Action Potential

Nobel prize-winning neuroscientist Linda Buck has retracted a 2001 Nature paper. In the retraction in this week's Nature, the authors report difficulty replicating the data and 'inconsistencies' between the original data and figures and data printed in the paper. Buck told Nature reporter Heidi Ledford that the figures and data in question were contributed by the first author, Zhihua Zou, who was unavailable for comment.

This is the highest profile retraction that I can recall in neuroscience, but so far, there has been little fallout. Perhaps that's because the original findings were notable only in the neuroscience community rather than in the general public. Regardless, it indicates that neuroscience and its well known labs are not immune from fraudulent data. Although I admire Buck's swift and direct action, it concerns me that the first author has been assigned the lion's share of the blame. This seems like a familiar refrain, and I find it troubling.

Posted by Debra Speert at 10:54 AM on March 06, 2008 | Permalink | Comments (13) | TrackBacks (0)
Categories: Debra Speert, Breaking News, Scientific Publishing

By now, you've likely read a shocking headline questioning the effectiveness of the latest generation of antidepressants. Kirsch et al. report that selective serotonin reuptake inhibitors (SSRIs) are only slightly more effective than placebos at reducing depression in a meta-analysis of US Food and Drug Administration (FDA) data. Are these data really worth all the fuss?

Continue reading "Anti antidepressants" »

Posted by Debra Speert at 11:14 AM on February 26, 2008 | Permalink | Comments (3) | TrackBacks (0)
Categories: Debra Speert, Breaking News

If a disease affects men and women differently, does the disease's mechanism differ by sex? My guess would be no. However, a recent article has me wondering. Schizophrenia symptoms, age of onset, and disease course differ in men and women, and some researchers report increased risk of schizophrenia in men relative to women. Now Shifman et al. report a single nucleotide polymorphism (SNP) associated with schizophrenia in women but not men in a recent article in PLoS Genetics.

Continue reading "Separate but not equal?" »

Posted by Debra Speert at 03:43 PM on February 20, 2008 | Permalink | Comments (1) | TrackBacks (0)
Categories: Debra Speert, Interesting Neuroscience, Neuroinformatics

How many neurons are required for learning and memory? None, according to Saigusa et al., who report basic learning behavior in unicellular amoebae in a recent article in Physical Review Letters.

The amoeba Physarum polycephalum is sensitive to environmental conditions. At room temperature, Physarum move at a constant rate. However, dry air slows the rate of Physarum movement.

The authors puffed dry air on Physarum once an hour for three hours. On the fourth hour, Physarum slowed down, even when no puff of air was delivered. Subsequent hours without air puffs slowly extinguished the periodic slowing of Physarum movement. However, one dry air puff six hours later reactivated the hourly behavior pattern.

These behaviors are consistent with rudimentary learning in higher organisms. Do these data indicate that unicellular organisms can learn? Physarum, like other organisms, have precise biological rhythms set by cellular oscillators. So, Physarum may be particularly sensitive to events occuring at regular intervals, and their periodic slow-down may represent the setting of a biological rhythm. However, rhythms alone do not explain extinction of the behavior in the absence of additional dry air puffs.

Do these data indicate a potential origin for learning, or do they indicate that our definition of learning in complex organisms is too simplistic? I'm a bit torn.

Posted by Debra Speert at 12:49 PM on January 23, 2008 | Permalink | Comments (2) | TrackBacks (0)
Categories: Debra Speert, Interesting Neuroscience

What causes autism? The lack of answers or even particularly good leads is frustrating to say the least. Not surprisingly, people both within the scientific community and the general public are hungry for answers, and my general opinion is that the more information the better. However, I'm a little puzzled by a report from the British Association for the Advancement of Science's annual Festival of Science.

According to Simon Baron-Cohen's 'extreme male brain' theory, people with autism show extreme versions of behaviors that are normal in men. In general, men tend to empathize less and systematize more than women. These drives are taken to an extreme degree in people with autism, resulting in the behaviors associated with autism, including reduced eye contact and verbal skills and increased repetitive behavior and orderliness, according to Baron-Cohen.

Is the hormone that causes male behaviors involved in autism? At the Festival of Science, Baron-Cohen and Bonnie Auyeng reported that fetal testosterone contributed to 'autistic traits' in normal eight-year-old children. The researchers calculated an 'autism spectrum quotient' from questionnaires about children's social behaviors and cognitive skills completed by their mothers. Fetal testosterone levels recorded eight years earlier accounted for more than 20% of the variability in this quotient.

According to the researchers, these data suggest that elevated testosterone levels in the womb may contribute to traits associated with autism. However, based on the researchers' reasoning, wouldn't an alternative explanation be that fetal testosterone correlates with male-typical behaviors? Animal studies have shown that testosterone produced in the fetal testes masculinizes the brain (allowing male-typical behavioral patterns). Perhaps the present study indicates that male-typical behaviors are graded, with high levels of fetal testosterone producing 'super males'.

While interesting, it's not clear to me that these data are directly relatable to autism. For that, we'll need to see Baron-Cohen's next study, involving clinical data and amniotic samples from 90,000 people with and without autism.

Posted by Debra Speert at 10:04 AM on September 18, 2007 | Permalink | Comments (0) | TrackBacks (0)
Categories: Debra Speert, Interesting Neuroscience

Nominations open Monday for the first Kavli prizes in neuroscience, astrophysics and nanoscience. One $1,000,000 prize will be awarded for each of the three fields in Norway next year. Sound like another Scandanavian award? Unlike Nobel prizes, which tend to reward scientists at the ends of their careers, the Kavli Prize will recognize innovation, according to a recent article in Time magazine. Fred Kavli, a Norwegian physicist/business mogul/philanthropist, has been funding giant awards for (the odd mix of scientific pursuits) neuroscience, astrophysics and nanoscience research at universities, like Caltech, Harvard, MIT and Cambridge. So, if you know of a deserving neuroscientist, the application deadline is 15 December.

Posted by Debra Speert at 01:37 PM on September 07, 2007 | Permalink | Comments (0) | TrackBacks (0)
Categories: Debra Speert

If you think managing chemical waste in your lab is like throwing money down the drain, imagine how Daniel Storm feels. According to the Seattle Post Intelligencer, rather than paying $15,000 to properly dispose of 5 cans of ethyl ether, the professor of pharmacology at the University of Washington took an axe to them and poured them down the drain. According to Nature, Storm falsified waste manifest sheets in an attempt to cover up the crime. Storm was sentenced to 3 years of probation, 80 hours of community service and a $5,000 fine in U. S. District Court and is undergoing university disciplinary review.

Like most people who have had to sit through the courses and fill out the monthly paperwork required to dispose of anything other than water, I can understand Storm's frustration. Do people in hazmat suits really need to close down a building over a broken thermometer? However, you don't have to be an environmentalist to realize that pouring an extremely flammable liquid into university pipes isn't a terribly smart thing to do.

Posted by Debra Speert at 01:53 PM on September 05, 2007 | Permalink | Comments (0) | TrackBacks (0)
Categories: Debra Speert

That's what Gary Lynch said of the physiological mechanism of memory in 2005 when L. A. Times reporter Terry McDermott asked to visit Lynch's University of California, Irvine lab. McDermott returned repeatedly, and his findings were featured last week in an epic four-part series in the L. A. Times.

The series reads like engrossing Greek drama, complete with a misunderstood hero and the tragicomedy of high stakes science. Lynch is painted as the lone wolf battling evil editors and competitors to get the truth out. Although it's over-dramatized and Lynch's role is perhaps a bit overstated, the science, aimed entirely at the lay person, is quite good. According to a recent report from the Pew Research Center, few Americans (19%) follow science news, so if it takes high drama to sell science stories to the public, I'm all for it. McDermott should be congratulated for getting neuroscience on the front page.

Posted by Debra Speert at 10:15 AM on August 28, 2007 | Permalink | Comments (1) | TrackBacks (0)
Categories: Debra Speert

It's been a tough month for parents. Open a newspaper, and you are virtually guaranteed to read about the latest environmental toxin seeping into children's blood and endangering neuronal or reproductive development. Mattel recalled toys that may be coated in lead paint. Meanwhile, a committee at the National Institute of Environmental Health Sciences (NIEHS) declared 'some concern' that a compound in many plastics, bisphenol A (BPA), affects neuronal development. And finally, the University of California at Davis announced a several million dollar study of possible environmental triggers for autism.

If you are a parent and also a scientist, what is the proper response to the conflicting urges to protect your children and evaluate the data? Rebecca Roberts, a biochemist who studies BPA, writes in PLoS Biology:

The mother in me still waits anxiously for the regulatory agencies and the legislature to catch up with the research on BPA that the scientist in me appreciates. I have switched my brand of sippy cups to one that doesn't contain BPA (a quick internet search will yield many sites describing these and other BPA-free baby products). Nevertheless, while I feel proactive as I watch my daughter happily drink her water, I still cringe a little bit when she drops the sippy cup, toddles over to her toy bin, and starts to gnaw on her plastic turtle instead.

Posted by Debra Speert at 12:30 PM on August 17, 2007 | Permalink | Comments (0) | TrackBacks (0)
Categories: Debra Speert

Keeping the commoners happy is easy when you have pharmacology on your side. Complex caste systems exist throughout the animal kingdom, but is it purely social feedback that keeps us all in our places? Vergoz, Shreurs and Mercer report that a pheromone prevents worker honeybees from forming aversive associations while they serve the queen in a recent article in Science.

In the honeybee society, the females do all of the work. Young females attend to the queen and her hive. Later in life, they leave the hive to collect nectar and pollen (the average honeybee lifespan is 4-6 weeks). Queen mandibular pheromone (QMP), which is produced by the queen and transferred to the rest of the hive by her caretakers, prevents the ovarian development of other females.

Honeybees show both appetitive (positively reinforced) and aversive (negatively reinforced) learning. In response to odors, honeybees can be trained to extend their tongues in anticipation of a sweet reward or extend their stingers in anticipation of a shock. Octopamine and dopamine are important in appetitive and aversive learning, respectively. QMP alters brain dopamine levels. Does QMP affect aversive learning?

The authors found that QMP blocked aversive, but not appetitive learning in 6-day-old female bees. However, QMP had no effect on aversive learning in 15-day-old female bees.

How does QMP affect aversive learning? The QMP component homovanillyl alcohol (HVA) blocked aversive learning, whereas another QMP component hydroxybenzoate (HOB) did not. HVA is similar in structure to dopamine, so HVA may be responsible for the QMP-mediated reduction in brain dopamine and the decline in dopamine-mediated aversive learning.

Why block aversive learning in subordinates? The authors speculate that QMP prevents young attendants from forming aversive associations with the queen and therefore promotes loyalty and diligence. Perhaps the age-dependent decline in QMP's effect on aversive learning induces older honeybees to leave the hive.

It is highly unlikely that humans have an Orwellian pheromone mediating subservience. However, there probably is a QMP keeping us in our societal places: the Quantity of Money in our Pockets.

Posted by Debra Speert at 10:20 AM on July 23, 2007 | Permalink | Comments (0) | TrackBacks (0)
Categories: Debra Speert

Instead of a tough-talking mayor, new windows may be to thank for the drop in violent crime in New York City. The Washington Post reports that according to economist Rick Nevin, 65-95% of the variation in violent crime in 9 countries can be explained by lead. Nevins claims that crime rates rise and fall approximately 20 years after environmental lead concentrations increase and decrease, respectively. This theory isn't new, but its relation to American politics is. Rudy Giuliani, former New York City mayor and current presidential candidate, claims that his law enforcement policies reduced homicides by 67% and total crime by 57% during his tenure as mayor from 1994-2001. Nevins argues that Giuliani benefited from policies in the 1960s to replace old lead windows (to reduce deadly falls) and in the 1970s and 1980s to reduce lead in paint and gasoline.

Lead is a neurotoxin that passes through the blood-brain barrier. Lidsky and Schneider report that lead mimics calcium in brain cells, disturbing endogenous calcium levels and inducing cytochrome C release from mitochondria. Lead also increases basal levels of acetylcholine, dopamine and amino acid neurotransmitters but reduces their activity-dependent release. Because children often put their hands in their mouths, they are susceptible to exposure to lead in paint. What are the behavioral effects of lead? Herbert Needleman, a psychiatrist at the University of Pittsburgh, reported increased lead levels in the bones of 11-year-old children with antisocial and delinquent behaviors and adolescents who had been through the penal system relative to their peers, suggesting that lead increases sociopathic behaviors and impulsivity.

Perhaps these data indicate that it's time for political candidates to pipe down about their past achievements and speak up about how they intend to clean up the environment.

Posted by Debra Speert at 10:41 AM on July 10, 2007 | Permalink | Comments (0) | TrackBacks (0)
Categories: Debra Speert

It's double-blind or nothing when it comes to phase III clinical trials. Although placebo groups are absolutely vital to the clinical validity of medical treatments, a recent article in The Lancet has me thinking about the ethics of treating desperate patients with saline.

The subthalamic nucleus is overactive in people with Parkinson's disease, presumably because it loses GABAergic input from the globus pallidus. Subthalamic nucleus lesions improve Parkinson's disease symptoms. Kaplitt et al. generated a gene therapy agent that would silence but not destroy subthalamic nuclei neurons. They inserted glutamic acid decarboxylase (GAD), the enzyme responsible for GABA production, into a viral vector and injected it into subthalamic nuclei of people with Parkinson's disease. In their phase I trial in 12 patients, the authors showed that their therapy was safe and virtually side-effect-free. Unlike most phase I trials, the authors also showed that their treatment was effective: intra-thalamic injections of the GAD agent reduced Parkinson's symptoms.

That's great news for a possible new treatment for Parkinson's disease. But it also means that at some point soon, people with advanced Parkinson's symptoms will volunteer for brain surgery and a 50% chance at treatment. Some would argue that even placebos have their upside, and I certainly understand their importance. I also understand that the patients who volunteer for these studies are often at the end of their medical ropes and are willing to roll the dice. I just feel for the folks who wake up 6 months after surgery and realize that their symptoms haven't improved.

Posted by Debra Speert at 02:52 PM on July 01, 2007 | Permalink | Comments (4) | TrackBacks (0)
Categories: Debra Speert

Enough with the cranes already! Richard Powers's 2006 novel The Echo Maker, a National Book Award winner, is a great book to take to the beach (or the bench while the PCR machine is running), even if it is about 100 pages too long.

The Echo Maker follows Mark Schluter's recovery from a mysterious car accident that leaves him with Capgras syndrome, the delusion that one's loved ones have been replaced by imposters. His sister Karin calls in a celebrity neuroscientist, the Oliver Sacks-ish Dr. Gerald Weber, and all three struggle with issues of identity and self. Oh, and there are also those blasted cranes, who pass through this book far more frequently than they do the Nebraska Platte described in the novel.

Capgras is a fascinating disorder worthy of fiction and nonfiction alike. Ramachandran describes Capgras, in which familiar faces fail to illicit proper emotional responses, as the mirror to prosapagnosia, the inability to recognize faces. He has suggested that injury-induced Capgras (approximately 33% of all Capgras cases) may be caused by lesions of the connections between the inferior temporal cortex and the amygdala. Capgras patients, unlike people with amygdala lesions, show elevated galvanic skin responses to emotional stimuli, but not to pictures of people they know, suggesting that it's not the amygdala itself that is affected, but the information flow to the amygdala from the visual cortex.

Like Ramachandran's case study D. S. (not me, I swear), Mark Schluter doubles himself, describing his pre-injury self as 'old Mark', someone who looks very much like the person he used to be. Powers sprinkles references to 9/11 throughout The Echo Maker, perhaps implying that we are all quite different than the people we used to be. A point very elegantly made, but one that used way too many birds in the making.

Posted by Debra Speert at 04:20 PM on June 18, 2007 | Permalink | Comments (0) | TrackBacks (0)
Categories: Debra Speert

TV's Mr. Wizard, Don Herbert, died yesterday. He was the first (and favorite) science teacher for several generations of children. He will be greatly missed.

Posted by Debra Speert at 09:43 AM on June 13, 2007 | Permalink | Comments (1) | TrackBacks (0)
Categories: Debra Speert

"One is 95 percent certainty, and the other is...50 percent and a feather"

According to attorney Kevin Conway (quoted in the Washington Post), that is the difference between the scientific and legal burden of proof that autism is related to childhood vaccines. Conway represents one of more than 4800 families who believe that a vaccine preservative caused autism in their loved ones and are suing for compensation from the Vaccine Injury Compensation Fund. The first test case is before the U. S. Court of Federal Claims today.

An editorial in the May issue described the lack of scientific data supporting this claim. However, the timing of this hearing is particularly interesting. Just days ago, the media generated a frenzy over Andrew Speaker, the American lawyer with a drug resistant form of tuberculosis who flew on commercial airplanes. Perhaps because vaccines have worked so well in combating diseases like polio, many in the west have been lulled into a false sense of security when it comes to diseases that are common in 'the rest of the world'. The court should certainly weigh the global health impact of a generation of American children who are not vaccinated. Conversely, we must continue to ensure that despite our hysteria over modern health threats, like small pox and avian flu, vaccine companies test and retest their products (and publish their data!) before rushing them out to nervous consumers.

The Post points out the biggest losers in the autism court battle: autistic children. Although my heart goes out to the plaintiffs in this case, one has to wonder what therapies and services could be purchased for the price of the legal blame game.

Posted by Debra Speert at 12:20 PM on June 11, 2007 | Permalink | Comments (0) | TrackBacks (0)
Categories: Debra Speert

If you could look into a crystal ball to find out how your life ends, would you? Yesterday, James Watson (yes, that James Watson) decided that he didn't want to know. His personal genome was sequenced by 454 Life Sciences and the Human Genome Sequencing Center at the Baylor College of Medicine. Dr. Watson will make his entire genome publicly available with the exception of one gene: apolipoprotein E, the gene most strongly associated with Alzheimer's disease, which killed his grandmother.

There is no correct answer to the genetic testing dilemma. The children and grandchildren of victims of diseases with much clearer genetic causes have struggled with this question for years. But if Watson's genome announces the dawn of pharmacogenomics, many more of us will have to decide for ourselves what we do and what we don't want to know.

Watson is not a man who shies away from controversy. Perhaps that is why I am slightly surprised by such a human decision from such a brazen pioneer.

Posted by Debra Speert at 06:01 PM on June 01, 2007 | Permalink | Comments (0) | TrackBacks (0)
Categories: Debra Speert

As the news out of Blacksburg, Virginia continues to unfold, it is difficult not to reflect on the importance of mental health services for young adults. In a sad coincidence, a meta-analysis published today in JAMA suggests that despite earlier reports of increased suicide risk, the benefits of antidepressant treatment in children and young adults outweigh the risks. Bridge et al. report that antidepressants helped young people with major depressive disorder, obsessive compulsive disorder and anxiety and increased their risk of suicidal thoughts or attempts by less than 1%. Improved treatment protocols specific for children and teenagers will hopefully help young adults in need. Unfortunately, we all know that treatments can only help those who seek them.

Posted by Debra Speert at 11:46 AM on April 18, 2007 | Permalink | Comments (0) | TrackBacks (0)
Categories: Debra Speert

Just a few weeks can separate a splash from a quiet ripple. On 5 April, Neuron and Nature both published articles reporting genetically targeted silencing of mammalian neurons. In Neuron, Lerchner et al. detailed drug-induced hyperpolarization of neurons expressing a C. elegans chloride channel within hours of treatment. In Nature, Zhang et al. reported light-induced hyperpolarization of neurons expressing an archaea opsin within milliseconds of illumination. The media took note of Zhang's article, but not Lerchner's.

To be fair, the two articles are quite different in scope. Zhang et al. reported not just inducible neuron silencing, but a neuron on/off switch. In the same neuron, the authors induced firing with a blue light-activated cation channel and inhibited endogenous firing with a yellow-light induced chloride pump. They turned behaviors on and off with blue and yellow light, respectively, in C. elegans expressing both the cation channel and the chloride pump. The ability to control neuron function is nothing short of stunning and will undoubtedly impact both bench and bedside.

Although their scope was much smaller, Lerchner et al. approached neuronal silencing cleverly. Ivermectin is a chloride channel agonist in C. elegans, but not mammals, making it a potent antiparasitic agent that literally puts worms to sleep, sparing mammalian hosts. The authors silenced mammalian neurons expressing the C. elegans ivermectin-gated chloride channel and suppressed behavior with systemic treatment of ivermectin.

Systemic drug treatment is virtually guaranteed to take longer than illumination to achieve inhibition. And an off switch alone can't compare to the deluxe on/off model. But I can't help wondering if I'd be more excited about Lerchner's article if it came out a few weeks earlier.

There is one interesting postscript to Zhang's amazing achievement. Han and Boyden reported an identical yellow-light induced chloride pump earlier in the month in PLoS ONE. They examined the properties of blue and yellow light-induced excitation and inhibition in cultured hippocampal neurons. Although Han and Boyden don't show any in vivo data, their study technically preceded Zhang et al. So, in the grand scheme of things, who will be credited with the discovery? Maybe timing isn't everything.

Posted by Debra Speert at 11:47 AM on April 10, 2007 | Permalink | Comments (7) | TrackBacks (0)
Categories: Debra Speert

We may have to thank body builders for the next big breakthrough in the battle against Parkinson disease. Companies that market powders and potions to those obsessed with their glutes and pecs claim that the dietary supplement creatine changes physiques. However, the NIH National Institute of Neurological Disorders and Stroke (NINDS) recently announced a phase III clinical trial examining the ability of creatine to slow symptom progression in people with Parkinson disease.

Although its body-bulking effect may be caused by simple weight gain, creatine is thought to boost exercise performance. Phosphocreatine donates phosphate groups to ADP, increasing the supply of ATP available in muscle, which allows muscles to work longer and harder.

Creatine is also neuroprotective. Klivenyi et al. reported that creatine prevented neuron loss but did not affect muscle weight in a mouse model of ALS. Zhu et al. reported that ischemia caused smaller stroke volumes in mice treated with creatine relative to vehicle. Ischemia induced less cytochrome c release and caspase activation in creatine-treated relative to vehicle-treated mice.

Creatine performed well in small clinical trials. Now NINDS plans to study 1720 people in the early stages of Parkinson disease in a double-blind study of creatine's effects. This study, the first of a series of clinical trials called NIH exploratory trials in Parkinson disease (NET-PD), is slated to last five to seven years.

Posted by Debra Speert at 05:05 PM on March 26, 2007 | Permalink | Comments (0) | TrackBacks (0)
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In response to my comments, Juan Carlos Lopez had this reply on Spoonful of Medicine:

Candidate genes? We already have many more candidate genes than we know what to do with. I'd argue that candidate genes are, in fact, part of the "genetic noise" Debra refers to.

What this field needs is, among other things, new animal models that allow us to make more thoughtful experiments on the biological basis of psychiatric disease.

In the absence of good models in which to test the functional relevance of whatever genes the screening process identifies, the massive investment that Apoorva highlighted will bring rather paltry returns.

He makes an excellent point, but I'm sticking to my guns. Groups of genes that are subtly affected (not wiped out entirely) would not have been found in the small populations studied thus far. Furthermore, the absence of good animal models underscores the need for more information on variation in the only disease model we have: the human.

Posted by Debra Speert at 10:34 AM on March 13, 2007 | Permalink | Comments (3) | TrackBacks (0)
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We can agree to disagree. Although I'm a huge, geeky fan of hers, I have to respectfully disagree with Apoorva's post on Spoonful of Medicine about the Stanley Medical Research Institute's $100 million gift to the Broad Institute (originally reported in the Boston Globe). The Broad Institute, which is arguably the be all and end all of genomics research, plans to compile genetic and clinical data from thousands of people in order to identify candidate genes that associate with psychiatric disorders, including schizophrenia and bipolar disorder. Apoorva said:

But these are extremely complex disorders, each involving multiple genes. What roles do those genes play in the disease? Without understanding how the different genes interact and what the impact is of the different variations, the data will be all but meaningless.

I would argue that the very complexity of these diseases is the reason that such large datasets (and the bioinformaticians to make sense of them) are necessary. A really good example is in this month's Nature Genetics. The Autism Genome Project Consortium identified new gene candidates associated with autism from a dataset containing genetic information from nearly 8000 people. Have they poof! figured out what causes autism? No, but they have identified a place to start.

Finding a place to start is really the whole point. These are disorders for which there just isn't a lot to go on. Apoorva's concern about understanding the roles of candidate genes in health and disease is really putting the cart before the horse. The molecular interactions between disease-related genes and their roles in psychiatric disorders can only be deciphered once candidates are in hand. With this fantastic grant, maybe the Broad Institute will get that far. That would really be something.

Posted by Debra Speert at 05:01 PM on March 09, 2007 | Permalink | Comments (0) | TrackBacks (0)
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In case you missed it, the New York Times profiled Joseph LeDoux's rock band, which is appropriately named the Amygdaloids. The band's fans may be even more impressive than its members, who are all neuroscientists. Nobel prize-winning mathematician John Nash (subject of A Beautiful Mind) describes the Amygdaloids music as "psychoanalytic".

Posted by Debra Speert at 04:27 PM on March 08, 2007 | Permalink | Comments (0) | TrackBacks (0)
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If you lose your marbles in zero gravity, your fellow astronauts are assigned to catch them. According to the LA Times, NASA has a detailed, if slightly barbaric plan for dealing with an astronaut's psychotic or suicidal behavior while in space. To prevent a distraught astronaut from harming his colleagues, crewmates are instructed to physically restrain him with bungee cords and administer tranquilizers. Then what? The written plan does not elaborate, but a NASA spokesman quoted in the Times suggests that officials on the ship and on the ground would decide if the mission should be aborted. This report comes in the wake of astronaut Lisa Nowak's arrest in Orlando for attempted kidnapping.

Although I have no issue with NASA's concern for the safety of its astronauts in an understandably delicate situation, I am a little uncomfortable with the brutality of its plan. Yes, a suicidal or psychotic astronaut could endanger the lives of his crewmates, and the seriousness of the situation is unquestionable. However, I wonder about the criteria fellow astronauts would use to evaluate a troubled crewmate. Will astronauts be educated about signs of deteriorating mental health, or will they be trusted to 'know it when they see it'?

Coincidentally, a bill before the US Senate will make it easier for Americans to seek treatment for mental health. The Mental Health Parity Act of 2007 would require health insurance companies to cover treatments for psychiatric and neurological disorders, including substance abuse, comparably to other health disorders.

Posted by Debra Speert at 11:55 AM on February 26, 2007 | Permalink | Comments (0) | TrackBacks (0)
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If you were happy with the level of NIH funding in 2006, you're in luck! According to the 2008 budget proposed by US President George Bush on Monday, NIH funding will remain flat. Oh sure, the numbers sound good. On paper, the proposal includes a $232 million increase relative to 2006 (Congress has yet to pass 2007's doozy of a budget). However, $200 million of that is already promised to the Global Fund to Fight HIV/AIDS, Tuberculosis and Malaria. The remaining $32 million increases NIH's budget by 0.1% relative to 2006, far less than the 3.7% yearly inflation rate estimated by NIH. Although the budget includes allotments for new grants, no inflationary increases are planned to increase grant size. That means you, students and post docs with NRSAs: the proposal freezes student and post doc stipends at fiscal year 2007 levels.

Posted by Debra Speert at 05:04 PM on February 08, 2007 | Permalink | Comments (0) | TrackBacks (0)
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The very special episode of Family Ties that guest starred Tom Hanks as Alex Keaton's cough syrup-guzzling, alcoholic uncle scarred me for life. Tom Hanks will be happy to know that he has finally been outdone. News reports circulated this week that people are ingesting hand sanitizers to get drunk. Hand sanitizers contain nearly twice the amount of alcohol as vodka and are toxic because they contain isopropanol, not ethanol. So, hand sanitizers make poor beverages.

Perhaps those in search of a quick high should instead open their wallets and inhale. According to Science Daily, 100% of Euro notes tested near Dublin contained traces of cocaine. Approximately 62% of the Euro notes contained in excess of 2 and 5% contained more than 200 nanograms per note, suggesting these bills might have been used during drug inhalation or transactions. Relative to 5 and 10 Euro notes, 20 and 50 Euro notes tended to have more cocaine residue. Previous studies in the U. S. showed that 65% of dollar bills held traces of cocaine. Researchers believe that cocaine adsorbs to bank notes and rubs off on other bills. Are most people, let alone bankers, therefore sensitized to small amounts of cocaine?

How about LSD? Hallucinogens, like LSD, act at 5-HT2a receptors, as do non-hallucinogens, including lisuride, which is used to treat Parkinson disease. How do 5-HT2a receptors differentially respond to different types of ligand? Gonzalez-Maeso et al. report that hallucinogens activate different cell signaling pathways than do non-hallucinogens in an article published yesterday in Neuron. Both LSD and lisuride act at 5-HT2a receptors to activate phospholipase C-beta via Gq/11 proteins. The authors showed that LSD, but not lisuride, increased the expression of the early growth response-2 (egr-2) gene. A phospholipase C-beta inhibitor, a Src inhibitor and pertussis toxin all blocked LSD-induced increases in egr-2. Therefore, the authors concluded that unlike non-hallucinogens, LSD acts at 5-HT2a receptors to activate pertussis toxin-sensitive Gi/o proteins and Src, which may mediate its hallucinogenic effects.

Posted by Debra Speert at 05:08 PM on February 02, 2007 | Permalink | Comments (2) | TrackBacks (0)
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Nicorette be damned! Quitting smoking is easy...if you've had a stroke. Naqvi et al. report that stroke-induced damage to the insula associates with smoking cessation in today's issue of Science.

The insula lies in the pocket separating the temporal lobe from the parietal lobe and is thought to provide emotional context for sensory information. Sixteen of nineteen smokers who suffered strokes that affected the insula quit smoking immediately. Smokers who sustained damage to the insula were more likely to quit than smokers who had sustained damage to other brain regions. Although several of the patients with insular damage also sustained damage to the putamen, which is part of the striatum thought to be involved in learning drug use behaviors, no other brain region associated with smoking cessation in the stroke patients.

Do smokers with insular damage lose pleasure in smoking? After smoking cessation, none of the patients with insular damage reported losing pleasure in eating or drinking, suggesting that they had not lost motivation or the ability to experience pleasure. Do these patients lose other habits? Unfortunately, the authors did not address this possibility.

These findings suggest that the insula is important in experiencing the need to smoke and is therefore a target for smoking cessation therapy. Considering the insula's proximity to language centers, surgical lesion of the insula is certainly not advisable. However, targeted pharmacological therapy might some day help smokers quit. According to the authors, the efficacy of smoking cessation programs might be determined by imaging insular activation.

Posted by Debra Speert at 11:27 AM on January 26, 2007 | Permalink | Comments (2) | TrackBacks (0)
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Despite my best efforts to stop it, my most productive planning always occurs in the last five minutes of a yoga class. Relax my mind? I don't think so! What goes on in the brain when we let our minds wander? Mason et al. report that a network of brain structures is active during daydreaming in a recent article in Science.

The authors had people do repetitive (i. e. boring) tasks, like memorizing and rehearsing the same short list of words forward and backward, for 30 minutes each day. The subjects reported that their minds wandered more during this task than when they were given a new task to do. On the fifth day, the subjects did the same task in an MRI machine. The authors identified regions of the brain that were active during this literally mind-numbing activity relative to those that were active when participants worked on a novel task. Then they correlated the activity of these brain regions to the participants' daydream frequencies. BOLD signal in the medial prefrontal cortex, cingulate, precuneus, right superior frontal gyrus and the left and right insula associated with daydreaming. In addition to daydreaming, the authors believe that these brain regions might be important in 'housekeeping' functions or might cause people to be aware of their daydreams.

Why do we daydream? I'll look that up once I stop thinking about a beach vacation...

Posted by Debra Speert at 05:00 PM on January 19, 2007 | Permalink | Comments (1) | TrackBacks (0)
Categories: Debra Speert

Several sources, including news@nature and the Washington Post, reported today that relative to the early 1990s, the average blood level of folate in women is declining. Folate deficiency is associated with neural tube defects during fetal development. So women of child-bearing age are encouraged to take folate supplements even if they are not pregnant or actively trying to get pregnant. Incidence of neural tube defects has declined by approximately 25%, presumably because we are all taking folate.

So why are folate levels declining? It's not clear, but officials from the U. S. Centers for Disease Control and Prevention have several ideas. Obese individuals metabolize folate differently than thin people and may need to consume more folate than their thin counterparts. Because obesity is on the rise, that may explain the decline in average folate levels. Alternatively, diet trends may be to blame. In the U. S., the Food and Drug Administration requires that enriched flour used in cereals and breads be fortified with folic acid. But in 2003, the Atkins diet craze encouraged us all to trade in our Cheerios for steaks. Now diet gurus are encouraging people to eat whole grains, which unlike their processed counterparts, are not supplemented with folic acid.

So, women should consume far more folate. That is, unless you remember this bizarre news item from last spring, reporting that each generation of obese pregnant mice fed folate and other methyl donors had increasingly heavier offspring.

Posted by Debra Speert at 05:29 PM on January 05, 2007 | Permalink | Comments (0) | TrackBacks (0)
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What's new in neuroscience? A physical scientist asked me this question at a holiday party last week. I'd already been thinking about the highs and lows (but mainly highs) of what I've seen in 2006, so I told him about my favorite group of papers to come out in the last few months.

The genes that make us human are expressed in the brain and may be involved in brain development. This is the basic gist of several recent papers that sit on the fence between evolutionary genetics and neuroscience. Pollard et al. (my favorite of the bunch) report that among all genes, the non-coding gene HAR1F has had the most accelerated changes in the human relative to other species. HAR1F is expressed in Cajal-Retzius cells, which are important in cortical development, and is developmentally regulated. Since the cortex is specifically enlarged in humans relative to other species, these data may suggest that HAR1F is important in the evolutionary expansion of the human brain.

Popesco et al. looked for genes with the biggest copy-number expansion in humans relative to other species. They report that humans have more copies of the MGC8902 gene than other species. Humans have approximately 50 copies, whereas chimps and macaques have 10 and 4 copies, respectively. MGC8902 encodes repeats of a protein domain called DUF1220, whose function is unknown. DUF1220 domains are only found in primates. In humans, DUF1220 is found in neurons in the hippocampus, cortex and cerebellum.

Finally, Prabhakar et al. report that non-coding genes with the most human-specific substitutions are disproportionately involve