Thursday, May 24, 2012
— Researchers at New York University and Albert Einstein College of Medicine of Yeshiva University have discovered new ways neurons work together to ease the transition between sleep and wakefulness. Their findings, which appear in the journal Neuron, provide additional insights into sleep-wake patterns and offer methods to explore what may disrupt them.
Their study explored the biological, or circadian, clocks of Drosophila fruit flies, which are commonly used for research in this area. This is because it is relatively easy to find mutants with malfunctioning biological clocks and then to identify the genes underlying the altered behavior. Such studies in fruit flies have allowed the identification of similar "clock genes" in mammals, which function in largely the same manner as they do in a fly's clock.
In the Neuron study, the researchers moved up a level to study how pacemaker clock neurons -- which express clock genes -- interact with each other. Specifically, they looked at the relationship between master pacemaker neurons, which control the overall pace of the circadian system, and non-master pacemaker neurons, whose role in circadian rhythms has been less clear.
To do so, they examined flies with normally functioning master and non-master clock neurons and compared them with mutant flies in which the signaling of these neurons was either increased or decreased. These comparisons allowed the researchers to isolate the individual roles of these neurons and, in particular, to understand how master and non-master pacemaker neurons work together to control circadian rhythms.
Their results revealed a previously unknown role for non-master pacemaker neurons. Specifically, these neurons employ a neurotransmitter, glutamate, which suppresses signaling of the master pacemaker neurons during the evening. Artificially increasing this suppression by the non-master clock neurons in the morning made it much harder for flies to wake up. So in normal flies, these non-master pacemaker neurons have to stand aside at dawn, allowing the master pacemaker neurons to fire to wake up the fly. The authors concluded that the balance between signaling of these two groups of clock neurons helps to set the precise time of the transition between sleep and wakefulness.
"Our work shifts the emphasis away from clock genes and starts to address how clock neurons function in a neural network to regulate behavior," explained Justin Blau, an associate professor in NYU's Department of Biology and one of the study's co-authors. "And it shows the importance of studying individual groups of clock neurons, since different subsets can have opposite effects on animal behavior."
"This work helps to elucidate the neurotransmitters and receptors that facilitate communication between specific groups of nerve cells that regulate circadian rhythm," said co-author Myles Akabas, professor of Physiology & Biophysics and of Neuroscience at Albert Einstein College of Medicine. "It demonstrates the power of collaborative interdisciplinary research to address the molecular and cellular basis for behavior."
The study's other co-authors are: Ben Collins, a post-doctoral fellow in NYU's Department of Biology; Elizabeth Kane, an undergraduate in NYU's College of Arts and Science at the time of the study and now a doctoral student at Harvard University's Center for Brain Science; and David Reeves, a post-doctoral researcher at Einstein.
The research was supported by grants from the National
Institutes of Health.
It is great news that infant Psychobiological Health is continuously revisited as Neuroscience guides all related fields from Pediatrics to Infant Traumatology.
Fever During Pregnancy More Than Doubles the Risk of Autism or Developmental Delay
— A team of UC Davis researchers has found that mothers who had fevers during their pregnancies were more than twice as likely to have a child with autism or developmental delay than were mothers of typically developing children, and that taking medication to treat fever countered its effect.
"Our study provides strong evidence that controlling fevers while pregnant may be effective in modifying the risk of having a child with autism or developmental delay," said Ousseny Zerbo, lead author of the study, who was a Ph.D. candidate with UC Davis when the study was conducted and is now a postdoctoral researcher with the Kaiser Permanente Northern California Division of Research. "We recommend that pregnant women who develop fever take anti-pyretic medications and seek medical attention if their fever persists."
Published online in the Journal of Autism and Developmental Disorders, the study is believed to be the first to consider how fever from any cause, including the flu, and its treatment during pregnancy could affect the likelihood of having a child with autism or developmental delay.
The results are based on data from a large, case-control investigation known as the Childhood Autism Risk from Genetics and the Environment (CHARGE) Study. Another recent study based on CHARGE data found that mothers who were obese or diabetic had a higher likelihood of having children with autism.
Irva Hertz-Picciotto, a professor of public health sciences at UC Davis and principal investigator of CHARGE, pointed out that fever is produced by acute inflammation -- the short-term, natural immune system reaction to infection or injury -- and that chronic inflammation, which no longer serves a beneficial purpose and can damage healthy tissue, may be present in mothers with metabolic abnormalities like diabetes and obesity.
"Since an inflammatory state in the body accompanies obesity and diabetes as well as fever," said Hertz-Picciotto, "the natural question is: Could inflammatory factors play a role in autism?"
She explained that when people are infected by bacteria or viruses, the body generally reacts by mounting a healing response that involves the release of pro-inflammatory cytokines from white blood cells into the bloodstream. Some cytokines are able to cross the placenta, and therefore could reach the fetal central nervous system, potentially altering levels of neurotransmitters and brain development.
"We definitely think more research is necessary to pinpoint the ways that inflammation could alter brain development," said Hertz-Picciotto.
CHARGE includes an ethnically diverse population of children aged 2 to 5 years born in California and living in Northern California. The current study included 538 children with autism, 163 children with developmental delay but not autism, and 421 typically developing children whose mothers answered standardized questionnaires about whether they had the flu and/or fever during pregnancy and if they took medications to treat their illnesses.
The results showed that flu during pregnancy was not associated with greater risks of having a child with autism or developmental delay. Fever from any cause during pregnancy, however, was far more likely to be reported by mothers of children with autism (2.12 times higher odds) or developmental delay (2.5 times higher odds), as compared with mothers of children who were developing typically. For children of mothers who took anti-fever medication, the risk of autism was not different from the risk in children whose mothers reported no fever.
According to Irva Hertz-Picciotto, results based on CHARGE data are noteworthy because of the study's large population-based sample and detailed information on participants. Other CHARGE evaluations have found that taking prenatal vitamins prior to and during the first month of pregnancy may help prevent autism and that living near a freeway or in areas with high regional air pollution is associated with higher risk of autism in children.
"CHARGE has obtained a wealth of environmental, demographic and medical information on young children and their parents and provides a solid basis for a variety of epidemiologic studies," said Hertz-Picciotto. "Those studies are helping us find ways to protect childhood neurodevelopment."
In addition to Zerbo and Hertz-Picciotto, other UC Davis authors were Robin Hansen of the Department of Pediatrics, Sally Ozonoff of the Department of Psychiatry and Behavioral Sciences, Cheryl Walker of the Department of Obstetrics and Gynecology and Ana-Maria Iosif of the Department of Public Health Sciences. Hertz-Picciotto, Hansen, Ozonoff and Walker are also affiliated with the UC Davis MIND (Medical
Investigation of Neurodevelopmental Disorders) Institute.ScienceDaily (May 23, 2012)
Thursday, May 17, 2012
The national institute of Diabetes, Digestive & Kidney Diseases
M.I.T.-trained mathematician and physicist: Dr. Chow
has the latest word on weight loss.
M.I.T.-trained mathematician and physicist: Dr. Chow
has the latest word on weight loss.
Any practical advice from your number crunching?
One of the things the numbers have shown us is that weight change, up or down, takes a very, very long time. All diets work. But the reaction time is really slow: on the order of a year.
People don’t wait long enough to see what they are going to stabilize at. So if you drop weight and return to your old eating habits, the time it takes to crawl back to your old weight is something like three years. To help people understand this better, we’ve posted an interactive version of our model at bwsimulator.niddk.nih.gov. People can plug in their information and learn how much they’ll need to reduce their intake and increase their activity to lose. It will also give them a rough sense of how much time it will take to reach the goal. Applied mathematics in action!
Wednesday, May 16, 2012
Chronic Child Abuse Strong Indicator
of Negative Adult Experiences
ScienceDaily (May 15, 2012) — Child abuse or neglect are strong predictors of major health and emotional problems, but little is known about how the chronicity of the maltreatment may increase future harm apart from other risk factors in a child's life.
In a new study published in the current issue of the journalPediatrics, Melissa Jonson-Reid, PhD, child welfare expert and a professor at the Brown School at Washington University in St. Louis, looked at how chronic maltreatment impacted the future health and behavior of children and adults.
The study tracked children by number of child maltreatment reports (zero to four or more) and followed the children into early adulthood, by which time some of the children had become parents.
The study sought to determine how well the number of child maltreatment reports predicted poor outcomes in adolescence, such as delinquency, substance abuse in the teen years or getting a sexually transmitted disease.
"For every measure studied, a more chronic history of child maltreatment reports was powerfully predictive of worse outcomes," Jonson-Reid says.
"For most outcomes, having a single maltreatment report put children at a 20 percent to 50 percent higher risk than non-maltreated comparison children.
In addition, a series of adult outcomes were tracked to see if the chronicity of maltreatment still mattered after controlling for the poor outcomes in adolescence. Adult outcomes included adult substance abuse or growing up and having children whom they then maltreated.
"In models of adult outcomes, children with four or more reports were about least twice as likely to later abuse their own children and have contact with the mental health system, even when controlling for the negative outcomes during adolescence." Jonson-Reid says that there appears to be good reason to put resources into preventing ongoing maltreatment.
"Successfully interrupting chronic child maltreatment may well reduce risk of a wide range of other costly child and adolescent health and behavioral problems," she says.
Jonson-Reid cites a recently published Centers for Disease Control and Prevention study estimating lifetime costs for a single year's worth of children reported for maltreatment at $242 billion.
"What our study illustrates is that these costs are even more likely to accrue for children who continue to be re-reported," she says.
The study also found that maltreatment predicts a range of negative adolescent outcomes, and those adolescent outcomes then predict poor adult outcomes.
"If the poor outcomes in adolescence can be dealt with effectively, then later adult outcomes may also be forestalled," Jonson-Reid says.
"Our findings could therefore be interpreted as supporting many current evidence-based interventions that seek to improve behavioral and social functioning among children and adolescents who have experienced trauma like abuse or neglect."
Jonson-Reid co-authored the study, "Child and Adult Outcomes of Chronic Child Maltreatment," with fellow Brown School faculty members Patricia L. Kohl, PhD, associate professor, and F. Brett Drake, PhD,
Thursday, May 10, 2012
Scientists Identify Neurotranmitters That Lead to Forgetting
ScienceDaily (May 9, 2012) — While we often think of memory as a way of preserving the essential idea of who we are, little thought is given to the importance of forgetting to our wellbeing, whether what we forget belongs in the "horrible memories department" or just reflects the minutia of day-to-day living.
Despite the fact that forgetting is normal, exactly how we forget -- the molecular, cellular, and brain circuit mechanisms underlying the process -- is poorly understood.
Now, in a study that appears in the May 10, 2012 issue of the journalNeuron, scientists from the Florida campus of The Scripps Research Institute have pinpointed a mechanism that is essential for forming memories in the first place and, as it turns out, is equally essential for eliminating them after memories have formed.
"This study focuses on the molecular biology of active forgetting," said Ron Davis, chair of the Scripps Research Department of Neuroscience who led the project. "Until now, the basic thought has been that forgetting is mostly a passive process. Our findings make clear that forgetting is an active process that is probably regulated."
The Two Faces of Dopamine
To better understand the mechanisms for forgetting, Davis and his colleagues studied Drosophila or fruit flies, a key model for studying memory that has been found to be highly applicable to humans. The flies were put in situations where they learned that certain smells were associated with either a positive reinforcement like food or a negative one, such as a mild electric shock. The scientists then observed changes in the flies' brains as they remembered or forgot the new information.
The results showed that a small subset of dopamine neurons actively regulate the acquisition of memories and the forgetting of these memories after learning, using a pair of dopamine receptors in the brain. Dopamine is a neurotransmitter that plays an important role in a number of processes including punishment and reward, memory, learning and cognition.
But how can a single neurotransmitter, dopamine, have two seemingly opposite roles in both forming and eliminating memories? And how can these two dopamine receptors serve acquiring memory on the one hand, and forgetting on the other?
The study suggests that when a new memory is first formed, there also exists an active, dopamine-based forgetting mechanism -- ongoing dopamine neuron activity -- that begins to erase those memories unless some importance is attached to them, a process known as consolidation that may shield important memories from the dopamine-driven forgetting process.
The study shows that specific neurons in the brain release dopamine to two different receptors known as dDA1 and DAMB, located on what are called mushroom bodies because of their shape; these densely packed networks of neurons are vital for memory and learning in insects. The study found the dDA1 receptor is responsible for memory acquisition, while DAMB is required for forgetting.
When dopamine neurons begin the signaling process, the dDA1 receptor becomes overstimulated and begins to form memories, an essential part of memory acquisition. Once that memory is acquired, however, these same dopamine neurons continue signaling. Except this time, the signal goes through the DAMB receptor, which triggers forgetting of those recently acquired, but not yet consolidated, memories.
Jacob Berry, a graduate student in the Davis lab who led the experimentation, showed that inhibiting the dopamine signaling after learning enhanced the flies' memory. Hyperactivating those same neurons after learning erased memory. And, a mutation in one of the receptors, dDA1, produced flies unable to learn, while a mutation in the other, DAMB, blocked forgetting.
While Davis was surprised by the mechanisms the study uncovered, he was not surprised that forgetting is an active process. "Biology isn't designed to do things in a passive way," he said. "There are active pathways for constructing things, and active ones for degrading things. Why should forgetting be any different?"
The study also brings into a focus a lot of intriguing issues, Davis said -- savant syndrome, for example.
"Savants have a high capacity for memory in some specialized areas," he said. "But maybe it isn't memory that gives them this capacity, maybe they have a bad forgetting mechanism. This also might be a strategy for developing drugs to promote cognition and memory -- what about drugs that inhibit forgetting as cognitive enhancers?