Astronomers discover unusual monster galaxy in the very early universe

W. M. Keck Observatory (stock image).

An international team of astronomers led by scientists at the University of California, Riverside, has found an unusual monster galaxy that existed about 12 billion years ago, when the universe was only 1.8 billion years old.

Dubbed XMM-2599, the galaxy formed stars at a high rate and then died. Why it suddenly stopped forming stars is unclear.

"Even before the universe was 2 billion years old, XMM-2599 had already formed a mass of more than 300 billion suns, making it an ultramassive galaxy," said Benjamin Forrest, a postdoctoral researcher in the UC Riverside Department of Physics and Astronomy and the study's lead author. "More remarkably, we show that XMM-2599 formed most of its stars in a huge frenzy when the universe was less than 1 billion years old, and then became inactive by the time the universe was only 1.8 billion years old."

The team used spectroscopic observations from the W. M. Keck Observatory's powerful Multi-Object Spectrograph for Infrared Exploration, or MOSFIRE, to make detailed measurements of XMM-2599 and precisely quantify its distance.

Study results appear in the Astrophysical Journal.

"In this epoch, very few galaxies have stopped forming stars, and none are as massive as XMM-2599," said Gillian Wilson, a professor of physics and astronomy at UCR in whose lab Forrest works. "The mere existence of ultramassive galaxies like XMM-2599 proves quite a challenge to numerical models. Even though such massive galaxies are incredibly rare at this epoch, the models do predict them. The predicted galaxies, however, are expected to be actively forming stars. What makes XMM-2599 so interesting, unusual, and surprising is that it is no longer forming stars, perhaps because it stopped getting fuel or its black hole began to turn on. Our results call for changes in how models turn off star formation in early galaxies."

The research team found XMM-2599 formed more than 1,000 solar masses a year in stars at its peak of activity -- an extremely high rate of star formation. In contrast, the Milky Way forms about one new star a year.

"XMM-2599 may be a descendant of a population of highly star-forming dusty galaxies in the very early universe that new infrared telescopes have recently discovered," said Danilo Marchesini, an associate professor of astronomy at Tufts University and a co-author on the study.

The evolutionary pathway of XMM-2599 is unclear.

"We have caught XMM-2599 in its inactive phase," Wilson said. "We do not know what it will turn into by the present day. We know it cannot lose mass. An interesting question is what happens around it. As time goes by, could it gravitationally attract nearby star-forming galaxies and become a bright city of galaxies?"

Co-author Michael Cooper, a professor of astronomy at UC Irvine, said this outcome is a strong possibility.

"Perhaps during the following 11.7 billion years of cosmic history, XMM-2599 will become the central member of one of the brightest and most massive clusters of galaxies in the local universe," he said. "Alternatively, it could continue to exist in isolation. Or we could have a scenario that lies between these two outcomes."

The team has been awarded more time at the Keck Observatory to follow up on unanswered questions prompted by XMM-2599.

"We identified XMM-2599 as an interesting candidate with imaging alone," said co-author Marianna Annunziatella, a postdoctoral researcher at Tufts University. "We used Keck to better characterize and confirm its nature and help us understand how monster galaxies form and die. MOSFIRE is one of the most efficient and effective instruments in the world for conducting this type of research."

Other researchers taking part include Daniel Lange-Vagle and Theodore Peña of Tufts University; Adam Muzzin and Cemile Marsan of York University, Canada; Ian McConachie and Jeffrey Chan of UCR; Percy Gomez of Keck Observatory; Erin Kado-Fong of Princeton University; Francesco La Barbera of INAF-Osservatorio Astronomico di Capodimonte, Italy; Ivo Labbe of Swinburne University of Technology, Australia; Julie Nantais of Andrés Bello National University, Santiago, Chile; Mario Nonino of Astronomical Observatory of Trieste, Italy; Paolo Saracco of Astronomical Observatory of Brera, Italy; Mauro Stefanon of Leiden University, Netherlands; and Remco F. J. van der Burg of the European Southern Observatory, Germany.

Wilson led the W. M. Keck Observatory data acquisition. Forrest led the processing and analysis.

The study was supported by grants from the National Science Foundation and NASA.

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Materials provided by University of California - Riverside. Original written by Iqbal Pittalwala. Note: Content may be edited for style and length.

Scientists discover key neural circuit regulating alcohol consumption

Scientists discover key neural circuit regulating alcohol consumption

Scientists have known that a region of the brain called the central nucleus of the amygdala (CeA) plays a role in behaviors related to alcohol use and consumption in general. It's been less known which precise populations of brain cells and their projections to other brain regions mediate these behaviors. Now, UNC School of Medicine scientists discovered that specific neurons in the CeA contribute to reward-like behaviors, alcohol consumption in particular.

Published in the Journal of Neuroscience, this research pinpoints a specific neural circuit that when altered caused animal models to drink less alcohol.

"The fact that these neurons promote reward-like behavior, that extremely low levels of alcohol consumption activate these cells, and that activation of these neurons drive alcohol drinking in animals without extensive prior drinking experience suggests that they may be important for early alcohol use and reward," said senior author Zoe McElligott, PhD, assistant professor of psychiatry and pharmacology. "It's our hope that by understanding the function of this circuit, we can better predict what happens in the brains of people who transition from casual alcohol use to subsequent abuse of alcohol, and the development of alcohol use disorders."

McElligott, who is also a member of the UNC Bowles Center for Alcohol Studies, set out to investigate if a population of neurons that express a specific neuropeptide (neurotensin or NTS) contributes to reward-like behaviors and alcohol drinking. She was especially interested in these neurons in the context of inexperienced alcohol use, such as when a person first begins to drink alcohol. Also, NTS neurons are a subpopulation of other neurons in this CeA brain region that have been implicated in anxiety and fear -- known as the somatostatin and corticotropin releasing factor neurons.

Using modern genetic and viral technologies in male mice, McElligott and colleagues found that selectively lesioning or ablating the NTS neurons in the CeA, while maintaining other types of CeA neurons, would cause the animals to drink less alcohol. This manipulation did not alter anxiety-like behavior. It also did not affect the consumption of other palatable liquids such as sucrose, saccharin, and bitter quinine solutions.

"We found that these NTS neurons in the CeA send a strong projection to the hindbrain, where they inhibit the parabrachial nucleus, near the brainstem," McElligott said.

Using optogenetics -- a technique where light activates these neurons -- the researchers stimulated the terminal projections of the CeA-NTS neurons in the parabrachial and found that this stimulation inhibited the neurons in the parabrachial. When the scientists stimulated this projection with a laser in one half of the animal's box, animals would spend more time where the stimulation would occur.

Animals also learned to perform a task to get the laser stimulation to turn on, and they would do this repeatedly, suggesting that they found this stimulation to be rewarding.

"Furthermore, when we stimulated this projection, animals would drink more alcohol as compared to when they had an opportunity to drink alcohol without laser stimulation," McElligott said. "In contrast to our study where we ablated the NTS neurons, laser stimulation of this parabrachial pathway also caused the animals to consume caloric and non-caloric sweetened beverages. When the animals were presented with regular food and a sweet food, however, laser stimulation did not enhance the consumption regardless of the mouse's hunger state. This suggests that different circuits may regulate the consumption of rewarding fluids and solids."

McElligott and her graduate student María Luisa Torruella Suarez, the first author of this study, hope to explore how alcohol experience may change these neurons over time.

"Would these cells respond differently after animals have been drinking high quantities of alcohol over time?" McElligott said. "We also want to discover which populations of neurons in the parabrachial are receiving inputs from these neurons. Fully understanding this circuit could be the key to developing therapeutics to help people with alcohol use disorders."

The National Institutes of Health, The North Carolina Translational Clinical Science (NC TraCS) Institute, the Alcohol Beverage Medical Research Foundation, and The UNC Bowles Center for Alcohol Studies funded this research.

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Materials provided by University of North Carolina Health Care. Note: Content may be edited for style and length.

Bioengineer Researchers Discover New Type of Cell Communication

Collective intercellular communication through ultra-fast hydrodynamic trigger waves:

Researchers studying one of the longest single cell organisms—Spirostomum ambiguum—which can grow up to lengths of 4mm (a unicellular organism observable to the naked eye) have discovered that it is also one of the fastest cells ever documented. The gargantuan protist can contract its long body by 60% within milliseconds, experiencing an acceleration force of up to 14g.

The contractile behavior protects the unicellular organism from would-be predators, as small vacuoles along the cellular membrane containing toxins are dispersed when undergoing the extreme g forces of the contraction. Remarkably, researchers have discovered that the contractions also generate long-ranged vortex flows that function as hydrodynamic signals to other Spirostomum.

This is the first time that hydrodynamic cellular signaling has been documented, and opens the door to investigating other instances where cells are communicating via long-range vorticular hydrodynamic signals.

RSF—in perspective:

RSF—in perspective: the subcellular components that allow for this blazingly fast contractile motion are microtubules. Microtubules are a central facet of current theories of quantum consciousness and cellular information processing producing memory and intelligent behavior.

As such, it is perhaps not so surprising that the intelligent behavior and communication via hydrodynamic signaling from rapid contraction by this unicellular organism involves microtubules.

Related article: https://www.biorxiv.org/content/10.1101/428573v1

Researchers discover brain circuit linked to food impulsivity

Eating popcorn at a movie (stock image).

Credit: © Zoriana / Adobe Stock

You're on a diet, but the aroma of popcorn in the movie theater lobby triggers a seemingly irresistible craving.

Within seconds, you've ordered a tub of the stuff and have eaten several handfuls.

Impulsivity, or responding without thinking about the consequences of an action, has been linked to excessive food intake, binge eating, weight gain and obesity, along with several psychiatric disorders including drug addiction and excessive gambling.

A team of researchers that includes a faculty member at the University of Georgia has now identified a specific circuit in the brain that alters food impulsivity, creating the possibility scientists can someday develop therapeutics to address overeating.

The team's findings were published recently in the journal Nature Communications.

"There's underlying physiology in your brain that is regulating your capacity to say no to (impulsive eating)," said Emily Noble, an assistant professor in the UGA College of Family and Consumer Sciences who served as lead author on the paper. "In experimental models, you can activate that circuitry and get a specific behavioral response."

Using a rat model, researchers focused on a subset of brain cells that produce a type of transmitter in the hypothalamus called melanin concentrating hormone (MCH).

While previous research has shown that elevating MCH levels in the brain can increase food intake, this study is the first to show that MCH also plays a role in impulsive behavior, Noble said.

"We found that when we activate the cells in the brain that produce MCH, animals become more impulsive in their behavior around food," Noble said.

To test impulsivity, researchers trained rats to press a lever to receive a "delicious, high-fat, high-sugar" pellet, Noble said. However, the rat had to wait 20 seconds between lever presses. If the rat pressed the lever too soon, it had to wait an additional 20 seconds.

Researchers then used advanced techniques to activate a specific MCH neural pathway from the hypothalamus to the hippocampus, a part of the brain involved with learning and memory function.

Results indicated MCH doesn't affect how much the animals liked the food or how hard they were willing to work for the food. Rather, the circuit acted on the animals' inhibitory control, or their ability to stop themselves from trying to get the food."Activating this specific pathway of MCH neurons increased impulsive behavior without affecting normal eating for caloric need or motivation to consume delicious food," Noble said. "Understanding that this circuit, which selectively affects food impulsivity, exists opens the door to the possibility that one day we might be able to develop therapeutics for overeating that help people stick to a diet without reducing normal appetite or making delicious foods less delicious."

---

Story Source:

Materials provided by University of Georgia. Original written by Cal Powell. Note: Content may be edited for style and length.

Scientists discover key neural circuit regulating alcohol consumption

Scientists discover key neural circuit regulating alcohol consumption

Scientists have known that a region of the brain called the central nucleus of the amygdala (CeA) plays a role in behaviors related to alcohol use and consumption in general. It's been less known which precise populations of brain cells and their projections to other brain regions mediate these behaviors. Now, UNC School of Medicine scientists discovered that specific neurons in the CeA contribute to reward-like behaviors, alcohol consumption in particular.

Published in the Journal of Neuroscience, this research pinpoints a specific neural circuit that when altered caused animal models to drink less alcohol.

"The fact that these neurons promote reward-like behavior, that extremely low levels of alcohol consumption activate these cells, and that activation of these neurons drive alcohol drinking in animals without extensive prior drinking experience suggests that they may be important for early alcohol use and reward," said senior author Zoe McElligott, PhD, assistant professor of psychiatry and pharmacology. "It's our hope that by understanding the function of this circuit, we can better predict what happens in the brains of people who transition from casual alcohol use to subsequent abuse of alcohol, and the development of alcohol use disorders."

McElligott, who is also a member of the UNC Bowles Center for Alcohol Studies, set out to investigate if a population of neurons that express a specific neuropeptide (neurotensin or NTS) contributes to reward-like behaviors and alcohol drinking. She was especially interested in these neurons in the context of inexperienced alcohol use, such as when a person first begins to drink alcohol. Also, NTS neurons are a subpopulation of other neurons in this CeA brain region that have been implicated in anxiety and fear -- known as the somatostatin and corticotropin releasing factor neurons.

Using modern genetic and viral technologies in male mice, McElligott and colleagues found that selectively lesioning or ablating the NTS neurons in the CeA, while maintaining other types of CeA neurons, would cause the animals to drink less alcohol. This manipulation did not alter anxiety-like behavior. It also did not affect the consumption of other palatable liquids such as sucrose, saccharin, and bitter quinine solutions.

"We found that these NTS neurons in the CeA send a strong projection to the hindbrain, where they inhibit the parabrachial nucleus, near the brainstem," McElligott said.

Using optogenetics -- a technique where light activates these neurons -- the researchers stimulated the terminal projections of the CeA-NTS neurons in the parabrachial and found that this stimulation inhibited the neurons in the parabrachial. When the scientists stimulated this projection with a laser in one half of the animal's box, animals would spend more time where the stimulation would occur.

Animals also learned to perform a task to get the laser stimulation to turn on, and they would do this repeatedly, suggesting that they found this stimulation to be rewarding.

"Furthermore, when we stimulated this projection, animals would drink more alcohol as compared to when they had an opportunity to drink alcohol without laser stimulation," McElligott said. "In contrast to our study where we ablated the NTS neurons, laser stimulation of this parabrachial pathway also caused the animals to consume caloric and non-caloric sweetened beverages. When the animals were presented with regular food and a sweet food, however, laser stimulation did not enhance the consumption regardless of the mouse's hunger state. This suggests that different circuits may regulate the consumption of rewarding fluids and solids."

McElligott and her graduate student María Luisa Torruella Suarez, the first author of this study, hope to explore how alcohol experience may change these neurons over time.

"Would these cells respond differently after animals have been drinking high quantities of alcohol over time?" McElligott said. "We also want to discover which populations of neurons in the parabrachial are receiving inputs from these neurons. Fully understanding this circuit could be the key to developing therapeutics to help people with alcohol use disorders."

The National Institutes of Health, The North Carolina Translational Clinical Science (NC TraCS) Institute, the Alcohol Beverage Medical Research Foundation, and The UNC Bowles Center for Alcohol Studies funded this research.

---

Story Source:

Materials provided by University of North Carolina Health Care. Note: Content may be edited for style and length.

Scientists discover key neural circuit regulating alcohol consumption

Scientists discover key neural circuit regulating alcohol consumption

Scientists have known that a region of the brain called the central nucleus of the amygdala (CeA) plays a role in behaviors related to alcohol use and consumption in general. It's been less known which precise populations of brain cells and their projections to other brain regions mediate these behaviors. Now, UNC School of Medicine scientists discovered that specific neurons in the CeA contribute to reward-like behaviors, alcohol consumption in particular.

Published in the Journal of Neuroscience, this research pinpoints a specific neural circuit that when altered caused animal models to drink less alcohol.

"The fact that these neurons promote reward-like behavior, that extremely low levels of alcohol consumption activate these cells, and that activation of these neurons drive alcohol drinking in animals without extensive prior drinking experience suggests that they may be important for early alcohol use and reward," said senior author Zoe McElligott, PhD, assistant professor of psychiatry and pharmacology. "It's our hope that by understanding the function of this circuit, we can better predict what happens in the brains of people who transition from casual alcohol use to subsequent abuse of alcohol, and the development of alcohol use disorders."

McElligott, who is also a member of the UNC Bowles Center for Alcohol Studies, set out to investigate if a population of neurons that express a specific neuropeptide (neurotensin or NTS) contributes to reward-like behaviors and alcohol drinking. She was especially interested in these neurons in the context of inexperienced alcohol use, such as when a person first begins to drink alcohol. Also, NTS neurons are a subpopulation of other neurons in this CeA brain region that have been implicated in anxiety and fear -- known as the somatostatin and corticotropin releasing factor neurons.

Using modern genetic and viral technologies in male mice, McElligott and colleagues found that selectively lesioning or ablating the NTS neurons in the CeA, while maintaining other types of CeA neurons, would cause the animals to drink less alcohol. This manipulation did not alter anxiety-like behavior. It also did not affect the consumption of other palatable liquids such as sucrose, saccharin, and bitter quinine solutions.

"We found that these NTS neurons in the CeA send a strong projection to the hindbrain, where they inhibit the parabrachial nucleus, near the brainstem," McElligott said.

Using optogenetics -- a technique where light activates these neurons -- the researchers stimulated the terminal projections of the CeA-NTS neurons in the parabrachial and found that this stimulation inhibited the neurons in the parabrachial. When the scientists stimulated this projection with a laser in one half of the animal's box, animals would spend more time where the stimulation would occur.

Animals also learned to perform a task to get the laser stimulation to turn on, and they would do this repeatedly, suggesting that they found this stimulation to be rewarding.

"Furthermore, when we stimulated this projection, animals would drink more alcohol as compared to when they had an opportunity to drink alcohol without laser stimulation," McElligott said. "In contrast to our study where we ablated the NTS neurons, laser stimulation of this parabrachial pathway also caused the animals to consume caloric and non-caloric sweetened beverages. When the animals were presented with regular food and a sweet food, however, laser stimulation did not enhance the consumption regardless of the mouse's hunger state. This suggests that different circuits may regulate the consumption of rewarding fluids and solids."

McElligott and her graduate student María Luisa Torruella Suarez, the first author of this study, hope to explore how alcohol experience may change these neurons over time.

"Would these cells respond differently after animals have been drinking high quantities of alcohol over time?" McElligott said. "We also want to discover which populations of neurons in the parabrachial are receiving inputs from these neurons. Fully understanding this circuit could be the key to developing therapeutics to help people with alcohol use disorders."

The National Institutes of Health, The North Carolina Translational Clinical Science (NC TraCS) Institute, the Alcohol Beverage Medical Research Foundation, and The UNC Bowles Center for Alcohol Studies funded this research.

---

Story Source:

Materials provided by University of North Carolina Health Care. Note: Content may be edited for style and length.

Scientists discover key neural circuit regulating alcohol consumption

Scientists have known that a region of the brain called the central nucleus of the amygdala (CeA) plays a role in behaviors related to alcohol use and consumption in general. It's been less known which precise populations of brain cells and their projections to other brain regions mediate these behaviors. Now, UNC School of Medicine scientists discovered that specific neurons in the CeA contribute to reward-like behaviors, alcohol consumption in particular.

Published in the Journal of Neuroscience, this research pinpoints a specific neural circuit that when altered caused animal models to drink less alcohol.

"The fact that these neurons promote reward-like behavior, that extremely low levels of alcohol consumption activate these cells, and that activation of these neurons drive alcohol drinking in animals without extensive prior drinking experience suggests that they may be important for early alcohol use and reward," said senior author Zoe McElligott, PhD, assistant professor of psychiatry and pharmacology. "It's our hope that by understanding the function of this circuit, we can better predict what happens in the brains of people who transition from casual alcohol use to subsequent abuse of alcohol, and the development of alcohol use disorders."

McElligott, who is also a member of the UNC Bowles Center for Alcohol Studies, set out to investigate if a population of neurons that express a specific neuropeptide (neurotensin or NTS) contributes to reward-like behaviors and alcohol drinking. She was especially interested in these neurons in the context of inexperienced alcohol use, such as when a person first begins to drink alcohol. Also, NTS neurons are a subpopulation of other neurons in this CeA brain region that have been implicated in anxiety and fear -- known as the somatostatin and corticotropin releasing factor neurons.

Using modern genetic and viral technologies in male mice, McElligott and colleagues found that selectively lesioning or ablating the NTS neurons in the CeA, while maintaining other types of CeA neurons, would cause the animals to drink less alcohol. This manipulation did not alter anxiety-like behavior. It also did not affect the consumption of other palatable liquids such as sucrose, saccharin, and bitter quinine solutions.

"We found that these NTS neurons in the CeA send a strong projection to the hindbrain, where they inhibit the parabrachial nucleus, near the brainstem," McElligott said.

Using optogenetics -- a technique where light activates these neurons -- the researchers stimulated the terminal projections of the CeA-NTS neurons in the parabrachial and found that this stimulation inhibited the neurons in the parabrachial. When the scientists stimulated this projection with a laser in one half of the animal's box, animals would spend more time where the stimulation would occur.

Animals also learned to perform a task to get the laser stimulation to turn on, and they would do this repeatedly, suggesting that they found this stimulation to be rewarding.

"Furthermore, when we stimulated this projection, animals would drink more alcohol as compared to when they had an opportunity to drink alcohol without laser stimulation," McElligott said. "In contrast to our study where we ablated the NTS neurons, laser stimulation of this parabrachial pathway also caused the animals to consume caloric and non-caloric sweetened beverages. When the animals were presented with regular food and a sweet food, however, laser stimulation did not enhance the consumption regardless of the mouse's hunger state. This suggests that different circuits may regulate the consumption of rewarding fluids and solids."

McElligott and her graduate student María Luisa Torruella Suarez, the first author of this study, hope to explore how alcohol experience may change these neurons over time.

"Would these cells respond differently after animals have been drinking high quantities of alcohol over time?" McElligott said. "We also want to discover which populations of neurons in the parabrachial are receiving inputs from these neurons. Fully understanding this circuit could be the key to developing therapeutics to help people with alcohol use disorders."

The National Institutes of Health, The North Carolina Translational Clinical Science (NC TraCS) Institute, the Alcohol Beverage Medical Research Foundation, and The UNC Bowles Center for Alcohol Studies funded this research.

---

Story Source:

Materials provided by University of North Carolina Health Care. Note: Content may be edited for style and length.

Researchers discover brain circuit linked to food impulsivity

Eating popcorn at a movie 

You're on a diet, but the aroma of popcorn in the movie theater lobby triggers a seemingly irresistible craving.

Within seconds, you've ordered a tub of the stuff and have eaten several handfuls.

Impulsivity, or responding without thinking about the consequences of an action, has been linked to excessive food intake, binge eating, weight gain and obesity, along with several psychiatric disorders including drug addiction and excessive gambling.

A team of researchers that includes a faculty member at the University of Georgia has now identified a specific circuit in the brain that alters food impulsivity, creating the possibility scientists can someday develop therapeutics to address overeating.

The team's findings were published recently in the journal Nature Communications.

"There's underlying physiology in your brain that is regulating your capacity to say no to (impulsive eating)," said Emily Noble, an assistant professor in the UGA College of Family and Consumer Sciences who served as lead author on the paper. "In experimental models, you can activate that circuitry and get a specific behavioral response."

Using a rat model, researchers focused on a subset of brain cells that produce a type of transmitter in the hypothalamus called melanin concentrating hormone (MCH).

While previous research has shown that elevating MCH levels in the brain can increase food intake, this study is the first to show that MCH also plays a role in impulsive behavior, Noble said.

"We found that when we activate the cells in the brain that produce MCH, animals become more impulsive in their behavior around food," Noble said.

To test impulsivity, researchers trained rats to press a lever to receive a "delicious, high-fat, high-sugar" pellet, Noble said. However, the rat had to wait 20 seconds between lever presses. If the rat pressed the lever too soon, it had to wait an additional 20 seconds.

Researchers then used advanced techniques to activate a specific MCH neural pathway from the hypothalamus to the hippocampus, a part of the brain involved with learning and memory function.

Results indicated MCH doesn't affect how much the animals liked the food or how hard they were willing to work for the food. Rather, the circuit acted on the animals' inhibitory control, or their ability to stop themselves from trying to get the food."Activating this specific pathway of MCH neurons increased impulsive behavior without affecting normal eating for caloric need or motivation to consume delicious food," Noble said. "Understanding that this circuit, which selectively affects food impulsivity, exists opens the door to the possibility that one day we might be able to develop therapeutics for overeating that help people stick to a diet without reducing normal appetite or making delicious foods less delicious."

---

Story Source:

Materials provided by University of Georgia. Original written by Cal Powell. Note: Content may be edited for style and length.