Chapter 11. Motor Control and Plasticity
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David Cyranoski For more than a decade, neuroscientist Grégoire Courtine has been flying every few months from his lab at the Swiss Federal Institute of Technology in Lausanne to another lab in Beijing, China, where he conducts research on monkeys with the aim of treating spinal-cord injuries. The commute is exhausting — on occasion he has even flown to Beijing, done experiments, and returned the same night. But it is worth it, says Courtine, because working with monkeys in China is less burdened by regulation than it is in Europe and the United States. And this week, he and his team report1 the results of experiments in Beijing, in which a wireless brain implant — that stimulates electrodes in the leg by recreating signals recorded from the brain — has enabled monkeys with spinal-cord injuries to walk. “They have demonstrated that the animals can regain not only coordinated but also weight-bearing function, which is important for locomotion. This is great work,” says Gaurav Sharma, a neuroscientist who has worked on restoring arm movement in paralysed patients, at the non-profit research organization Battelle Memorial Institute in Columbus, Ohio. The treatment is a potential boon for immobile patients: Courtine has already started a trial in Switzerland, using a pared-down version of the technology in two people with spinal-cord injury. © 2016 Macmillan Publishers Limited
Ian Sample Science editor Partially-paralysed monkeys have learned to walk again with a brain implant that uses wireless signals to bypass broken nerves in the spinal cord and reanimate the useless limbs. The implant is the first to restore walking ability in paralysed primates and raises the prospect of radical new therapies for people with devastating spinal injuries. Scientists hope the technology will help people who have lost the use of their legs, by sending movement signals from their brains to electrodes in the spine that activate the leg muscles. One rhesus macaque that was fitted with the new implant regained the ability to walk only six days after it was partially paralysed in a surgical procedure that severed some of the nerves that controlled its right hind leg. “It was a big surprise for us,” said Grégoire Courtine, a neuroscientist who led the research at the Swiss Federal Institute of Technology. “The gait was not perfect, but it was almost like normal walking. The foot was not dragging and it was fully weight bearing.” A second animal in the study that received more serious damage to the nerves controlling its right hind leg recovered the ability to walk two weeks after having the device fitted, according to a report published in the journal, Nature. Both monkeys regained full mobility in three months. The “brain-spine interface” is the latest breakthrough to come from the rapidly-advancing area of neuroprosthetics. Scientists in the field aim to read intentions in the brain’s activity and use it to control computers, robotic arms and even paralysed limbs. © 2016 Guardian News and Media Limited
By Neuroskeptic A new paper could prompt a rethink of a basic tenet of neuroscience. It is widely believed that the motor cortex, a region of the cerebral cortex, is responsible for producing movements, by sending instructions to other brain regions and ultimately to the spinal cord. But according to neuroscientists Christian Laut Ebbesen and colleagues, the truth may be the opposite: the motor cortex may equally well suppress movements. Ebbesen et al. studied the vibrissa motor cortex (VMC) of the rat, an area which is known to be involved in the movement of the whiskers. First, they determined that neurons within the VMC are more active during periods when the rat’s whiskers are resting: for instance, like this: whiskerThe existence of cells whose firing negatively correlates with movement is interesting, but by itself it doesn’t prove that much. Maybe those cells are just doing something else than controlling movement? However, Ebbesen et al. went on to show that electrical stimulation of the VMC caused whiskers to stop moving, while applying a drug (lidocaine) to suppress VMC activity caused the rat’s whiskers to whisk harder. Ebbesen et al. go on to say that the inhibitory role of VMC may extend to other regions of the rat motor cortex, and to other movements beyond the whiskers: Rats can perform long sequences of skilled, learned motor behaviors after motor cortex ablation, but motor cortex is required for them to learn a task of behavioral inhibition (they must learn to postpone lever presses)35. When swimming, intact rats hold their forelimbs still and swim with only their hindlimbs. After forelimb motor cortex lesions, however, rats swim with their forelimbs also36.
Keyword: Movement Disorders
Link ID: 22837 - Posted: 11.07.2016
Laura Sanders A protein that can switch shapes and accumulate inside brain cells helps fruit flies form and retrieve memories, a new study finds. Such shape-shifting is the hallmark move of prions — proteins that can alternate between two forms and aggregate under certain conditions. In fruit flies’ brain cells, clumps of the prionlike protein called Orb2 stores long-lasting memories, report scientists from the Stowers Institute for Medical Research in Kansas City, Mo. Figuring out how the brain forms and calls up memories may ultimately help scientists devise ways to restore that process in people with diseases such as Alzheimer’s. The new finding, described online November 3 in Current Biology, is “absolutely superb,” says neuroscientist Eric Kandel of Columbia University. “It fills in a lot of missing pieces.” People possess a version of the Orb2 protein called CPEB, a commonality that suggests memory might work in a similar way in people, Kandel says. It’s not yet known whether people rely on the prion to store long-term memories. “We can’t be sure, but it’s very suggestive,” Kandel says. When neuroscientist Kausik Si and colleagues used a genetic trick to inactivate Orb2 protein, male flies were worse at remembering rejection. These lovesick males continued to woo a nonreceptive female long past when they should have learned that courtship was futile. In different tests, these flies also had trouble remembering that a certain odor was tied to food. |© Society for Science & the Public 2000 - 2016. All rights reserved.
By Dan Hurley The Centers for Disease Control and Prevention has confirmed 89 cases of the paralyzing disease in the United States through September. A 6-year-old boy suspected of having AFM died in Seattle on Sunday, the first death believed to be caused by the disease. One of the drugs in development, pocapavir, was used briefly on a few patients during a 2014 outbreak of AFM under a compassionate-use exception that allows extremely sick patients to be given unapproved drugs without the usual kinds of placebo-controlled trials required by the Food and Drug Administration. “There were a couple of kids who got pocapavir in the Colorado outbreaks,” said Benjamin Greenberg, a neurologist who has treated children with AFM at the University of Texas Southwestern in Dallas. “It had relatively weak but measurable impact on viral replication. A larger study would definitely be warranted. We'll take anything we can get.” Although the CDC says no cause has been conclusively linked to AFM, many researchers suspect a family of viruses known as enteroviruses. “I have been studying enteroviruses for 40 years now,” said John Modlin, deputy director of the polio eradication program at the Bill and Melinda Gates Foundation. “If I had a child with acute flaccid myelitis, I would be on the phone in a second to the companies making these drugs.” © 1996-2016 The Washington Post
Keyword: Movement Disorders
Link ID: 22830 - Posted: 11.04.2016
By Helen Thomson IN THE 2009 Bruce Willis movie Surrogates, people live their lives by embodying themselves as robots. They meet people, go to work, even fall in love, all without leaving the comfort of their own home. Now, for the first time, three people with severe spinal injuries have taken the first steps towards that vision by controlling a robot thousands of kilometres away, using thought alone. The idea is that people with spinal injuries will be able to use robot bodies to interact with the world. It is part of the European Union-backed VERE project, which aims to dissolve the boundary between the human body and a surrogate, giving people the illusion that their surrogate is in fact their own body. In 2012, an international team went some way to achieving this by taking fMRI scans of the brains of volunteers while they thought about moving their hands or legs. The scanner measured changes in blood flow to the brain area responsible for such thoughts. An algorithm then passed these on as instructions to a robot. “The feeling of embodying the robot was good, although the sensation varied over time“ The volunteers could see what the robot was looking at via a head-mounted display. When they thought about moving their left or right hand, the robot moved 30 degrees to the left or right. Imagining moving their legs made the robot walk forward. © Copyright Reed Business Information Ltd.
Link ID: 22795 - Posted: 10.27.2016
Richard Harris Researchers have launched an innovative medical experiment that's designed to provide quick answers while meeting the needs of patients, rather than drug companies. Traditional studies can cost hundreds of millions of dollars, and can take many years. But patients with amyotrophic lateral sclerosis, or Lou Gehrig's disease don't have the time to wait. This progressive muscle-wasting disease is usually fatal within a few years. Scientists in an active online patient community identified a potential treatment and have started to gather data from the participants virtually rather than requiring many in-person doctor's visits. How is that possible? In this case, doctors and patients alike got interested in an extraordinary ALS patient whose symptoms actually got better, which rarely occurs. He'd been taking a dietary supplement called lunasin, "and lo and behold six months later, [his] speech [was] back to normal, swallowing back to normal, doesn't use his feeding tube, [and he was] significantly stronger as measured by his therapists," said Richard Bedlack, a neurologist who runs the ALS clinic at Duke University. Of course, it could just be a coincidence that the man who got better happened to be taking these supplements. To find out, Bedlack teamed up to run a study with Paul Wicks, a neuropsychologist and vice president for innovation at a web-based patient organization called PatientsLikeMe. © 2016 npr
Keyword: ALS-Lou Gehrig's Disease
Link ID: 22788 - Posted: 10.26.2016
Ian Sample Science editor Experiments with a fake body part have revealed how the brain becomes confused during a party trick known as the rubber hand illusion. Researchers in Italy performed the trick on a group of volunteers to explore how the mind combines information from the senses to create a feeling of body ownership. Under the illusion, people feel that a rubber hand placed on the table before them is their own, a bizarre but convincing shift in perception that is accompanied by a sense of disowning their real hand. The scientists launched the study after noticing that some stroke patients in their care experienced similar sensations, at times becoming certain that a paralysed limb was not their own, and even claiming ownership over other people’s appendages. “It is a very strong belief,” said Francesca Garbarini at the University of Turin. “We know that the feeling of body ownership can be dramatically altered after brain damage.” For the study, healthy volunteers sat with their forearms resting on a table and their right hand hidden inside a box. A lifelike rubber hand was then placed in front of them and lined up with their right shoulder. A cloth covered the stump of the hand, but the fingers remained visible. To induce the illusion, one of the researchers stroked the middle finger of the participant’s real hand while simultaneously stroking the same finger on the rubber hand. © 2016 Guardian News and Media Limited
Keyword: Pain & Touch
Link ID: 22780 - Posted: 10.24.2016
Linda Geddes For the first time, a paralysed man has gained a limited sense of touch, thanks to an electric implant that stimulates his brain and allows him to feel pressure-like sensations in the fingers of a robotic arm. The advance raises the possibility of restoring limited sensation to various areas of the body, as well as giving people with spinal-cord injuries better control over prosthetic limbs. But restoring human-like feeling, such as sensations of heat or pain, will prove more challenging, the researchers say. Nathan Copeland had not been able to feel or move his legs and lower arms since a car accident snapped his neck and injured his spinal cord when he was 18. Now, some 12 years later, he can feel when a robotic arm has its fingers touched, because sensors on the fingers are linked to an implant in his brain. Brain implant restores paralysed man's sense of touch Rob Gaunt, a biomedical engineer at the University of Pittsburgh, performs a sensory test on a blindfolded Nathan Copeland. Nathan, who is paralysed, demonstrates his ability to feel by correctly identifying different fingers through a mind-controlled robotic arm. Video credit: UPMC/Pitt Health Sciences. “He says the sensations feel like they’re coming from his own hand,” says Robert Gaunt, a biomedical engineer at the University of Pittsburgh who led the study. © 2016 Macmillan Publishers Limited
Urine could potentially be used for a quick and simple way to test for CJD or "human mad cow disease", say scientists in the journal JAMA Neurology. The Medical Research Council team say their prototype test still needs honing before it could be used routinely. Currently there is no easy test available for this rare but fatal brain condition. Instead, doctors have to take a sample of spinal fluid or brain tissue, or wait for a post-mortem after death. What they look for is tell-tale deposits of abnormal proteins called prions, which cause the brain damage. Building on earlier US work, Dr Graham Jackson and colleagues, from University College London, have now found it is also possible to detect prions in urine. This might offer a way to diagnose CJD rapidly and earlier, they say, although there is no cure. Creutzfeldt-Jakob disease (CJD): CJD is a rare, but fatal degenerative brain disorder caused by abnormal proteins called prions that damage brain cells. There are several forms of the disease: sporadic, which occurs naturally in the human population, and accounts for 85% of all CJD cases variant CJD, linked to eating beef infected by bovine spongiform encephalopathy (BSE) iatrogenic infection, caused by contamination during medical or surgical treatment In the 1990s it became clear that a brain disease could be passed from cows to humans. The British government introduced a ban on beef on the bone. Since then, officials have kept a close check on how many people have become sick or died from CJD. © 2016 BBC
Link ID: 22724 - Posted: 10.05.2016
By Carl Luepker For the past 35 years, a relentless neurological disorder has taken over my body, causing often painful muscle spasms that make it hard for me to walk and write and that cause my speech to be garbled enough that people often can’t understand me I can live with my bad luck in getting this condition, which showed up when I was 10; what’s harder to accept is that I have passed on this disorder, carried in my genes, to my 11-year-old son, Liam. As a parent, you hope that your child’s life will follow an upward trend, one of emotional and physical growth toward an adulthood of wide-open possibilities where they can explore the world, challenge themselves emotionally and physically, and perhaps play on a sports team. And you hope that you can pass down to your child at least some of what was passed down to you. Yet my generalized dystonia, as my progressive condition is called, was one thing I had hoped would end with me. Liam poses for a photograph just months before his diagnosis with dystonia. He “has just moved into middle school,” his father writes, where “he will have to both advocate for himself and educate his new teachers and peers about this genetic disorder.” When my wife and I started thinking of having kids, the statistics were fairly reassuring: There was a 1-in-2 chance that our child would inherit the gene that causes the disorder, but most people who have the gene don’t go on to manifest dystonia. We wanted a family and rolled the dice — twice. Our daughter does not have the gene. © 1996-2016 The Washington Post
By Jessica Boddy Activity trackers like Fitbits and Jawbones help fitness enthusiasts log the calories they burn, their heart rates, and even how many flights of stairs they climb in a day. Biologist Cory Williams of Northern Arizona University in Flagstaff is using similar technology to track the energy consumption of arctic ground squirrels in Alaska—insight that may reveal how the animals efficiently forage for food while avoiding being picked off by golden eagles. This week, Williams published a study in Royal Society Open Science that compared the activity levels of male and female squirrels. He found that although males spend a lot more time outside of their burrows, they’re pretty lazy, and sometimes just bask in the sun during warmer months. Females, on the other hand, have limited time to spare when caring for their young, and use it to run around and forage for themselves and their babies. In addition to previous work on arctic ground squirrel hibernation and seasonal differences in behavior, the finding is helping his team figure out why males tend to be more susceptible to being eaten. Williams sat down with Science to talk about creating a squirrel Fitbit, catching the animals in the wild, and how technology is improving ecological research. This interview has been edited for brevity and clarity. Q: What got you interested in studying arctic ground squirrels? A: It’s one of the only arctic animals that keeps a rigid schedule even when there’s no light/dark cycle for 6 week—meaning, they emerge from and return to their burrows the same time every day and they eat the same time each day, even though the sun stays in the sky for weeks and weeks. So I started to deploy the energy tracking technologies to better understand how the squirrels use energy through the seasons. © 2016 American Association for the Advancement of Science
Keyword: Sexual Behavior
Link ID: 22714 - Posted: 09.30.2016
By GRETCHEN REYNOLDS Before you skip another workout, you might think about your brain. A provocative new study finds that some of the benefits of exercise for brain health may evaporate if we take to the couch and stop being active, even just for a week or so. I have frequently written about how physical activity, especially endurance exercise like running, aids our brains and minds. Studies with animals and people show that working out can lead to the creation of new neurons, blood vessels and synapses and greater overall volume in areas of the brain related to memory and higher-level thinking. Presumably as a result, people and animals that exercise tend to have sturdier memories and cognitive skills than their sedentary counterparts. Exercise prompts these changes in large part by increasing blood flow to the brain, many exercise scientists believe. Blood carries fuel and oxygen to brain cells, along with other substances that help to jump-start desirable biochemical processes there, so more blood circulating in the brain is generally a good thing. Exercise is particularly important for brain health because it appears to ramp up blood flow through the skull not only during the actual activity, but throughout the rest of the day. In past neurological studies, when sedentary people began an exercise program, they soon developed augmented blood flow to their brains, even when they were resting and not running or otherwise moving. But whether those improvements in blood flow are permanent or how long they might last was not clear. So for the new study, which was published in August in Frontiers in Aging Neuroscience, researchers from the department of kinesiology at the University of Maryland in College Park decided to ask a group of exceedingly fit older men and women to stop exercising for awhile. © 2016 The New York Times Company
By Alison F. Takemura Bodies like to keep their pH close to 7.4, whether that means hyperventilating to make the blood alkaline, or burning energy, shifting to anaerobic metabolism, and producing lactate to make the blood acidic. The lungs and kidneys can regulate pH changes systemically, but they may not act quickly on a local scale. Because even small pH changes can dramatically affect the nervous system, a study led by Sten Grillner of Karolinska Institute in Sweden looked for a mechanism for pH homeostasis in the spinal cord. Using the lamprey as a model system, the researchers observed that a type of spinal canal neuron, called CSF-c, fired more rapidly when they bathed it with high pH (7.7) or low pH (7.1) media. They could suspend the elevated activity by blocking two ion channels: PKD2L1 channels, which stimulate neurons in alkaline conditions, or ASIC3 channels, which, the team showed previously, do the same in acidic states. As the neurons fired, they released the hormone somatostatin, which inhibited the lamprey’s locomotor network. These results suggest that, whichever direction pH deviates, “the response of the system is just to reduce activity as much as possible,” Grillner says. The pH-regulating role of CSF-c neurons is likely conserved among animals, the authors suspect, given the presence of these neurons across vertebrate taxa. © 1986-2016 The Scientist
Keyword: Movement Disorders
Link ID: 22688 - Posted: 09.24.2016
By Michael Price A soft brush that feels like prickly thorns. A vibrating tuning fork that produces no vibration. Not being able to tell which direction body joints are moving without looking at them. Those are some of the bizarre sensations reported by a 9-year-old girl and 19-year-old woman in a new study. The duo, researchers say, shares an extremely rare genetic mutation that may shed light on a so-called “sixth sense” in humans: proprioception, or the body’s awareness of where it is in space. The new work may even explain why some of us are klutzier than others. The patients’ affliction doesn’t have a name. It was discovered by one of the study’s lead authors, pediatric neurologist Carsten Bönnemann at the National Institutes of Health (NIH) in Bethesda, Maryland, who specializes in diagnosing unknown genetic illnesses in young people. He noticed that the girl and the woman shared a suite of physical symptoms, including hips, fingers, and feet that bent at unusual angles. They also had scoliosis, an unusual curvature of the spine. And, significantly, they had difficulty walking, showed an extreme lack of coordination, and couldn’t physically feel objects against their skin. Bönnemann screened their genomes and looked for mutations that they might have in common. One in particular stood out: a catastrophic mutation in PIEZO2, a gene that has been linked to the body’s sense of touch and its ability to perform coordinated movements. At about the same time, in a “very lucky accident,” Bönnemann attended a lecture by Alexander Chesler, a neurologist also at NIH, on PIEZO2. Bönnemann invited Chesler to help study his newly identified patients. © 2016 American Association for the Advancement of Science.
By SABRINA TAVERNISE WASHINGTON — The Food and Drug Administration approved the first drug to treat patients with the most common childhood form of muscular dystrophy, a vivid example of the growing power that patients and their advocates wield over the federal government’s evaluation of drugs. The agency’s approval went against the recommendation of its experts. The main clinical trial of the drug was small, involving only 12 boys with the disease known as Duchenne muscular dystrophy, and did not have an adequate control group of boys who had the disease but did not take the drug. A group of independent experts convened by the agency this spring said there was not enough evidence that it was effective. But the vote was close. Large and impassioned groups of patients, including boys in wheelchairs, and their advocates, weighed in. The muscular dystrophy community is well organized and has lobbied for years to win approval for the drug, getting members of Congress to write letters to the agency. A decision on the drug had been delayed for months. The approval was so controversial that F.D.A. employees fought over it, a dispute that was taken to the agency’s commissioner, Dr. Robert M. Califf, who ultimately decided that it would stand. The approval delighted the drug’s advocates and sent the share price of the drug’s maker, Sarepta Therapeutics, soaring. But it was taken as a deeply troubling sign among drug policy experts who believe the F.D.A. has been far too influenced by patient advocates and drug companies, and has allowed the delicate balance in drug approvals to tilt toward speedy decisions based on preliminary data and away from more conclusive evidence of effectiveness and safety. © 2016 The New York Times Company
Carrie Arnold Could a protein that originated in a virus explain why men are more muscular than women? Viruses are notorious for their ability to cause disease, but they also shape human biology in less obvious ways. Retroviruses, which insert their genetic material into our genomes to copy themselves, have left behind genes that help to steer our immune systems and mold the development of embryos and the placenta. Now researchers report in PLOS Genetics that syncytin, a viral protein that enables placenta formation, also helps to increase muscle mass in male mice1. These results could partially explain a lingering mystery in biology: why the males of many mammalian species tend to be more muscular than females. “As soon as I read it, my mind started racing with the potential implications,” says evolutionary virologist Aris Katzourakis of the University of Oxford, UK. About 8% of the 3 billion pairs of As, Ts, Gs and Cs that make up our DNA are viral detritus. Many of those viral hand-me-downs have degraded into useless junk — but not all, as a series of discoveries over the past 15 years has revealed. In 2000, scientists discovered that syncytin, a protein that enables the formation of the placenta, actually originated as a viral protein that humans subsequently ‘borrowed’2. That original viral protein enables the retrovirus to fuse with host cells, depositing its entire genome into the safe harbour of the cytoplasm. Syncytin has changed little from this ancestral protein form; it directs certain placental cells to fuse with cells in the mother’s uterus, forming the outer layer of the placenta. © 2016 Macmillan Publishers Limited
By Karen Weintraub Researchers have long believed that problems with mitochondria—the power plants of cells—underlie some cases of Parkinson’s disease. Now a new study details those problems, and suggests that they may form a common thread linking previously unexplained cases of the disease with those caused by different genetic anomalies or toxins. Finding a common mechanism behind different suspected causes of Parkinson’s suggests that there might also be a common means to measure, treat or cure it, says Marco Baptista, research director at the nonprofit Michael J. Fox Foundation, a leading center for study and advocacy in the fight against Parkinson’s. The study, published Thursday in Cell Stem Cell, did identify a possible way to reverse the damage of Parkinson’s—but only in individual cells and fruit flies. Finding a treatment that does the same thing in people will be challenging, Baptista says. Roughly one million Americans have Parkinson’s disease, which is characterized by motor problems and can cause other symptoms including cognitive and gastrointestinal difficulties. About 1 to 2 percent of cases are linked to mutations in the LRRK2 gene, with far fewer associated with genes known as PINK1 and Parkin. Exposure to environmental factors such as toxic chemicals can also lead to Parkinson’s, although most cases have no obvious cause. In the new paper Xinnan Wang, an assistant professor of neurosurgery at Stanford University, and her colleagues show that mitochondria are underpowered in several types of Parkinson’s and that these mitochondria also release toxic chemicals. Looking at fly models of the disease as well as cells taken from patients, the researchers found that they could correct these problems and reverse neurodegeneration if they reduced levels of a protein involved in mitochondrial activity. © 2016 Scientific American
Link ID: 22642 - Posted: 09.10.2016
By Abby Olena Mammalian prions are notoriously difficult as structural biology subjects, given their insolubility and tendency to aggregate. Researchers have now overcome these challenges to figure out the preliminary structure of a shortened form of infectious prion (PrPSc), which they report today (September 8) in PLOS Pathogens. “For the first time, we have a structure of an infectious mammalian prion,” said Giuseppe Legname of Scuola Internazionale Superiore di Studi Avanzati in Trieste, Italy, who was not involved in this study. “It’s a very important paper,” he added. “What we have done is to obtain a very simple, very preliminary idea of what the structure of these mammalian prions are,” said study coauthor Jesús Requena of the University of Santiago de Compostela in Spain. Requena and colleagues generated a shortened form of PrPSc by injecting a laboratory strain of prions into transgenic mice that express a truncated form of normal cellular prion protein (PrPC), which lacks the attachment of a membrane anchor present in full-length PrPSc. In nature, PrPC transforms into full-length PrPSc, which causes Creutzfeldt-Jakob disease in humans, scrapie in sheep, and mad cow disease. The absence of the membrane anchor in shortened PrPSc from the transgenic mice allowed the researchers to isolate a fairly homogeneous population of PrPSc. They confirmed that this population was infectious by inoculating wild-type mice, which then developed symptoms of prion disease. © 1986-2016 The Scientist
Link ID: 22638 - Posted: 09.10.2016
By The Scientist Staff Growing up, we learn that there are five senses: sight, smell, touch, taste, and hearing. For the past five years, The Scientist has taken deep dives into each of those senses, explorations that revealed diverse mechanisms of perception and the impressive range of these senses in humans and diverse other animals. But as any biologist knows, there are more than just five senses, and it’s difficult to put a number on how many others there are. Humans’ vestibular sense, for example, detects gravity and balance through special organs in the bony labyrinth of the inner ear. Receptors in our muscles and joints inform our sense of body position. (See “Proprioception: The Sense Within.”) And around the animal kingdom, numerous other sense organs aid the perception of their worlds. The comb jelly’s single statocyst sits at the animal’s uppermost tip, under a transparent dome of fused cilia. A mass of cells called lithocytes, each containing a large, membrane-bound concretion of minerals, forms a statolith, which sits atop four columns called balancers, each made up of 150–200 sensory cilia. As the organism tilts, the statolith falls towards the Earth’s core, bending the balancers. Each balancer is linked to two rows of the ctenophore’s eight comb plates, from which extend hundreds of thousands of cilia that beat together as a unit to propel the animal. As the balancers bend, they adjust the frequency of ciliary beating in their associated comb plates. “They’re the pacemakers for the beating of the locomotor cilia,” says Sidney Tamm, a researcher at the Marine Biological Laboratory in Woods Hole, Massachusetts, who has detailed the structure and function of the ctenophore statocyst (Biol Bull, 227:7-18, 2014; Biol Bull, 229:173-84, 2015). © 1986-2016 The Scientist