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Olinguito 

On Tuesday, Bill Stanley grabbed my arm and pulled me into a side hallway as we were walking towards the mammal collections on the third floor. He looked around suspiciously before leaning in, and in a hushed tone he said

there’s a new raccoon.

What do you mean? 

There’s a new raccoon. You can’t tell anyone. It’s in the pipeline. Going live on Thursday.

Wha- I wasn’t going to-

You can’t tell anyone. Guess where it was discovered?

Oh, geez. I don’t know. Maybe Per-

Here. It was discovered here. 

Then he patted my shoulder, winked, and kept walking. 

Such was my introduction to the olinguito - and yesterday Bill brought it out to show me. In front of us were two drawers, one with the previously known species and the newly described animals on the right. It was immediately obvious to me that before us were two different animals - the size, color and length of the fur, the size of the ears - but without the previous knowledge that they were not one in the same, would I have seen the same dissimilarities? 

This is what sparks me. This is what drives my enthusiasm. In these drawers for sixty years, side-by-side these animals remained, their full potential not realized until a curious researcher took the quiet time to sit down and take a concentrated look at them. It’s the romance of the discovery – it was here all along! – and once you see the striking inconsistencies there comes a feeling of empowerment, the thought that we are the next big discoverers. The thrill of the breakthrough remains attainable, accessible. It’s not beyond our reach or out of grasp - I look forward to seeing what you find next. 

For more posts like these, go to @mypsychology​

Be greater than average.

Why Number Are The Way They Are

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(Image caption: The above image compares the neural activation patterns between images from the participants’ brains when reading “O eleitor foi ao protesto” (observed) and the computational model’s prediction for “The voter went to the protest” (predicted))

Brain “Reads” Sentences the Same in English and Portuguese

An international research team led by Carnegie Mellon University has found that when the brain “reads” or decodes a sentence in English or Portuguese, its neural activation patterns are the same.

Published in NeuroImage, the study is the first to show that different languages have similar neural signatures for describing events and scenes. By using a machine-learning algorithm, the research team was able to understand the relationship between sentence meaning and brain activation patterns in English and then recognize sentence meaning based on activation patterns in Portuguese. The findings can be used to improve machine translation, brain decoding across languages and, potentially, second language instruction.

“This tells us that, for the most part, the language we happen to learn to speak does not change the organization of the brain,” said Marcel Just, the D.O. Hebb University Professor of Psychology and pioneer in using brain imaging and machine-learning techniques to identify how the brain deciphers thoughts and concepts.

“Semantic information is represented in the same place in the brain and the same pattern of intensities for everyone. Knowing this means that brain to brain or brain to computer interfaces can probably be the same for speakers of all languages,” Just said.

For the study, 15 native Portuguese speakers — eight were bilingual in Portuguese and English — read 60 sentences in Portuguese while in a functional magnetic resonance imaging (fMRI) scanner. A CMU-developed computational model was able to predict which sentences the participants were reading in Portuguese, based only on activation patterns.

The computational model uses a set of 42 concept-level semantic features and six markers of the concepts’ roles in the sentence, such as agent or action, to identify brain activation patterns in English.

With 67 percent accuracy, the model predicted which sentences were read in Portuguese. The resulting brain images showed that the activation patterns for the 60 sentences were in the same brain locations and at similar intensity levels for both English and Portuguese sentences.

Additionally, the results revealed the activation patterns could be grouped into four semantic categories, depending on the sentence’s focus: people, places, actions and feelings. The groupings were very similar across languages, reinforcing the organization of information in the brain is the same regardless of the language in which it is expressed.

“The cross-language prediction model captured the conceptual gist of the described event or state in the sentences, rather than depending on particular language idiosyncrasies. It demonstrated a meta-language prediction capability from neural signals across people, languages and bilingual status,” said Ying Yang, a postdoctoral associate in psychology at CMU and first author of the study.

Newly discovered windows of brain plasticity may help with treatment of stress-related disorders

Chronic stress can lead to changes in neural circuitry that leave the brain trapped in states of anxiety and depression. But even under repeated stress, brief opportunities for recovery can open up, according to new research at The Rockefeller University.

(Image caption: Routine versus disruptive: A familiar stressor (left) did not increase NMDA receptors (dark spots), a booster of potentially harmful glutamate signaling, in the brains of mice. However, when subjected to an unfamiliar stress (right), mice expressed more NMDA receptors)

“Even after a long period of chronic stress, the brain retains the ability to change and adapt. In experiments with mice, we discovered the mechanism that alters expression of key glutamate-controlling genes to make windows of stress-related neuroplasticity—and potential recovery—possible,” says senior author Bruce McEwen, Alfred E. Mirsky Professor, and head of the Harold and Margaret Milliken Hatch Laboratory of Neuroendocrinology. Glutamate is a chemical signal implicated in stress-related disorders, including depression.

“This sensitive window could provide an opportunity for treatment, when the brain is most responsive to efforts to restore neural circuitry in the affected areas,” he adds.

The team, including McEwen and first author Carla Nasca, wanted to know how a history of stress could alter the brain’s response to further stress. To find out, they accustomed mice to a daily experience they dislike, confinement in a small space for a short period. On the 22nd day, they introduced some of those mice to a new stressor; others received the now-familiar confinement.

Then, the researchers tested both groups for anxiety- or depression-like behaviors. A telling split emerged: Mice tested shortly after the receiving the familiar stressor showed fewer of those behaviors; meanwhile those given the unfamiliar stressor, displayed more. The difference was transitory, however; by 24 hours after the final stressor, the behavioral improvements seen in half of the mice had disappeared.

Molecular analyses revealed a parallel fluctuation in a part of the hippocampus, a brain region involved in the stress response. A key molecule, mGlu2, which tamps down the release of the neurotransmitter glutamate, increased temporarily in mice subjected to the familiar confinement stress. Meanwhile, a molecular glutamate booster, NMDA, increased in other mice that experienced the unfamiliar stressor. In stress-related disorders, excessive glutamate causes harmful structural changes in the brain.

The researchers also identified the molecule regulating the regulator, an enzyme called P300. By adding chemical groups to proteins known as histones, which give support and structure to DNA, P300 increases expression of mGlu2, they found.

In other experiments, they looked at mice genetically engineered to carry a genetic variant associated with development of depression and other stress-related disorders in humans, and present in 33 percent of the population.

“Here again, in experiments relevant to humans, we saw the same window of plasticity, with the same up-then-down fluctuations in mGlu2 and P300 in the hippocampus,” Nasca says. “This result suggests we can take advantage of these windows of plasticity through treatments, including the next generation of drugs, such as acetyl carnitine, that target mGlu2—not to ‘roll back the clock’ but rather to change the trajectory of such brain plasticity toward more positive directions.”