Chapter 13. Memory, Learning, and Development
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By Andy Coghlan The switching-off of genes in the human brain has been watched live for the first time. By comparing this activity in different people’s brains, researchers are now on the hunt for abnormalities underlying disorders such as Alzheimer’s disease and schizophrenia. To see where genes are most and least active in the brain, Jacob Hooker at Harvard Medical School and his team developed a radioactive tracer chemical that binds to a type of enzyme called an HDAC. This enzyme deactivates genes inside our cells, stopping them from making the proteins they code for. When injected into people, brain scans can detect where this tracer has bound to an enzyme, and thus where the enzyme is switching off genes. Live epigenetics The switching-off of genes by HDACs is a form of epigenetics – physical changes to the structure of DNA that modify how active genes are without altering their code. Until now, the only way to examine such activity in the brain has been by looking at post-mortem brain tissue. In the image above from the study, genes are least active in the red regions, such as the bulb-shaped cerebellum area towards the bottom right. The black and blue areas show the highest levels of gene activity – where barely any HDACs are present – and the yellow and green areas fall in between. © Copyright Reed Business Information Ltd.
Nicola Davis Scientists say that they have discovered a possible explanation for how Alzheimer’s disease spreads in the brain. Alzheimer’s is linked to a buildup of protein plaques and tangles that spread across particular tissues in the brain as the disease progresses. But while the pattern of this spread is well-known, the reason behind the pattern is not. Now scientists say they have uncovered a potential explanation as to why certain tissues of the brain are more vulnerable to Alzheimer’s disease. The vulnerability appears to be linked to variations in the levels of proteins in the brain that protect against the clumping of other proteins - variations that are present decades before the onset of the disease. Hope for Alzheimer's treatment as researchers find licensed drugs halt brain degeneration Read more “Our results indicate that within healthy brains a tell-tale pattern of protein levels predicts the progression of Alzheimer’s disease through the brain [in those that are affected by the disease],” said Rosie Freer, a PhD student at the University of Cambridge and first author of the study. The results could open up the possibility of identifying individuals who are at risk of developing Alzheimer’s long before symptoms appear, as well as offering new insights to those attempting to tackle the disease. Charbel Moussa, director of the Laboratory for Dementia and Parkinsonism at Georgetown University Medical Center said that he agreed with the conclusions of the study. “It is probably true that in cases of diseases like Alzheimer’s and Parkinson’s we may have deficiencies in quality control mechanisms like cleaning out bad proteins that collect in the brain cells,” he said, although he warned that using such findings to predict those more at risk of such disease is likely to be difficult. © 2016 Guardian News and Media Limited
By Robert Lavine Just the briefest eye contact can heighten empathetic feelings, giving people a sense of being drawn together. But patients who suffer from autism, even in its most high-functioning forms, often have trouble establishing this sort of a social connection with other people. Researchers are delving into what’s going on behind the eyes when these magical moments occur, and the hormones and neural substrates involved may offer hope of helping people with autism. University of Cambridge neuroscientist Bonnie Auyeung and colleagues gave oxytocin—a compound commonly referred to as the “love hormone,” as it’s been found to play roles in maternal and romantic bonding—to both normal men and those with a high-functioning form of autism also called Asperger’s syndrome. The scientists then tracked the eye movements of the study subjects and found that, compared with controls, those who received oxytocin via nasal spray showed increases in the number of fixations—pauses of about 300 milliseconds—on the eye region of an interviewer’s face and in the fraction of time spent looking at this region during a brief interview (Translational Psychiatry, doi:10.1038/tp.2014.146, 2015). Oxytocin, a neuropeptide hormone secreted by the pituitary gland, has long been known to activate receptors in the uterus and mammary glands, facilitating labor and milk letdown. But research on the neural effects of oxytocin has been accelerated by the availability of a nasal spray formulation of the hormone, which can deliver it more directly to the brain, also rich with oxytocin receptors. Auyeung adds that her study used a unique experimental setup. “Other studies have shown that [oxytocin] increases looking at the eye region when presented with a picture of a face,” Auyeung says. “The new part is that we are using a live interaction.”
By Virginia Morell Fourteen years ago, a bird named Betty stunned scientists with her humanlike ability to invent and use tools. Captured from the wild and shown a tiny basket of meat trapped in a plastic tube, the New Caledonian crow bent a straight piece of wire into a hook and retrieved the food. Researchers hailed the observation as evidence that these crows could invent new tools on the fly—a sign of complex, abstract thought that became regarded as one of the best demonstrations of this ability in an animal other than a human. But a new study casts doubt on at least some of Betty’s supposed intuition. Scientists have long agreed that New Caledonian crows (Corvus moneduloides), which are found only on the South Pacific island of the same name, are accomplished toolmakers. At the time of Betty’s feat, researchers knew that in the wild these crows could shape either stiff or flexible twigs into tools with a tiny, barblike hook at one end, which they used to lever grubs from rotting logs. They also make rakelike tools from the leaves of the screw pine (Pandanus) tree. But Betty appeared to take things to the next level. Not only did she fashion a hook from a material she’d never previously encountered—a behavior not observed in the wild—she seemed to know she needed this specific shape to solve her particular puzzle. © 2016 American Association for the Advancement of Science. A
Laura Sanders A busy protein known for its role in aging may also have a hand in depression, a study on mice hints. Under certain circumstances, the aging-related SIRT1 protein seems to make mice despondent, scientists report August 10 in the Journal of Neuroscience. The results are preliminary, but they might ultimately help find new depression treatments. Today’s treatments aren’t always effective, and new approaches are sorely needed. “This is one potential new avenue,” says study coauthor Deveroux Ferguson of the University of Arizona College of Medicine in Phoenix. Ferguson and colleagues subjected mice to 10 days of stressful encounters with other mice. After their demoralizing ordeal, the mice showed signs of depression, such as eschewing sugar water and giving up attempts to swim. Along with these signs of rodent despair, the mice had more SIRT1 gene activity in the nucleus accumbens, a brain area that has been linked to motivation and depression. Resveratrol, a compound found in red grapes, supercharges the SIRT1 protein, making it more efficient at its job. When Ferguson and colleagues delivered resveratrol directly to the nucleus accumbens, mice displayed more signs of depression and anxiety. When the researchers used a different compound to hinder SIRT1 activity, the mice showed the opposite effect, appearing bolder in some tests than mice that didn’t receive the compound. |© Society for Science & the Public 2000 - 2016.
By Ann Griswold, Autism shares genetic roots with obsessive-compulsive disorder (OCD) andattention deficit hyperactivity disorder (ADHD). The three conditions have features in common, such as impulsivity. New findings suggest that they also share a brain signature. The first comparison of brain architecture across these conditions has found that all are associated with disruptions in the structure of the corpus callosum. The corpus callosum is a bundle of nerve fibers that links the brain’s left and right hemispheres. The results appeared July 1 in the American Journal of Psychiatry. Clinicians may find it difficult to distinguish autism from ADHD based on symptoms alone. But if the conditions are marked by similar structural problems in the brain, the same interventions might be useful no matter what the diagnosis is, says lead researcher Stephanie Ameis, assistant professor of psychiatry at the University of Toronto. The unique aspects of each condition might arise from other brain attributes, such as differences in the connections between neurons, says Thomas Frazier, director of research at the Cleveland Clinic Foundation. “A reasonable conclusion is that autism and ADHD don’t differ dramatically in a structural way, but could differ in connectivity,” says Frazier, who was not involved in the study. Ameis’ team examined the brains of 71 children with autism, 31 with ADHD, 36 with OCD and 62 typical children using diffusion tensor imaging. This method provides a picture of the brain’s white matter, the long fibers that connect nerve cells, by measuring the diffusion of water across these fibers. © 2016 Scientific American
BENEDICT CAREY As a boy growing up in Massachusetts, Luke Dittrich revered his grandfather, a brain surgeon whose home was full of exotic instruments. Later, he learned that he was not only a prominent doctor but had played a significant role in modern medical history. In 1953, at Hartford Hospital, Dr. William Scoville had removed two slivers of tissue from the brain of a 27-year-old man with severe epilepsy. The operation relieved his seizures but left the patient — Henry Molaison, a motor repairman — unable to form new memories. Known as H. M. to protect his privacy, Mr. Molaison went on to become the most famous patient in the history of neuroscience, participating in hundreds of experiments that have helped researchers understand how the brain registers and stores new experiences. By the time Mr. Dittrich was out of college — and after a year and a half in Egypt, teaching English — he had become fascinated with H. M., brain science and his grandfather’s work. He set out to write a book about the famous case but discovered something unexpected along the way. His grandfather was one of a cadre of top surgeons who had performed lobotomies and other “psycho-surgeries” on thousands of people with mental problems. This was not a story about a single operation that went wrong; it was far larger. The resulting book — “Patient H. M.: A Story of Memory, Madness, and Family Secrets,” to be published Tuesday — describes a dark era of American medicine through a historical, and deeply personal, lens. Why should scientists and the public know this particular story in more detail? The textbook story of Patient H. M. — the story I grew up with — presents the operation my grandfather performed on Henry as a sort of one-off mistake. It was not. Instead, it was the culmination of a long period of human experimentation that my grandfather and other leading doctors and researchers had been conducting in hospitals and asylums around the country. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22531 - Posted: 08.09.2016
By Julia Shaw Every memory you have ever had is chock-full of errors. I would even go as far as saying that memory is largely an illusion. This is because our perception of the world is deeply imperfect, our brains only bother to remember a tiny piece of what we actually experience, and every time we remember something we have the potential to change the memory we are accessing. I often write about the ways in which our memory leads us astray, with a particular focus on ‘false memories.’ False memories are recollections that feel real but are not based on actual experience. For this particular article I invited a few top memory researchers to comment on what they wish everyone knew about their field. First up, we have Elizabeth Loftus from the University of California, Irvine, who is one of the founders of the area of false memory research, and is considered one of the most ‘eminent psychologists of the 20th century.’ Elizabeth Loftus says you need independent evidence to corroborate your memories. According to Loftus: “The one take home message that I have tried to convey in my writings, and classes, and in my TED talk is this: Just because someone tells you something with a lot of confidence and detail and emotion, it doesn't mean it actually happened. You need independent corroboration to know whether you're dealing with an authentic memory, or something that is a product of some other process.” Next up, we have memory scientist Annelies Vredeveldt from the Vrije Universiteit Amsterdam, who has done fascinating work on how well we remember when we recall things with other people. © 2016 Scientific American,
Keyword: Learning & Memory
Link ID: 22530 - Posted: 08.09.2016
Pete Etchells Mind gamers: How good do you reckon your memory is? We might forget things from time to time, but the stuff we do remember is pretty accurate, right? The trouble is, our memory isn’t as infallible as we might want to believe, and you can test this for yourself using the simple experiment below. All done? Great. Now we’re going to do a simple recognition test – below is another list of words for you to look at. Without looking back, note down which of them appeared in the three lists you just scanned. No cheating! If you said that top, seat and yawn were in the lists, you’re spot on. Likewise, if you think that slow, sweet and strong didn’t appear anywhere, you’re also right. What about chair, mountain and sleep though? They sound like they should have been in the lists, but they never made an appearance. Some of you may have spotted this, but a lot of people tend to say, with a fair amount of certainty, that the words were present. This experiment comes from a classic 1995 study by Henry L. Roediger and Kathleen McDermott at Rice University in Texas. Based on earlier work by James Deese (hence the name Deese-Roediger-McDermott, or DRM, paradigm), participants heard a series of word lists, which they then had to recall from memory. After a brief conversation with the researcher, the participants were then given a new list of words. Critically, this new list contained some words that were associated with every single item on each of the initial lists – for example, while sleep doesn’t appear on list 3 above, it’s related to each word that does appear (bed, rest, tired, and so on). © 2016 Guardian News and Media Limited
Keyword: Learning & Memory
Link ID: 22526 - Posted: 08.08.2016
Tina Hesman Saey Alcoholism may stem from using genes incorrectly, a study of hard-drinking rats suggests. Rats bred either to drink heavily or to shun alcohol have revealed 930 genes linked to a preference for drinking alcohol, researchers in Indiana report August 4 in PLOS Genetics. Human genetic studies have not found most of the genetic variants that put people at risk for alcoholism, says Michael Miles, a neurogenomicist at Virginia Commonwealth University in Richmond. The new study takes a “significant and somewhat novel approach” to find the genetic differences that separate those who will become addicted to alcohol from those who drink in moderation. It took decades to craft the experiment, says study coauthor William Muir, a population geneticist at Purdue University in West Lafayette, Ind. Starting in the 1980s, rats bred at Indiana University School of Medicine in Indianapolis were given a choice to drink pure water or water mixed with 10 percent ethanol, about the same amount of alcohol as in a weak wine. For more than 40 generations, researchers selected rats from each generation that voluntarily drank the most alcohol and bred them to create a line of rats that consume the rat equivalent of 25 cans of beer a day. Simultaneously, the researchers also selected rats that drank the least alcohol and bred them to make a line of low-drinking rats. A concurrent breeding program produced another line of high-drinking and teetotaling rats. For the new study, Muir and colleagues collected DNA from 10 rats from each of the high- and low-drinking lines. Comparing complete sets of genetic instructions from all the rats identified 930 genes that differ between the two lines. |© Society for Science & the Public 2000 - 2016.
By Nicholas Bakalar A drug used to treat rheumatoid arthritis may have benefits against Alzheimer’s disease, researchers report. Rheumatoid arthritis is an autoimmune disease believed to be driven in part by tumor necrosis factor, or T.N.F., a protein that promotes inflammation. Drugs that block T.N.F., including an injectable drug called etanercept, have been used to treat rheumatoid arthritis for many years. T.N.F. is also elevated in the cerebrospinal fluid of Alzheimer’s patients. Researchers identified 41,109 men and women with a diagnosis of rheumatoid arthritis and 325 with both rheumatoid arthritis and Alzheimer’s disease. In people over 65, the prevalence of Alzheimer’s disease was more than twice as high in people with rheumatoid arthritis as in those without it. The study is in CNS Drugs. But unlike patients treated with five other rheumatoid arthritis drugs, those who had been treated with etanercept showed a significantly reduced risk for Alzheimer’s disease. Still, the lead author, Dr. Richard C. Chou, an assistant professor of medicine at Dartmouth, said that it is too early to think of using etanercept as a treatment for Alzheimer’s. “We’ve identified a process in the brain, and if you can control this process with etanercept, you may be able to control Alzheimer’s,” he said. “But we need clinical trials to prove and confirm it.” © 2016 The New York Times Company
Link ID: 22520 - Posted: 08.06.2016
By LUKE DITTRICH ‘Can you tell me who the president of the United States is at the moment?” A man and a woman sat in an office in the Clinical Research Center at the Massachusetts Institute of Technology. It was 1986, and the man, Henry Molaison, was about to turn 60. He was wearing sweatpants and a checkered shirt and had thick glasses and thick hair. He pondered the question for a moment. “No,” he said. “I can’t.” The woman, Jenni Ogden, was a visiting postdoctoral research fellow from the University of Auckland, in New Zealand. One of the greatest thrills of her time at M.I.T. was the chance to have sit-down sessions with Henry. In her field — neuropsychology — he was a legendary figure, something between a rock star and a saint. “Who’s the last president you remember?” “I don’t. ... ” He paused for a second, mulling over the question. He had a soft, tentative voice, a warm New England accent. “Ike,” he said finally. Dwight D. Eisenhower’s inauguration took place in 1953. Our world had spun around the sun more than 30 times since, though Henry’s world had stayed still, frozen in orbit. This is because 1953 was the year he received an experimental operation, one that destroyed most of several deep-seated structures in his brain, including his hippocampus, his amygdala and his entorhinal cortex. The operation, performed on both sides of his brain and intended to treat Henry’s epilepsy, rendered him profoundly amnesiac, unable to hold on to the present moment for more than 30 seconds or so. That outcome, devastating to Henry, was a boon to science: By 1986, Patient H.M. — as he was called in countless journal articles and textbooks — had become arguably the most important human research subject of all time, revolutionizing our understanding of how memory works. © 2016 The New York Times Company
Keyword: Learning & Memory
Link ID: 22519 - Posted: 08.04.2016
By Megan Scudellari In late 2013, psychologist Raphael Bernier welcomed a 12-year-old girl and her parents into his office at the University of Washington (UW) in Seattle. The girl had been diagnosed with autism spectrum disorder, and Bernier had invited the family in to discuss the results of a genetic analysis his collaborator, geneticist Evan Eichler, had performed in search of the cause. As they chatted, Bernier noticed the girl’s wide-set eyes, which had a slight downward slant. Her head was unusually large, featuring a prominent forehead. The mother described how her daughter had gastrointestinal issues and sometimes wouldn’t sleep for two to three days at a time. The girl’s presentation was interesting, Bernier recalls, but he didn’t think too much of it—until a week later, when he met an eight-year-old boy with similarly wide-set eyes and a large head. Bernier did a double take. The “kiddos,” as he calls children who come to see him, could have been siblings. According to the boy’s parents, he also suffered from gastrointestinal and sleep problems. The similarities between the unrelated children were remarkable, especially for a disorder so notoriously complex that it has been said, “If you’ve met one child with autism, you’ve met one child with autism.” But Bernier knew that the patients shared another similarity that might explain the apparent coincidence: both harbored a mutation in a gene known as chromodomain helicase DNA binding protein 8 (CHD8). © 1986-2016 The Scientist
by Helen Thompson Pinky and The Brain's smarts might not be so far-fetched. Some mice are quicker on the uptake than others. While it might not lead to world domination, wits have their upside: a better shot at staying alive. Biologists Audrey Maille and Carsten Schradin of the University of Strasbourg in France tested reaction time and spatial memory in 90 African striped mice (Rhabdomys pumilio) over the course of a summer. For this particular wild rodent, surviving harsh summer droughts means making it to mating season in the early fall. The team saw some overall trends: Females were more likely to survive if they had quick reflexes, and males were more likely to survive if they had good spatial memory. Cognitive traits like reacting quickly and remembering the best places to hide are key to eluding predators during these tough times but may come with trade-offs for males and females. The results show that an individual mouse’s cognitive strengths are linked to its survival odds, suggesting that the pressure to survive can shape basic cognition, Maille and Schradin write August 3 in Biology Letters. |© Society for Science & the Public 2000 - 2016
Meghan Rosen Exercise may not erase old memories, as some studies in animals have previously suggested. Running on an exercise wheel doesn’t make rats forgetprevious trips through an underwater maze, Ashok Shetty and colleagues report August 2 in the Journal of Neuroscience. Exercise or not, four weeks after learning how to find a hidden platform, rats seem to remember the location just fine, the team found. The results conflict with two earlier papers that show that running triggers memory loss in some rodents by boosting the birth of new brain cells. Making new brain cells rejiggers memory circuits, and that can make it hard for animals to remember what they’ve learned, says Paul Frankland, a neuroscientist at the Hospital for Sick Children in Toronto. He has reported this phenomenon in mice, guinea pigs and degus (SN: 6/14/14, p. 7). Maybe rats are the exception, he says, “but I’m not convinced.” In 2014, Frankland and colleagues reported that brain cell genesis clears out fearful memories in three different kinds of rodents. Two years later, Frankland’s team found similar results with spatial memories. After exercising, mice had trouble remembering the location of a hidden platform in a water maze, the team reported in February in Nature Communications. Again, Frankland and colleagues pinned the memory wipeout on brain cell creation — like a chalkboard eraser that brushes away old information. The wipe seemed to clear the way for new memories to form. Shetty, a neuroscientist at Texas A&M Health Science Center in Temple, wondered if the results held true in rats, too. “Rats are quite different from mice,” he says. “Their biology is similar to humans.” |© Society for Science & the Public 2000 - 2016. All rights reserved.
Keyword: Learning & Memory
Link ID: 22510 - Posted: 08.03.2016
Nicola Davis Scientists have discovered 17 separate genetic variations that increase the risk of a person developing depression. The findings, which came from analysing DNA data collected from more than 300,000 people, are the first genetics links to the disease found in people of European ancestry. The scientists say the research will contribute to a better understanding of the disease and could eventually lead to new treatments. They also hope it will reduce the stigma that can accompany depression. According to Nice, up to 10% of people seen by practitioners in primary care have clinical depression, with symptoms including a continuously low mood, low self-esteem, difficulties making decisions and lack of energy. Both environmental and genetic factors are thought to be behind depression, with the interaction between the two also thought to be important. But with a large number of genetic variants each thought to make a tiny contribution to the risk of developing the condition, unravelling their identity has proved challenging. While previous studies have turned up a couple of regions in the genome of Chinese women that might increase the risk of depression, the variants didn’t appear to play a role in depression for people of European ancestry. © 2016 Guardian News and Media Limited
By Andy Coghlan Mysterious shrunken cells have been spotted in the human brain for the first time, and appear to be associated with Alzheimer’s disease. “We don’t know yet if they’re a cause or consequence,” says Marie-Ève Tremblay of Laval University in Québec, Canada, who presented her discovery at the Translational Neuroimmunology conference in Big Sky, Montana, last week. The cells appear to be withered forms of microglia – the cells that keep the brain tidy and free of infection, normally by pruning unwanted brain connections or destroying abnormal and infected brain cells. But the cells discovered by Tremblay appear much darker when viewed using an electron microscope, and they seem to be more destructive. “It took a long time for us to identify them,” says Tremblay, who adds that these shrunken microglia do not show up with the same staining chemicals that normally make microglia visible under the microscope. Compared with normal microglia, the dark cells appear to wrap much more tightly around neurons and the connections between them, called synapses. “It seems they’re hyperactive at synapses,” says Tremblay. Where these microglia are present, synapses often seem shrunken and in the process of being degraded. Tremblay first discovered these dark microglia in mice, finding that they increase in number as mice age, and appear to be linked to a number of things, including stress, the neurodegenerative condition Huntington’s disease and a mouse model of Alzheimer’s disease. “There were 10 times as many dark microglia in Alzheimer’s mice as in control mice,” says Tremblay. © Copyright Reed Business Information Ltd.
By Katherine S. Pollard When the first human genome sequence was published in 2001,1 I was a graduate student working as the statistics expert on a team of scientists. Hailing from academia and biotechnology, we aimed to discover differences in gene expression levels between tumors and healthy cells. Like many others, I had high hopes for what we could do with this enormous text file of more than 3 billion As, Cs, Ts, and Gs. Ambitious visions of a precise wiring diagram for human cells and imminent cures for disease were commonplace among my classmates and professors. But I was most excited about a different use of the data, and I found myself counting the months until the genome of a chimpanzee would be sequenced. Chimps are our closest living relatives on the tree of life. While their biology is largely similar to ours, we have many striking differences, ranging from digestive enzymes to spoken language. Humans also suffer from an array of diseases that do not afflict chimpanzees or are less severe in them, including autism, schizophrenia, Alzheimer’s disease, diabetes, atherosclerosis, AIDS, rheumatoid arthritis, and certain cancers. I had long been fascinated with hominin fossils and the way the bones morphed into different forms over evolutionary time. But those skeletons cannot tell us much about the history of our immune system or our cognitive abilities. So I started brainstorming about how to extend the statistical approaches we were using for cancer research to compare human and chimpanzee DNA. My immodest goal was to identify the genetic basis for all the traits that make humans unique. © 1986-2016 The Scientist
By Bahar Gholipour After reflexively reaching out to grab a hot pan falling from the stove, you may be able to withdraw your hand at the very last moment to avoid getting burned. That is because the brain's executive control can step in to break a chain of automatic commands. Several new lines of evidence suggest that the same may be true when it comes to the reflex of recollection—and that the brain can halt the spontaneous retrieval of potentially painful memories. Within the brain, memories sit in a web of interconnected information. As a result, one memory can trigger another, making it bubble up to the surface without any conscious effort. “When you get a reminder, the mind's automatic response is to do you a favor by trying to deliver the thing that's associated with it,” says Michael Anderson, a neuroscientist at the University of Cambridge. “But sometimes we are reminded of things we would rather not think about.” Humans are not helpless against this process, however. Previous imaging studies suggest that the brain's frontal areas can dampen the activity of the hippocampus, a crucial structure for memory, and therefore suppress retrieval. In an effort to learn more, Anderson and his colleagues recently investigated what happens after the hippocampus is suppressed. They asked 381 college students to learn pairs of loosely related words. Later, the students were shown one word and asked to recall the other—or to do the opposite and to actively not think about the other word. Sometimes between these tasks they were shown unusual images, such as a peacock standing in a parking lot. © 2016 Scientific American
Keyword: Learning & Memory
Link ID: 22500 - Posted: 08.01.2016
Aaron E. Carroll I remember thinking, after my pregnant wife’s water broke, minutes after I went to bed, anguishing really, over one thought as we drove to the hospital: “I’m never going to be well rested again.” If there’s one things all new parents wish for, it’s a good night’s sleep. Unfortunately, infants sometimes make that impossible. They wake up repeatedly, needing to be fed, changed and comforted. Eventually, they reach an age when they should sleep through the night. Some don’t, though. What to do with them continues to be a topic of a heated debate in parenting circles. One camp believes that babies should be left to cry it out. These people place babies in their cribs at a certain time, after a certain routine, and don’t interfere until the next morning. No matter how much the babies scream or cry, parents ignore them. After all, if babies learn that tantrums lead to the appearance of a loved one, they will continue that behavior in the future. The official name for this intervention is “Extinction.” The downside, of course, is that it’s unbelievably stressful for parents. Many can’t do it. And not holding fast to the plan can make everything worse. Responding to an infant’s crying after an extended period of time makes the behavior harder to extinguish. To a baby, it’s like a slot machine that hits just as you’re ready to walk away; it makes you want to play more. A modification of this strategy is known as “Graduated Extinction.” Parents allow their infant to cry it out for a longer period each night, until infants eventually put themselves to sleep. On the first night, for instance, parents might commit to not entering the baby’s room for five minutes. The next night, 10 minutes. Then 15, and so on. Or, they could increase the increments on progressive checks each night. When they do go in the room, it’s only to check and make sure the baby is O.K. – no picking up or comforting. This isn’t meant to be a reward for crying, but to allow parents to be assured that nothing is wrong. © 2016 The New York Times Company