Posts tagged memory
Posts tagged memory
New research from Karolinska Institutet shows that omega-3 fatty acids in dietary supplements can cross the blood brain barrier in people with Alzheimer’s disease, affecting known markers for both the disease itself and inflammation. The findings are presented in the Journal of Internal Medicine, and strengthen the evidence that omega-3 may benefit certain forms of this seriously debilitating disease.
"Earlier population studies indicate that omega-3 can protect against Alzheimer’s disease, which makes it interesting to study the effects of dietary supplements containing this group of fatty acids in patients who have already developed the disease," says the study’s lead author Dr Yvonne Freund-Levi.
Omega-3 and other essential polyunsaturated fatty acids accumulate in the central nervous system (CNS) during gestation. It has been assumed that these acids are continually replaced throughout life, but little is known about how this occurs and whether changes in diet can affect the transport of important fatty acids across the blood-brain barrier. The blood-brain barrier serves to protect the brain from harmful chemicals existing naturally in the blood, but also blocks the delivery of drug substances to the brain.
Several diseases can affect the fatty acid profile of the CNS; in patients with Alzheimer’s disease, for example, previous research has observed lower than normal brain concentrations of docosahexaenoic acid (DHA), an omega-3 fatty acid.
In the present study, part of the larger OmegAD project, scientists examined whether omega-3 dietary supplements change the fatty acid profile of the CNS in patients with mild Alzheimer’s disease. Thirty-three patients participated in the study, 18 of whom received a daily omega-3 supplement and 15 a placebo for six months. The results show that the first group had higher levels of both DHA and eicosapentaenoic acid (EPA, another omega-3 fatty acid) in their cerebrospinal fluid (which surrounds the CNS) and blood. No such change was seen in the placebo group.
Moreover, they also found that levels of DHA correlated directly with the degree of change in Alzheimer’s disease and inflammatory markers in the cerebrospinal fluid. Researchers in the field have long been interested in this link between Alzheimer’s disease and inflammation, but attempts to treat the disease using traditional anti-inflammatory drugs have failed to produce any improvements in memory function.
"In animals, DHA dietary supplements can lead to an increase in DHA concentrations in the CNS," says Professor Jan Palmblad, who initiated the study. "Here we show that the same applies to humans, which suggests that omega-3 fatty acids in dietary supplements cross the blood-brain barrier. However, much work remains to be done before we know how these fatty acids can be used in the treatment of Alzheimer’s disease to halt memory loss."
In a new paper published in the current issue of Neuron, McLean Hospital and Harvard Medical School researchers report that increased activity in the medial prefrontal cortex (mPFC) of the brain is linked to decreased activity in the amygdala, the portion of the brain used in the creation of memories of events that scared those exposed.
According to author Vadim Bolshakov, PhD, director of the Cellular Neurobiology Laboratory at McLean and professor at Harvard Medical School, this finding is significant in that it could lead to better methods to prevent PTSD.
"A single exposure to something traumatic or scary can be enough to create a fear memory—causing someone to expect and be afraid in similar situations in the future," said Bolshakov. "What we’re seeing is that we may one day be able to prevent those fear memories."
Bolshakov and his colleagues tested their theory using animal models. Dividing the mice into two groups, some were taught to fear an auditory stimulus while in others fear memory was extinguished Increased activation of mPFC in extinguished animals led to inhibition of the amygdala and significant decreases in fear responses.
"For example, if a sound ended with an extremely loud shriek, a subject would come to expect that scary noise at the end of the sound," explained Bolshakov. "What we found was when we suppressed the fear memory by decreasing activity in the amygdala, the subjects were not afraid of the end of the auditory stimulus any longer."
Bolshakov notes that this work could have serious implications for the treatment of a number of conditions including PTSD.
"While there is still a great deal of research that needs to be done before our work can be translated to clinical trials, what we are showing has the potential to ensure that individuals exposed to trauma were not haunted by the conditions surrounding their initial stressor."
Attention, parents: The messier your child gets while playing with food in the high chair, the more he or she is learning.
Researchers at the University of Iowa studied how 16-month-old children learn words for nonsolid objects, from oatmeal to glue. Previous research has shown that toddlers learn more readily about solid objects because they can easily identify them due to their unchanging size and shape. But oozy, gooey, runny stuff? Not so much.
New research shows that changes if you put toddlers in a setting they know well. In those instances, word learning increases, because children at that age are “used to seeing nonsolid things in this context, when they’re eating,” says Larissa Samuelson, associate professor in psychology at the UI who has worked for years on how children learn to associate words with objects. “And, if you expose them to these things when they’re in a highchair, they do better. They’re familiar with the setting and that helps them remember and use what they already know about nonsolids.”
In a paper published in the journal Developmental Science, Samuelson and her team at the UI tested their idea by exposing 16-month-olds to 14 nonsolid objects, mostly food and drinks such as applesauce, pudding, juice, and soup. They presented the items and gave them made-up words, such as “dax” or “kiv.” A minute later, they asked the children to identify the same food in different sizes or shapes. The task required the youngsters to go beyond relying simply on shape and size and to explore what the substances were made of to make the correct identification and word choice.
Not surprisingly, many children gleefully dove into this task by poking, prodding, touching, feeling, eating—and yes, throwing—the nonsolids in order to understand what they were and make the correct association with the hypothetical names. The toddlers who interacted the most with the foods—parents, interpret as you want—were more likely to correctly identify them by their texture and name them, the study determined. For example, imagine you were a 16-month-old gazing at a cup of milk and a cup of glue. How would you tell the difference by simply looking?
“It’s the material that makes many nonsolids,” Samuelson notes, “and how children name them.”
The setting matters, too, it seems. Children in a high chair were more apt to identify and name the food than those in other venues, such as seated at a table, the researchers found.
“It turns out that being in a high chair makes it more likely you’ll get messy, because kids know they can get messy there,” says Samuelson, the senior author on the paper.
The authors say the exercise shows how children’s behavior, environment (or setting), and exploration help them acquire an early vocabulary—learning that is linked to better later cognitive development and functioning.
“It may look like your child is playing in the high chair, throwing things on the ground, and they may be doing that, but they are getting information out of (those actions),” Samuelson contends. “And, it turns out, they can use that information later. That’s what the high chair did. Playing with these foods there actually helped these children in the lab, and they learned the names better.”
“It’s not about words you know, but words you’re going to learn,” Samuelson adds.
Certain symptoms of schizophrenia may arise from uncontrolled activation of neurons that help to build memories during periods of rest
Sufferers of schizophrenia experience a broad gamut of symptoms, including hallucinations and delusions as well as disorientation and problems with learning and memory. This diversity of neurological deficits has made schizophrenia extremely difficult for scientists to understand, thwarting the development of effective treatments. A research team led by Susumu Tonegawa from the RIKEN–MIT Center for Neural Circuit Genetics has now revealed disruptions in the activity of particular clusters of neurons that might account for certain core symptoms of this disorder.
Tonegawa’s laboratory previously found that mice lacking the protein calcineurin in certain regions of the brain exhibit many behavioral deficits that are characteristic of schizophrenia. In their most recent study, the researchers sought out physiological alterations at the single-cell or circuit level that could connect the absence of the calcineurin protein in the brain with these behavioral impairments.
Their study focused on the hippocampus, a region of the brain associated with memory and spatial learning. Within the hippocampus, specialized ‘place cells’ switch on and off as an animal explores its environment. During subsequent periods of wakeful rest, these place cells continue to fire in patterns that essentially ‘replay’ recent wanderings, allowing the brain to build memories based on these experiences. The researchers used precisely positioned electrodes to measure differences in brain activity in these cells for normal mice and the calcineurin-deficient mouse model of schizophrenia.
Remarkably, essentially identical place-cell activity patterns were observed for both sets of mice during active exploration. Once the animals were at rest, however, the calcineurin-deficient mice displayed a dramatic increase in place-cell activity. In the normal hippocampus, the resting replay process depended on sequential activity from place cells corresponding to specific, real-world spatial coordinates. In contrast, this correlation was all but lost in the calcineurin-deficient mice. Instead, these neurons often seemed to fire indiscriminately, creating high levels of ‘noise’ that overwhelmed actual location information and thwarted memory formation.
“Our study provides the first potential evidence of disorganized thinking processes in a schizophrenia model at the single-cell and circuit level,” says Junghyup Suh, a member of Tonegawa’s research team. These findings fit with an emerging model that suggests that schizophrenic symptoms may arise from excess activation of brain regions within a ‘default mode network’—which includes the hippocampus—during wakeful rest. “Neurobiological approaches that can calm down the default mode network may therefore open up new avenues to alleviating symptoms or curing this mental disorder,” says Suh.
Scientists have long suspected that corvids – the family of birds including ravens, crows and magpies – are highly intelligent. Now, Tübingen neurobiologists Lena Veit und Professor Andreas Nieder have demonstrated how the brains of crows produce intelligent behavior when the birds have to make strategic decisions. Their results are published in the latest edition of Nature Communications.
Crows are no bird-brains. Behavioral biologists have even called them “feathered primates” because the birds make and use tools, are able to remember large numbers of feeding sites, and plan their social behavior according to what other members of their group do. This high level of intelligence might seem surprising because birds’ brains are constructed in a fundamentally different way from those of mammals, including primates – which are usually used to investigate these behaviors.
The Tübingen researchers are the first to investigate the brain physiology of crows’ intelligent behavior. They trained crows to carry out memory tests on a computer. The crows were shown an image and had to remember it. Shortly afterwards, they had to select one of two test images on a touchscreen with their beaks based on a switching behavioral rules. One of the test images was identical to the first image, the other different. Sometimes the rule of the game was to select the same image, and sometimes it was to select the different one. The crows were able to carry out both tasks and to switch between them as appropriate. That demonstrates a high level of concentration and mental flexibility which few animal species can manage – and which is an effort even for humans.
The crows were quickly able to carry out these tasks even when given new sets of images. The researchers observed neuronal activity in the nidopallium caudolaterale, a brain region associated with the highest levels of cognition in birds. One group of nerve cells responded exclusively when the crows had to choose the same image – while another group of cells always responded when they were operating on the “different image” rule. By observing this cell activity, the researchers were often able to predict which rule the crow was following even before it made its choice.
The study published in Nature Communications provides valuable insights into the parallel evolution of intelligent behavior. “Many functions are realized differently in birds because a long evolutionary history separates us from these direct descendants of the dinosaurs,” says Lena Veit. “This means that bird brains can show us an alternative solution out of how intelligent behavior is produced with a different anatomy.” Crows and primates have different brains, but the cells regulating decision-making are very similar. They represent a general principle which has re-emerged throughout the history of evolution. “Just as we can draw valid conclusions on aerodynamics from a comparison of the very differently constructed wings of birds and bats, here we are able to draw conclusions about how the brain works by investigating the functional similarities and differences of the relevant brain areas in avian and mammalian brains,” says Professor Andreas Nieder.
Do fruit flies hold the key to treating dementia? Researchers at the University of Houston (UH) have taken a significant step forward in unraveling the mechanisms of Pavlovian conditioning. Their work will help them understand how memories form and, ultimately, provide better treatments to improve memory in all ages.
Gregg Roman, an associate professor of biology and biochemistry at UH, and Shixing Zhang, his postdoctoral associate, describe their findings in a paper titled “Presynaptic Inhibition of Gamma Lobe Neurons Is Required for Olfactory Learning in Drosophila,” appearing Nov. 27 in Current Biology, a scientific bimonthly journal published by Cell Press.
“Memory is essential to our daily function and is also central to our sense of self,” Roman said. “To a large degree, we are the sum of our experiences. When memories can no longer be retrieved or we have difficulty in forming new memories, the effects are frequently tragic. In the future, our work will enable us to have a better understanding of how human memories form.”
Roman and Zhang set about to unravel some of these mysteries by studying the brains of fruit flies (Drosophila). Within the fly brain, Roman says, there are nerve cells that play a role in olfactory learning and memory. Olfactory learning, he says, is an example of classical conditioning first described by Pavlov in his experiment with dogs. In their study, the flies were trained to associate a weak electric shock with an odor. After training, the flies avoided that odor.
“We found that these particular nerve cells – the gamma lobe neurons of the mushroom bodies in the insect brain – are activated by odors. Training the flies to associate an odor with an electric shock changed how these cells responded to odors by developing a modification in gamma lobe neuron activity, known as a memory trace,” he said. “Interestingly, we found that training caused the gamma lobe neurons to be more weakly activated by odors that were not paired with an electric shock, while the odors paired with electric shock maintained a strong activation of these neurons. Thus, the gamma lobe neurons responded more strongly to the trained odor than to the untrained odor.”
The team also showed that a specific protein – the heterotrimeric G(o) protein – is naturally involved in inhibiting gamma lobe neurons. Roman says removing the activity of this protein only within the gamma lobe neurons resulted in a loss of the memory trace and, thus, poor learning. Therefore, inhibiting the release of neurotransmitters from these neurons through the actions of the G(o) protein is key to forming the memory trace and associative memories.
The significance of using fruit flies is that while their brain structure is much simpler with far fewer neurons, the mushroom body is analogous to the perirhinal cortex in humans, which serves the same function of sensory integration and learning. This simplicity allows scientists to gain insights into how memories are acquired, stored and retrieved.
“Drosophila represents the Goldilocks principle of neural research, with sufficient behavioral complexity, while maintaining a huge advantage in neural simplicity,” Roman said. “The complex behaviors allow us to examine many behavioral processes like learning, attention, aggression and addiction-like behaviors, while the simplicity allows us to dissect the crucial neural activities down to single cells. Additionally, Drosophila has the most powerful genetic toolkit available for behavioral experimentation. In using these tools, we are genetically identifying the molecules necessary to perform these behaviors and dissecting the logic of the neural circuits that allow for changes in behavior to occur.”
The pair says all their experience to date suggests the molecules and logic will translate to most animals, including humans, leading to a more complete understanding of how memories form in humans, both at the level of molecules and through the activity of neural circuits.
Carrying a particular version of the gene for apolipoprotein E (APOE) is the major known genetic risk factor for the sporadic, late-onset form of Alzheimer’s disease, but exactly how that variant confers increased risk has been controversial among researchers. Now an animal study led by Massachusetts General Hospital (MGH) investigators shows that even low levels of the Alzheimer’s-associated APOE4 protein can increase the number and density of amyloid beta (A-beta) brain plaques, characteristic neuronal damage, and the amount of toxic soluble A-beta within the brain in mouse models of the disease. Introducing APOE2, a rare variant that has been associated with protection from developing Alzheimer’s disease, into the brains of animals with established plaques actually reduced A-beta deposition, retention and neurotoxicity, suggesting the potential for gene-therapy-based treatment.
"Using a technique developed by our collaborators at the University of Iowa, we were able to get long-term expression of these human gene variants in the fluid that bathes the entire brain," says Bradley Hyman, MD, PhD, of the MassGeneral Institute for Neurodegenerative Disease (MGH-MIND), senior author of the report in the Nov. 20 Science Translational Medicine. “Our results suggest that strategies aimed at decreasing levels of APOE4, the harmful form of the protein, and increasing concentrations of protective variant APOE2 could be helpful to patients.”
The association between the APOE4 variant and increased Alzheimer’s risk was first made more than 20 years ago. Subsequent research has established that carrying two copies of the harmful variant increases risk 12 times compared with having two copies of the more common form, APOE3. Inheriting the APOE2 variant, however, appears to cut the risk in half. The extremely rare gene variants that directly cause the familial forms of the disease all participate in the production and deposition of A-beta, but exactly how APOE variants contribute to the process has been poorly understood.
Secreted by certain brain cells, APOE is known to regulate cholesterol metabolism within the brain and can bind to A-beta peptides, suggesting that the different forms of the protein may affect whether and how toxic A-beta plaques form. While previous investigations into the protein’s effects have used either mice in which gene expression was knocked out or transgenic animals that expressed human gene variants throughout their lifetimes, the MGH-MIND-led study used a different approach to investigate the effects of introducing the variant forms of the protein into brains in which plaque formation had already begun. They directly injected into the cerebrospinal fluid of a mouse model of Alzheimer’s – adult animals in which plaques were well established – viral vectors carrying genes for one of the three APOE variants or a control protein.
Two month after the vectors had been injected, about 10 percent of the APOE in the brains of animals that received one of the variants was found to be the introduced human version. At five months after injection, examination of brain tissue revealed that the A-beta plaques in mice that received APOE4 injections were more numerous and significantly denser than those of mice receiving APOE2. The growth of plaques in animals receiving APOE3 was intermediate between that of the other two groups and similar to what was seen in control animals. Levels of A-beta in the blood of mice that received APOE2 were higher than in the other groups, suggesting that the protective variant had increased clearance of A-beta from the brain.
In a group of animals in which tiny implanted windows allowed direct imaging of brain tissue, the progression of A-beta plaque deposition was fastest in animals receiving APOE4 and slowest, sometimes even appearing to regress, in mice injected with APOE2. Signs of neuronal damage around plaques also varied depending on the APOE variant the animals received, and experiments in a different Alzheimer’s model in which plaques appear more slowly showed that injection of APOE4 increased levels of free, soluble A-beta in the fluid that bathes the brain.
"This study has allowed us to sort out, in mice, which effects of the different types of APOE were most important to variation in amyloid plaque deposition," says Eloise Hudry, PhD, of MGH-MIND, lead author of the Science Translational Medicine report. “Our results imply that APOE-based therapeutic approaches may help to alleviate the progression of Alzheimer’s disease. More study is needed to pursue that possibility and to investigate the potential use of this gene transfer technology to introduce other protective proteins into the brain.”
Researchers from TAU demonstrate hyperbaric oxygen therapy significantly revives brain functions and life quality
Every year, nearly two million people in the United States suffer traumatic brain injury (TBI), the leading cause of brain damage and permanent disabilities that include motor dysfunction, psychological disorders, and memory loss. Current rehabilitation programs help patients but often achieve limited success.
Now Dr. Shai Efrati and Prof. Eshel Ben-Jacob of Tel Aviv University’s Sagol School of Neuroscience have proven that it is possible to repair brains and improve the quality of life for TBI victims, even years after the occurrence of the injury.
In an article published in PLoS ONE, Dr. Efrati, Prof. Ben Jacob, and their collaborators present evidence that hyperbaric oxygen therapy (HBOT) should repair chronically impaired brain functions and significantly improve the quality of life of mild TBI patients. The new findings challenge the often-dismissive stand of the US Food and Drug Administration, Centers for Disease Control and Prevention, and the medical community at large, and offer new hope where there was none.
The research trial
The trial included 56 participants who had suffered mild traumatic brain injury one to five years earlier and were still bothered by headaches, difficulty concentrating, irritability, and other cognitive impairments. The patients’ symptoms were no longer improving prior to the trial.
The participants were randomly divided into two groups. One received two months of HBOT treatment while the other, the control group, was not treated at all. The latter group then received two months of treatment following the first control period. The treatments, administered at the Institute of Hyperbaric Medicine at Assaf Harofeh Medical Center, headed by Dr. Efrati, consisted of 40 one-hour sessions, administered five times a week over two months, in a high pressure chamber, breathing 100% oxygen and experiencing a pressure of 1.5 atmospheres, the pressure experienced when diving under water to a depth of 5 meters. The patients’ brain functions and quality of life were then assessed by computerized evaluations and compared with single photon emission computed tomography (SPECT) scans.
In both groups, the hyperbaric oxygen therapy sessions led to significant improvements in tests of cognitive function and quality of life. No significant improvements occurred by the end of the period of non-treatment in the control group. Analysis of brain imaging showed significantly increased neuronal activity after a two-month period of HBOT treatment compared to the control periods of non-treatment.
"What makes the results even more persuasive is the remarkable agreement between the cognitive function restoration and the changes in brain functionality as detected by the SPECT scans," explained Prof. Ben-Jacob. "The results demonstrate that neuroplasticity can be activated for months and years after acute brain injury."
"But most important, patients experienced improvements such as memory restoration and renewed use of language," Dr. Efrati said. "These changes can make a world of difference in daily life, helping patients regain their independence, go to work, and integrate back into society."
The regeneration process following brain injury involves complex processes, such as building new blood vessels and rebuilding connections between neurons, and requires much energy.
"This is where HBOT treatment can help," said Dr. Efrati. "The elevated oxygen levels during treatment supply the necessary energy for facilitating the healing process."
The findings offer new hope for millions of traumatic brain injury patients, including thousands of veterans wounded in action in Iraq and Afghanistan. The researchers call for additional larger scale, multi-center clinical studies to further confirm the findings and determine the most effective and personalized treatment protocols. But since the hyperbaric oxygen therapy is the only treatment proven to heal TBI patients, the researchers say that the medical community and the US Armed Forces should permit the victims of TBI benefit from the new hope right now, rather than waiting until additional studies are completed.
Based on the largest comprehensive systematic review to date, researchers at the Perelman School of Medicine at the University of Pennsylvania concluded that available evidence does not support an association between statins and memory loss or dementia. The new study, a collaborative effort between faculty in Penn Medicine’s Preventive Cardiovascular Program, the Penn Memory Center, and the Penn Center for Evidence-Based Practice, will be published in Annals of Internal Medicine.
“Statins are prescribed to approximately 30 million people in the United States, and these numbers may increase as a result of the national cholesterol guidelines recently released,” said senior study author Emil deGoma, MD, assistant professor of Medicine and medical director of the Preventive Cardiovascular Program at Penn. “A wealth of data supports a benefit of these cholesterol-lowering medications among individuals at risk for cardiovascular disease in terms of a reduction in the risk of heart attack and stroke; however, potential side effects of statins are less well understood. In February 2012, largely based on anecdotal reports, the U.S. Food and Drug Administration (FDA) issued a safety statement warning patients of possible adverse cognitive effects associated with statin use. Many concerned patients have asked if there is a relationship between statins and memory problems. Their concerns, along with the FDA statement, prompted us to pursue a rigorous analysis of all available evidence to better answer the question – are statins associated with changes in cognition?”
The research team conducted a systematic review of the published literature and identified 57 statin studies reporting measures of cognitive function. Dr. deGoma and colleagues found no evidence of an increased risk of dementia with statin therapy. In fact, in cohort studies, statin users had a 13 percent lower risk of dementia, a 21 percent lower risk of Alzheimer’s disease, and a 34 percent lower risk of mild cognitive impairment compared to people who did not take statins.
Most importantly, cognitive test scores were not adversely affected by statin treatment in randomized controlled trials. In these trials, roughly half of the study participants received statins and the other half received placebo. All study participants underwent formal testing of memory and other cognitive domains through tests such as the ability to recall a set of numbers. The analysis of 155 cognitive tests spanning eight categories of cognitive function, including 26 tests of memory, revealed no differences between study participants treated with statins and those provided placebo.
The research team additionally performed an analysis of the FDA post-marketing surveillance databases and found no difference in the frequency of cognitive adverse event reports between statins and two commonly prescribed cardiovascular medications that have not been associated with cognitive impairment, namely, clopidogrel and losartan.
“Overall, these findings are quite reassuring. I wouldn’t let concerns about adverse effects on cognition influence the decision to start a statin in patients suffering from atherosclerotic disease or at risk for cardiovascular disease. I also wouldn’t jump to the conclusion that statins are the culprit when an individual who is taking a statin describes forgetfulness. We may be doing more harm than good if we withhold or stop statins – medications proven to reduce the risk of heart attack and stroke – due to fears that statins might possibly cause memory loss,” said Dr. deGoma.
The team acknowledges that while their analysis is reassuring, large, high-quality randomized controlled trials are needed to confirm their findings.
“For many of the cognitive outcomes that we examined, the identified studies were small, were at risk for bias, used varying diagnostic tests to assess cognitive domains, and did not include patients on high-dose statins, which is important given the increasing use of high-dose statins for secondary prevention,” noted study co-author Craig Umscheid, MD, MSCE, assistant professor of Medicine and Epidemiology and director of the Penn Center for Evidence-based Practice. “Thus, additional trials addressing these limitations would strengthen our conclusions. Despite this, the totality of the evidence does reassure us that there’s unlikely to be a significant link between statins and cognitive impairment.”
New research on pond snails has revealed that high levels of stress can block memory processes. Researchers from the University of Exeter and the University of Calgary trained snails and found that when they were exposed to multiple stressful events they were unable remember what they had learned.
Previous research has shown that stress also affects human ability to remember. This study, published in the journal PLOS ONE, found that experiencing multiple stressful events simultaneously has a cumulative detrimental effect on memory.
Dr Sarah Dalesman, a Leverhulme Trust Early Career Fellow, from Biosciences at the University of Exeter, formally at the University of Calgary, said: “It’s really important to study how different forms of stress interact as this is what animals, including people, frequently experience in real life. By training snails, and then observing their behaviour and brain activity following exposure to stressful situations, we found that a single stressful event resulted in some impairment of memory but multiple stressful events prevented any memories from being formed.”
The pond snail, Lymnaea stagnalis, has easily observable behaviours linked to memory and large neurons in the brain, both useful benefits when studying memory processes. They also respond to stressful events in a similar way to mammals, making them a useful model species to study learning and memory.
In the study, the pond snails were trained to reduce how often they breathed outside water. Usually pond snails breathe underwater and absorb oxygen through their skin. In water with low oxygen levels the snails emerge and inhale air using a basic lung opened to the air via a breathing hole.
To train the snails not to breathe air they were placed in poorly oxygenated water and their breathing holes were gently poked every time they emerged to breathe. Snail memory was tested by observing how many times the snails attempted to breathe air after they had received their training. Memory was considered to be present if there was a reduction in the number of times they opened their breathing holes. The researchers also assessed memory by monitoring neural activity in the brain.
Immediately before training, the snails were exposed to two different stressful experiences, low calcium - which is stressful as calcium is necessary for healthy shells - and overcrowding by other pond snails.
When faced with the stressors individually, the pond snails had reduced ability to form long term memory, but were still able to learn and form short and intermediate term memory lasting from a few minutes to hours. However, when both stressors were experienced at the same time, results showed that they had additive effects on the snails’ ability to form memory and all learning and memory processes were blocked.
Future work will focus on the effects of stress on different populations of pond snail.