Posts tagged neural circuitry

Posts tagged neural circuitry
You wouldn’t hear the mating song of the male fruit fly as you reached for the infested bananas in your kitchen. Yet, the neural activity behind the insect’s amorous call could help scientists understand how you made the quick decision to pull your hand back from the tiny swarm.

Male fruit flies base the pitch and tempo of their mating song on the movement and behavior of their desired female, Princeton University researchers have discovered. In the animal kingdom, lusty warblers such as birds typically have a mating song with a stereotyped pattern. A fruit fly’s song, however, is an unordered series of loud purrs and soft drones made by wing vibrations, the researchers reported in the journal Nature. A male adjusts his song in reaction to his specific environment, which in this case is the distance and speed of a female — the faster and farther away she’s moving, the louder he “sings.”
While the actors are small, the implications of these findings could be substantial for understanding rapid decision-making, explained corresponding author Mala Murthy, a Princeton assistant professor of molecular biology and the Princeton Neuroscience Institute. Fruit flies are a common model for studying the systems of more advanced beings such as humans, and have the basic components of more complex nervous systems, she said.
The researchers have provided a possible tool for studying the neural pathways behind how an organism engaged in a task adjusts its behavior to sudden changes, be it a leopard chasing a zigzagging gazelle, or a commuter navigating stop-and-go traffic, Murthy said. She and her co-authors created a model that could predict a fly’s choice of song in response to its changing environment, and identified the neural pathways involved in these decisions.
"Here we have natural courtship behavior and we have this discovery that males are using information about their sensory environment in real time to shape their song. That makes the fly system a unique model to study decision-making in a natural context," Murthy said.
"You can imagine that if a fly can integrate visual information quickly to modulate his song, the way in which it does that is probably a very basic equivalent of how a more complicated animal solves a similar problem," she said. "To figure out at the level of individual neurons how flies perform sensory-motor integration will give us insight into how a mammalian brain does it and, ultimately, maybe how a human brain does it."
Insulin plays a role in mediating worms’ perceptions and behaviors
Using salt-sniffing roundworms, Salk scientists help explain how the nervous system processes sensory information
In the past few years, as imaging tools and techniques have improved, scientists have been working tirelessly to build a detailed map of neural connections in the human brain—with the ultimate hope of understanding how the mind works.
But determining how cells in the brain are physically connected is only the first clue for decoding our perceptions and behaviors. We also need to know the precise routes that information takes in the brain in a given context. Now, publishing their results September 8, 2013, in the journal Nature Neuroscience, researchers at the Salk Institute for Biological Studies have shown a striking example of the flexibility in neural circuitry and its influence on behaviors in worms, depending on the animals’ environment.
The roundworm Caenorhabditis elegans has exactly 302 neurons—far less than the estimated 100 billion neurons a person has—and we already know how each of them is connected. That, in addition to how easily the tiny creature’s cells can be manipulated, allows researchers to ask what sort of information passes through the circuits—in molecular-and circuit-level detail—and what are the behavioral consequences of this information flow.
Even with a comprehensive map of the worm’s neuronal connections in hand, however, scientists still don’t know how the animal can interact with its environment in thousands of different ways. That’s one big question that Sreekanth Chalasani, an assistant professor in Salk’s Molecular Neurobiology Laboratory and Sarah Leinwand, a doctoral student at the University of California, San Diego, sought to answer.
In C. elegans, thanks to studies performed more than 20 years ago, many sensory neurons were identified to have distinct roles such as sensing temperature, pheromones, salt and odors. To know what these cells did, scientists had zapped them one-by-one with a laser and measured the worms’ behaviors. These studies implicated one neuron in the detection of increased salt in the worm’s surroundings.
In the new study, rather than ablating individual sensory neurons, Leinwand and Chalasani imaged worms that expressed genetically encoded calcium indicators in their neurons, which caused the cells to light up when active. Surprisingly, after exposure to an attractive but high concentration of salt, the worms’ olfactory sensory neuron lit up.
"We were extremely surprised to see that with these new tools, these new calcium sensors, we could discover that there was more than one type of neuron involved in processing sensory cues that people had thought were only sensed by single neurons," says Leinwand.
Using additional genetic manipulations and behavioral assays, the researchers showed that the olfactory neuron—while still important for sensing odorants—was crucial for the worm’s movement toward salt within a certain concentration range. Unexpectedly, this neuron’s response to salt also required the previously identified salt-sensing neuron. In fact, the olfactory neuron was not directly sensing salt but instead was being activated by the salt sensory neuron, they found.
What information was the salt-sensing neuron sending to the olfactory neuron? Neurons communicate with each other by sending chemical and electrical signals through close contacts with their neighbors. By testing worms whose signaling molecules had been genetically knocked out, Chalasani and Leinwand could see which were playing a role in transmission when the worm was stimulated by higher salt. From these experiments, they saw that a neuropeptide, a small protein present in neurons, was being released by the salt-sensing neuron to shape the animal’s behavior.
Identifying the neuropeptide (or neuropeptides) responsible for the context-dependent signaling was the most challenging part of the study, because the worm has 115 genes that code for some 250 neuropeptides, Chalasani says. Luckily, there are only four different molecular machines that process all of these peptides; by using genetic knockouts of each of the four, Leinwand and Chalasani were quickly able to narrow the list down to about 40 genes which coded for insulin neuropeptides.
One by one, the team tracked olfactory neuron responses to high salt in worms missing each gene, finding that worms lacking the gene for an insulin neuropeptide known as INS-6 did not respond to increases in salt. Putting this peptide back restored the animal’s normal responses to high salt.
"It was rewarding to see that, while there might be more than one peptide signal, the contributions from INS-6 are certainly significant," Leinwand says. She and Chalasani also found the specific receptor on the receiving end of the olfactory neurons.
That insulin was the main signaling molecule recruiting the olfactory neuron into a salt-sensing circuit was a big surprise.
"Traditionally, neuropeptides have been thought to modulate neuronal function over many seconds to many minutes," Chalasani says. "But in this particular instance, it looks like the insulin is acting in less than a second to transfer information from the salt-sensing neuron to the neuron which normally responds to odor."
Similar neuropeptide communication may also create flexible neural circuits that mediate the diverse behaviors that other animals and people perform in their environments. Insulin has many roles in people—it has been implicated in aging and metabolism, for example—but so far it has only been shown to function on a slower, minute time-scale.
Chalasani and Leinwand plan to investigate whether there are other fast neural circuit switches in worms—and if so, whether those switches act through neuropeptide signaling or some other mechanism. They’re also interested in how the circuit switch changes as the animal ages. “You would expect that as the animal is aging, some of this communication becomes less efficient,” Chalasani says.
Dragonflies can see by switching “on” and “off”
Researchers at the University of Adelaide have discovered a novel and complex visual circuit in a dragonfly’s brain that could one day help to improve vision systems for robots.
Dr Steven Wiederman and Associate Professor David O’Carroll from the University’s Centre for Neuroscience Research have been studying the underlying processes of insect vision and applying that knowledge in robotics and artificial vision systems.
Their latest discovery, published this month in The Journal of Neuroscience, is that the brains of dragonflies combine opposite pathways - both an ON and OFF switch - when processing information about simple dark objects.
"To perceive the edges of objects and changes in light or darkness, the brains of many animals, including insects, frogs, and even humans, use two independent pathways, known as ON and OFF channels," says lead author Dr Steven Wiederman.
"Most animals will use a combination of ON switches with other ON switches in the brain, or OFF and OFF, depending on the circumstances. But what we show occurring in the dragonfly’s brain is the combination of both OFF and ON switches. This happens in response to simple dark objects, likely to represent potential prey to this aerial predator.
"Although we’ve found this new visual circuit in the dragonfly, it’s possible that many other animals could also have this circuit for perceiving various objects," Dr Wiederman says.
The researchers were able to record their results directly from ‘target-selective’ neurons in dragonflies’ brains. They presented the dragonflies with moving lights that changed in intensity, as well as both light and dark targets.
"We discovered that the responses to the dark targets were much greater than we expected, and that the dragonfly’s ability to respond to a dark moving target is from the correlation of opposite contrast pathways: OFF with ON," Dr Wiederman says.
"The exact mechanisms that occur in the brain for this to happen are of great interest in visual neurosciences generally, as well as for solving engineering applications in target detection and tracking. Understanding how visual systems work can have a range of outcomes, such as in the development of neural prosthetics and improvements in robot vision.
"A project is now underway at the University of Adelaide to translate much of the research we’ve conducted into a robot, to see if it can emulate the dragonfly’s vision and movement. This project is well underway and once complete, watching our autonomous dragonfly robot will be very exciting," he says.
A new study reveals that the representation of complex features in the brain may begin earlier—and play out in a more cumulative manner—than previously thought.
The finding represents a new view of how the brain creates internal representations of the visual world. “We are excited to see if this novel view will dominate the wider consensus” said senior author Dr. Miyashita, who is also Professor of Physiology at the University of Tokyo’s School of Medicine, “and also about the potential impact of our new computational principle on a wide range of views on human cognitive abilities.”
The brain recalls the patterns and objects we observe by developing distinct neuronal representations that go along with them (this is the same way it recalls memories). Scientists have long hypothesized that these neuronal representations emerge in a hierarchical process limited to the same cortical region in which the representations are first processed.
Because the brain perceives and recognizes the external world through these internal images, any new information about the process by which this takes place has the power to inform our understanding of related functions, including knowledge acquisition and memory.
However, studies attempting to uncover the functional hierarchy involved in the cortical process of visual stimuli have tried to characterize this hierarchy by analyzing the activity of single nerve cells, which are not necessarily correlated with neurons nearby, thus leaving these analyses lacking.
In a new study appearing in the 12 July issue of the journal Science, lead author Toshiyuki Hirabayashi and colleagues focus not on single neurons but instead on the relationship between neuron pairs, testing the possibility that the representation of an object in a single brain region emerges in a hierarchically lower brain area.
"I became interested in this work," said Dr. Hirabayashi, "because I was impressed by the elaborate neuronal circuitry in the early visual system, which is well-studied, and I wanted to explore the circuitry underlying higher-order visual processing, which is not yet fully understood."
Hirabayashi and colleagues analyzed nerve cell pairs in cortical areas TE and 36, the latter of which is hierarchically higher, in two adult macaques. After these animals looked at six sets of paired stimuli for several months to learn to associate related objects (a process that can lead to pair-coding neurons in the brain), the researchers recorded neuron responses in areas TE and 36 of both animals as they again performed this task.
The neurons exhibited pair association, but not where the researchers would have thought. “The most surprising result,” said senior author Dr. Yasushi Miyashita “was that the neuronal circuit that generated pair-association was found only in area TE, not in area 36.” Indeed, based on previous studies, which indicated that the number of pair-coding neurons in area TE is much smaller, the researchers would have expected the opposite.
During their study, Miyashita and other team members observed that in region TE of the macaque cortex, unit 1 neurons (or source neurons) provided input to unit 2 neurons (or target neurons), which—unlike unit 1 neurons—responded to both members of a stimulus pair.
"The representations generated in area TE did not reflect a mere random fluctuation of response patterns," explained Dr. Miyashita, "but rather, they emerged as a result of circuit processing inherent to that area of the brain."
In area 36, meanwhile, members of neuron pairs behaved differently; on average, unit 1 as well as unit 2 neurons responded to both members of a stimulus pair. Neurons in area 36 received input from area TE, but only from its unit 2 neurons.
Taken together, these findings lead the authors to hypothesize the existence of a hierarchical relationship between regions TE and 36, in which paired associations first established in the former region are propagated to the latter one. Here, area 36 represents the next level of a so-called feed forward hierarchy.
The work by Hirabayashi and colleagues suggests that the detailed representations of objects commonly observed in the brain are attained not by buildup of representations in a single area, but by emergence of these representations in a hierarchically prior area and their subsequent transfer to the brain region that follows. There, they become sufficiently prevalent for the brain to register. The work also reveals that the brain activity involved in recreating visual stimuli emerges in a hierarchically lower brain area than previously thought.
Moving forward, the Japanese research team has plans to expand upon this research, thus continuing to contribute to studies worldwide that aim to give scientists the best possible tools with which to obtain a dynamic picture of the brain. As a next step, the team hopes to further elucidate interactions between the various cortical microcircuits that operate in memory encoding. Dr. Miyashita has conjectured that these microcircuits are manipulated by a global brain network. Using the results of this latest study, he and colleagues are poised to further evaluate this assumption.
"It will also be important to weave the neuronal circuit mechanisms into a unified framework," said Dr. Hirabayashi," and to examine the effects of learning on these circuit organizations."
Equipped with their new view of cortical processing, the team also hopes to trace the causal chain of memory retrieval across different areas of the cortex. “I am excited by the recent development of genetic tools that will allow us to do this,” said Dr. Miyashita. A better understanding of object representations from one area of the brain to the next will shed even greater light on elusive aspects of this hierarchical organ.
(Source: eurekalert.org)
Researchers discover a gene’s key role in building the developing brain’s scaffolding
The gene, Arl13b, is necessary for the proper construction of the cerebral cortex. The finding offers new insights on normal brain development and illuminates some of the factors behind Joubert’s syndrome, a rare neurological disorder.
Researchers have pinpointed the role of a gene known as Arl13b in guiding the formation and proper placement of neurons in the early stages of brain development. Mutations in the gene could help explain brain malformations often seen in neurodevelopmental disorders.
The research, led by a team at the University of North Carolina School of Medicine, was published June 30 in the journal Nature Neuroscience.
“We wanted to get a better sense of how the cerebral cortex is constructed,” said senior study author Eva Anton, PhD, a professor in the Department of Cell Biology and Physiology and a member of the UNC Neuroscience Center. “The cells we studied — radial glial cells — provide a scaffolding for the formation of the brain by making neurons and guiding them to where they have to go. This is the first step in the formation of functional neuronal circuitry in the brain. This study gives us new information about the mechanisms involved in that process.”
The researchers became interested in the Arl13b gene because of its expression in a part of the cell called primary cilium and its association with a rare neurological disorder known as Joubert syndrome. The syndrome is characterized by brain malformations and autism like features.
“In addition to helping us understand an important cellular mechanism involved in normal brain development, this study may offer an explanation for some of the malformations seen in Joubert syndrome patients,” said Anton. Although there is no immediate clinical application for these patients, the study does help illuminate the factors behind the disease. “It shows what may have gone wrong in some of those patients that led to the malformations,” said Anton.
The cerebral cortex, the brain’s “gray matter,” is responsible for higher-order functions such as memory and consciousness. Like the scaffolding builders use to move people and materials during construction, radial glial cells provide an instructive matrix to create the basic structural features of the cerebral cortex. Mistakes in the formation and development of radial glial cells can translate into structural problems in the brain as it develops, said Anton.
Both mice and humans have the Arl13b gene. The researchers generated a series of mice with mutations on the Arl13b gene at different developmental stages to track the mutations’ effects on brain development. They discovered that the gene is crucial to the radial glial cells’ ability to sense signals through an appendage called the primary cilium. Without this signaling capability, the radial glia were unable to organize into an instructive scaffold capable of orchestrating the orderly formation of cerebral cortex. “The cilia in these cells play an important role in the initial setup of this scaffolding,” said Anton. “Without a functioning Arl13b gene, the cells were not able to determine polarity and formed haphazardly. As a result, they formed a malformed cerebral cortex with ectopic clusters of neurons, instead of the orderly layers of neurons with appropriate connectivity that would be expected, in the developing brain.
Genes Involved in Birth Defects May Also Lead to Mental Illness
Gene mutations that lead to major birth defects may also cause subtle disruptions in the brain that contribute to psychiatric disorders such as schizophrenia, autism, and bipolar disorder, according to new research by UC San Francisco scientists.
Over the past several years, researchers in the laboratory of psychiatrist Benjamin Cheyette, MD, PhD, have shown that mutations in a gene called Dact1 cause cell signaling networks to go awry during embryonic development. Researchers observed that mice with Dact1 mutations were born with a range of severe malformations, including some reminiscent of spina bifida in humans.
This new study was designed to explore whether Dact1 mutations exert more nuanced effects in the brain that may lead to mental illness. In doing so, Cheyette, John Rubenstein, MD, PhD, and colleagues in UCSF’s Nina Ireland Laboratory of Developmental Neurobiology used a genetic technique in adult mice to selectively delete the Dact1 protein only in interneurons, a group of brain cells that regulates activity in the cerebral cortex, including cognitive and sensory processes. Poor function of interneurons has been implicated in a range of psychiatric conditions.
As reported in the June 24 online issue of PLOS ONE, researchers found that the genetically altered interneurons appeared relatively normal and had managed to find their proper position in the brain’s circuitry during development. But the cells had significantly fewer synapses, the sites where communication with neighboring neurons takes place. In additional observations not included in the new paper, the team also noted that the cells’ dendrites – fine extensions that normally form bushy arbors studded with synapses – were poorly developed and sparsely branched.
“When you delete this gene function after initial, early development – just eliminating it in neurons after they’ve formed – they migrate to the right place and their numbers are correct, but their morphology is a little off,” Cheyette said. “And that’s very much in line with the kinds of pathology that people have been able to identify in psychiatric illness.
"Neurological illnesses tend to be focal, with lesions that you can identify or pathology you can see on an imaging study," Cheyette explained. "Psychiatric illnesses? Not so much. The differences are really subtle and hard to see.”
Key Gene’s Role in Development of Human Nervous System
The Dact1 protein is part of a fundamental biological system known as the Wnt (pronounced “wint”) signaling pathway. Interactions among proteins in the Wnt pathway orchestrate many processes essential to life in animals as diverse as fruit flies, mice and humans, including the proper development of the immensely complex human nervous system from a single fertilized egg cell.
One way the Wnt pathway manages this task is by maintaining the “polarity” of cells during development, said Cheyette, “a process of sequestering, increasing the concentration of one set of proteins on one side of the cell and a different set of proteins on the other side of the cell.” Polarity is particularly important as precursor cells transform into nerve cells, Cheyette said, because neurons are “the most polarized cells in the body,” with specialized input and output zones that must wind up in the proper spots if the cells are to function normally.
Cheyette said his group is now conducting behavioral experiments with the mice analyzed in the new PLOS ONE paper and with genetically related mouse lines to test whether these mice have behavioral abnormalities in sociability, sensory perception, anxiety or motivation that resemble symptoms in major psychiatric disorders.
He also hopes to collaborate with UCSF colleagues on follow-up experiments to determine whether the activity of neurons lacking Dact1 is impaired in addition to the structural flaws identified in the new study and prior published work from his lab.
Meanwhile, as-yet-unpublished findings from human genetics research conducted by Cheyette’s group suggest that individuals with autism are significantly more likely than healthy comparison subjects to carry mutations in a Wnt pathway gene called WNT1.
“Just because a gene plays an important role in the embryo doesn’t mean it isn’t also important in the brain later, and might be involved in psychiatric pathology,” said Cheyette. “When these genes are mutated, someone may look fine, develop fine and have no obvious medical problems at birth, but they may also develop autism in childhood or have a psychotic break in adulthood and develop schizophrenia.”
Scientists at the University of Massachusetts Medical School have developed a novel transgenic system which allows them to remotely activate individual brain cells in the model organism Drosophila using ambient temperature. This powerful new tool for identifying and characterizing neural circuitry has lead to the identification of a pair of neurons – now called Fdg neurons – in the fruit fly that decide when to eat and initiate the subsequent feeding action. Discovery of these neurons may help neurobiologists better understand how the brain uses memory and stimuli to produce classically conditioned responses, such as those often associated with phobias or drug tolerance. The study appears in the journal Nature.

"For any organism, the decision to eat is a complex integration of internal and external stimuli leading to the activation of an organized sequence of motor patterns," said Motojiro Yoshihara, PhD, assistant professor of neurobiology at the University of Massachusetts Medical School and lead author of the Nature study. “By developing genetic tools to remotely activate individual brain cells in Drosophila, we’ve been able to isolate a pair of neurons that are critical to the act of eating in fruit flies. More importantly, we now have a powerful new tool with which we can answer important questions about the function and composition of neural circuitry.”
To isolate the neurons responsible for sensing food and initiating the complex feeding program in Drosophila, UMMS scientists had to develop a method of studying the behavior of freely moving flies while targeting and manipulating individual neurons. To accomplish this, Dr. Yoshihara expressed temperature activated genes in random neurons in more than 800 Drosophila lines. Placing these genetically modified flies in a small temperature-controlled chamber, he was able to active these genes by increasing and decreasing the ambient temperature. This, in turn, activated the corresponding neurons.
Under wild conditions, when a hungry fly comes in contact with food it ceases motion and executives eight basic motor functions resulting in the consumption of the food. When the temperature in the chamber was increased, Yoshihara and colleagues were able to isolate a single Drosophila line which exhibited these eight motor functions, even in the absence of food or other stimuli. Subsequent experiments revealed that the feeding mechanism initiated by activating the transgenes was being controlled by a single pair of neurons in the fly’s brain. Furthermore, these feeding (Fdg) neurons were responsible for synthesizing cues about available food and hunger, and using them to start the feeding mechanism.
"Our results showed that these neurons become active in the presence of a food source for the fly, but the response was contingent on whether the animal was hungry," said Yoshihara. "This means that these neurons are integrating both internal and external stimuli in order to initiate a complex feeding behavior with multiple motor programs."
Yoshihara believes this discovery will provide researchers with a powerful new tool for isolating, analyzing and characterizing aspects of the brain’s neural circuitry and studying how information is integrated in the brain. In the future, Yoshihara plans to use the Fdg-neurons to study the biological basis of classical or Pavlovian conditioning. Doing so, he hopes to uncover how memory integrates stimuli to illicit a conditioned behavior.
(Source: eurekalert.org)
By trying it all, predatory sea slug learns what not to eat
Researchers have found that a type of predatory sea slug that usually isn’t picky when it comes to what it eats has more complex cognitive abilities than previously thought, allowing it to learn the warning cues of dangerous prey and thereby avoid them in the future.
The research appears in the Journal of Experimental Biology.
Pleurobranchaea californica is a deep-water species of sea slug found off the west coast of the United States. It has a relatively simple neural circuitry and set of behaviors. It is a generalist feeder, meaning, as University of Illinois professor of molecular and integrative physiology and leader of the study Rhanor Gillette put it, that members of this species “seem to try anything once.”
Another sea slug species, Flabellina iodinea, commonly known as the Spanish shawl because of the orange outgrowths called cerata that cover its purple back, also lives off the west coast. Unlike Pleurobranchaea, however, the Spanish shawl eats only one type of food, an animal called Eudendrium ramosum. According to Gillette, the Spanish shawl digests the Eudendrium’s entire body except for its embryonic, developing stinging cells. The Spanish shawl instead transports these stinging cells to its own cerata where they mature, thereby co-opting its victim’s body parts for its own defense.
The story of Gillette’s Pleurobranchaea-Flabellina research began with a happy accident that involved showing a lab visitor Pleurobranchaea’s penchant for predation.
“I had a Pleurobranchaea in a small aquarium that we were about to do a physiological experiment with, and my supplier from Monterey had just sent me these beautiful Spanish shawls,” Gillette said. “So I said to the visitor, ‘Would you like to see Pleurobranchaea eat another animal?’”
Gillette placed the Spanish shawl into the aquarium. The Pleurobranchaea approached, smelled, and bit the purple and orange newcomer. However, the Flabellina’s cerata stung the Pleurobranchaea, the Spanish shawl was rejected and left to do its typical “flamenco dance of escape,” and Pleurobranchaea also managed to escape with an avoidance turn.
Some minutes later, his curiosity piqued, Gillette placed the Spanish shawl back into the aquarium with the Pleurobranchaea. Rather than try to eat the Spanish shawl a second time, the Pleurobranchaea immediately started its avoidance turn. (Watch a video of this interaction.)
“I had never seen that before! We began testing them and found that they were learning the odor of the Spanish shawl very specifically and selectively,” Gillette said.
Gillette and his team later replicated that day’s events by placing a Pleurobranchaea in a training arena 12-15 centimeters from a Spanish shawl, then recorded the Pleurobranchaea’s behavior. They returned the Pleurobranchaea to the arena for four more trials in 20-minute intervals, then repeated the procedure 24 and 72 hours later.
In the experiments, those Pleurobranchaea whose feeding thresholds were too high (meaning they were already full) or too low (they were extremely hungry) would either not participate or completely consume the Spanish shawl, respectively. Those that were hungry, but not ravenously so, continued to exhibit the avoidance-turn behavior when placed with the Spanish shawl even 72 hours later.
This showed that Pleurobranchaea was selective in its food choices, but only on a case-by-case basis; the sea slugs already trained to avoid the Spanish shawl would readily eat a species closely related to Flabellina called Hermissenda crassicornis.
Such behaviors come in handy in Pleurobranchaea’s natural environment, Gillette said.
“If you’re a generalist like Pleurobranchaea, it’s highly strategic and advantageous to learn what’s good and what’s not good so you can decide whether or not to take the risk or of attacking certain types of prey,” he said.
These findings show that the “simple” Pleurobranchaea is much more complex than originally thought.
“We already knew the neuronal circuitry that mediates this kind of decision,” Gillette said. “Finding this highly selective type of learning enlarges our perspective of function, in terms of the animal’s ability to make cost-benefit decisions that place it on a rather higher plane of cognitive ability than previously thought for many sea slugs.”
Breakthrough in neuroscience could help re-wire appetite control
Researchers at the University of East Anglia (UEA) have made a discovery in neuroscience that could offer a long-lasting solution to eating disorders such as obesity.
It was previously thought that the nerve cells in the brain associated with appetite regulation were generated entirely during an embryo’s development in the womb and therefore their numbers were fixed for life.
But research published today in the Journal of Neuroscience has identified a population of stem cells capable of generating new appetite-regulating neurons in the brains of young and adult rodents.
Obesity has reached epidemic proportions globally. More than 1.4 billion adults worldwide are overweight and more than half a billion are obese. Associated health problems include type 2 diabetes, heart disease, arthritis and cancer. And at least 2.8 million people die each year as a result of being overweight or obese.
The economic burden on the NHS in the UK is estimated to be more than £5 billion annually. In the US, the healthcare cost tops $60 billion.
Scientists at UEA investigated the hypothalamus section of the brain – which regulates sleep and wake cycles, energy expenditure, appetite, thirst, hormone release and many other critical biological functions. The study looked specifically at the nerve cells that regulate appetite.
The researchers used ‘genetic fate mapping’ techniques to make their discovery – a method that tracks the development of stem cells and cells derived from them, at desired time points during the life of an animal.
They established that a population of brain cells called ‘tanycytes’ behave like stem cells and add new neurons to the appetite-regulating circuitry of the mouse brain after birth and into adulthood.
Lead researcher Dr Mohammad K. Hajihosseini, from UEA’s school of Biological Sciences, said: “Unlike dieting, translation of this discovery could eventually offer a permanent solution for tackling obesity.
“Loss or malfunctioning of neurons in the hypothalamus is the prime cause of eating disorders such as obesity.
“Until recently we thought that all of these nerve cells were generated during the embryonic period and so the circuitry that controls appetite was fixed.
“But this study has shown that the neural circuitry that controls appetite is not fixed in number and could possibly be manipulated numerically to tackle eating disorders.
“The next step is to define the group of genes and cellular processes that regulate the behaviour and activity of tanycytes. This information will further our understanding of brain stem cells and could be exploited to develop drugs that can modulate the number or functioning of appetite-regulating neurons.
“Our long-term goal of course is to translate this work to humans, which could take up to five or 10 years. It could lead to a permanent intervention in infancy for those predisposed to obesity, or later in life as the disease becomes apparent.”