Posts Tagged ‘Honor Whiteman’


When it comes to social behavior, there are clear differences between men and women, and a new study suggests cooperation with others is no exception.

Written by Honor Whiteman

Published in the journal Scientific Reports, the study reveals that men and women show significant differences in brain activity when working with others in order to complete a task.

The research team – co-led by Joseph Baker, Ph.D., a postdoctoral fellow at Stanford University School of Medicine – says the findings may shed light on the evolutionary differences in cooperation between men and women.

Additionally, they could help inform new strategies to enhance cooperation, which could prove useful for people with disorders that affect social behavior, such as autism.

This latest study is not the first to identify sex differences in cooperation – defined as “a situation in which people work together to do something.”

For example, previous research has shown that a pair of men tend to cooperate better than a pair of women. In mixed-sex pairs, however, women tend to cooperate better than men.

While a number of theories have been put forward to explain these differences, Baker and colleagues note that there is limited data on the neurological processes at play.


The cooperation task

To further investigate, the team enrolled 222 participants – of whom 110 were female – and assigned each of them a partner.

Each pair was made up of either two males, two females, or one male and one female.

The pairs were required to engage in a cooperation task, in which each partner sat in front of a computer opposite from one another. Each partner could see the other, but they were instructed not to talk.

Each individual was instructed to press a button when a circle on their computer screen changed color; their goal was to try and press the button at the same time as their partner.

The pairs were given 40 tries to get the timing of their button presses as close to each other as possible, and after each try, they were told which partner had pressed the button first.

During the task, the researchers recorded the brain activity of each participant simultaneously using hyperscanning and functional near-infrared spectroscopy (fNIRS).

“We developed this test because it was simple, and you could easily record responses,” notes senior study author Dr. Allan Reiss, professor of psychiatry and behavioral sciences and psychology at Stanford.

No ‘interbrain coherence’ when opposite-sex pairs cooperate

Overall, the team found that, compared with female-female pairs, male-male pairs were better at timing their button pushes more closely.

From the brain imaging results, however, the researchers noticed that both partners in each of the same-sex pairs had highly synchronized brain activity during the task – representing greater “interbrain coherence.”

“Within same-sex pairs, increased coherence was correlated with better performance on the cooperation task,” says Baker. “However, the location of coherence differed between male-male and female-female pairs.”

Interestingly, the cooperation performance of male-female pairs was just as good as that of male-male pairs, though opposite-sex pairs showed no evidence of interbrain coherence.

“It’s not that either males or females are better at cooperating or can’t cooperate with each other. Rather, there’s just a difference in how they’re cooperating.” – Dr. Allan Reiss

Baker cautions that their study is “pretty exploratory,” noting that it does not look at all forms of cooperation.

What is more, the researchers did not assess activity in all regions of participants’ brains, and they note that it is possible interbrain coherence in opposite-sex pairs arose in these unmeasured areas.

Still, they believe their findings may help researchers learn more about how cooperation has evolved differently between men and women, and they may even lead to new ways to boost cooperation, which could have clinical implications.

“There are people with disorders like autism who have problems with social cognition,” says Baker. “We’re absolutely hoping to learn enough information so that we might be able to design more effective therapies for them.”

http://www.medicalnewstoday.com/articles/310879.php

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Infection with the common parasite Toxoplasma gondii promotes accumulation of a neurotransmitter in the brain called glutamate, triggering neurodegenerative diseases in individuals predisposed to such conditions.

Written by Honor Whiteman

This is the finding of a new study conducted by researchers from the University of California-Riverside (UC-Riverside), recently published in PLOS Pathogens.

T. gondii is a single-celled parasite that can cause a disease known as toxoplasmosis.

Infection with the parasite most commonly occurs through eating undercooked, contaminated meat or drinking contaminated water.

It may also occur through accidentally swallowing the parasite after coming into contact with cat feces – by cleaning a litter tray, for example.

Though more than 60 million people in the United States are believed to be infected with T. gondii, few people become ill from it; a healthy immune system can normally stave it off.

As such, most people who become infected with the parasite are unaware of it.

Those who do become ill from T. gondii infection may experience flu-like symptoms – such as swollen lymph glands or muscle aches – that last for at least a month.

In severe cases, toxoplasmosis can cause damage to the eyes, brain, and other organs, though such complications usually only arise in people with weakened immune systems.

The new study, however, suggests there may be another dark side to T. gondii infection: it may lead to development of neurodegenerative disease in people who are predisposed to it.

To reach their findings, lead author Emma Wilson – an associate professor in the Division of Biomedical Sciences at the UC-Riverside School of Medicine – and colleagues focused on how T. gondii infection in mice affects glutamate production

How a build-up of glutamate can damage the brain

Glutamate is an amino acid released by nerve cells, or neurons. It is one of the brain’s most abundant excitatory neurotransmitters, aiding communication between neurons.

However, previous studies have shown that too much glutamate may cause harm; a build-up of glutamate is often found in individuals with traumatic brain injury (TBI) and people with certain neurodegenerative diseases, such as multiple sclerosis (MS) and amyotrophic lateral sclerosis (ALS).

The researchers explain that excess glutamate accumulates outside of neurons, and this build-up is regulated by astrocytes – cells in the central nervous system (CNS).

Astrocytes use a glutamate transporter called GLT-1 in an attempt to remove excess glutamate from outside of neurons and convert it into a less harmful substance called glutamine, which cells use for energy.

“When a neuron fires, it releases glutamate into the space between itself and a nearby neuron,” explains Wilson. “The nearby neuron detects this glutamate, which triggers a firing of the neuron. If the glutamate isn’t cleared by GLT-1 then the neurons can’t fire properly the next time and they start to die.”


T. gondii increases glutamate by inhibiting GLT-1

n mice infected with T. gondii, the researchers identified an increase in glutamate levels.

They found that the parasite causes astrocytes to swell, which impairs their ability to regulate glutamate accumulation outside of neurons.

Furthermore, the parasite prevents GLT-1 from being properly expressed, which causes an accumulation of glutamate and misfiring of neurons. This may lead to neuronal death, and ultimately, neurodegenerative disease.

“These results suggest that in contrast to assuming chronic Toxoplasma infection as quiescent and benign, we should be aware of the potential risk to normal neurological pathways and changes in brain chemistry.” – Emma Wilson

Next, the researchers gave the infected mice an antibiotic called ceftriaxone, which has shown benefits in mouse models of ALS and a variety of CNS injuries.

They found the antibiotic increased expression of GLT-1, which led to a reduction in glutamate build-up and restored neuronal function.

Wilson says their study represents the first time that T. gondii has been shown to directly disrupt a key neurotransmitter in the brain.

“More direct and mechanistic research needs to be performed to understand the realities of this very common pathogen,” she adds.

While their findings indicate a link between T. gondii infection and neurodegenerative disease, Wilson says they should not be cause for panic.

“We have been living with this parasite for a long time,” she says. “It does not want to kill its host and lose its home. The best way to prevent infection is to cook your meat and wash your hands and vegetables. And if you are pregnant, don’t change the cat litter.”

The team now plans to further investigate what causes the reduced expression of GLT-1 in T. gondii infection.

http://www.medicalnewstoday.com/articles/310865.php

Written by Honor Whiteman

Anew study has questioned the benefits of opioid painkillers, after finding the drugs might worsen chronic pain rather than ease it.

Study co-leader Prof. Peter Grace, of the University of Colorado at Boulder (CU-Boulder), and colleagues recently published their findings in the Proceedings of the National Academy of Sciences.

Opioids are among the most commonly used painkillers in the United States; almost 250 million opioid prescriptions were written in 2013 – the equivalent to one bottle of pills for every American adult.

Previous studies have suggested opioids – such as codeine, oxycodone, morphine, and fentanyl – are effective pain relievers. They bind to proteins in the brain, spinal cord, and gastrointestinal tract called opioid receptors, reducing pain perception.

Increasing use and abuse of opioids, however, has become a major public health concern in the U.S.; opioid overdoses are responsible for 78 deaths in the country every day.

Now, Prof. Grace and colleagues have questioned whether opioids really work for pain relief, after finding the opioid morphine worsened chronic pain in rats.

Just 5 days of morphine treatment increased chronic pain in rats
According to Prof. Grace, previous studies assessing morphine use have focused on how the drug affects pain in the short term.

With this in mind, the researchers set out to investigate the longer-term effects of morphine use for chronic pain.

For their study, the team assessed two groups of rats with chronic nerve pain. One group was treated with morphine, while the other was not.

Compared with the non-treatment group, the team found that the chronic pain of the morphine group worsened with just 5 days of treatment. What is more, this effect persisted for several months.

“We are showing for the first time that even a brief exposure to opioids can have long-term negative effects on pain,” says Prof. Grace. “We found the treatment was contributing to the problem.”

Another ‘ugly side’ to opioids
According to the authors, the combination of morphine and nerve injury triggered a “cascade” of glial cell signaling, which increased chronic pain.

Glial cells are the “immune cells” of the central nervous system, which support and insulate nerve cells and aid nerve injury recovery.

They found that this cascade activated signaling from a protein called interleukin-1beta (IL-1b), which led to overactivity of nerve cells in the brain and spinal cord that respond to pain. This process can increase and prolong pain.

The researchers say their findings have important implications for individuals with chronic pain – a condition that is estimated to affect around 100 million Americans.

“The implications for people taking opioids like morphine, oxycodone and methadone are great, since we show the short-term decision to take such opioids can have devastating consequences of making pain worse and longer lasting. This is a very ugly side to opioids that had not been recognized before.”

Study co-leader Prof. Linda Watkins, CU-Boulder

It is not all bad news, however. The researchers found they were able to reverse morphine’s pain-increasing effect using a technique called “designer receptor exclusively activated by designer drugs” (DREADD), which involves the use of a targeted drug that stops glial cell receptors from recognizing opioids.

“Importantly, we’ve also been able to block the two main receptors involved in this immune response, including Toll-Like receptor 4 (TLR4) and another one called P2X7R, which have both been separately implicated in chronic pain before,” notes Prof. Grace.

“By blocking these receptors, we’re preventing the immune response from kicking in, enabling the painkilling benefits of morphine to be delivered without resulting in further chronic pain.”

He adds that drugs that can block such receptors are currently in development, but it is likely to be at least another 5 years before they are available for clinical use.

http://www.medicalnewstoday.com/articles/310645.php

Thanks to Kebmnodee for bringing this to the attention of the It’s Interesting community.