using both this method and by analyzing the gene and protein expression in the brain the researchers discovered that the mGluR5 largely disappear in the glial cells of adult mice meaning that these cells do not directly respond to synaptic neuronal signalling, thus calling into question the concepts that drive most of ongoing research in the field.

“The process of neuron-glial transmission as conceived by the tripartite synapse model appears to just be a simplistic signaling pathway that ‘teaches’ the synapse how to behave,” said Nedergaard. “Once the brain matures, it goes away.”