Can't Dance? Blame GABA, Not ABBA

Can't Dance? Blame GABA, Not ABBA

Очень интересная статья, объясняющая неспособность людей к точному повторению танцевальных движений, через призму ГАМК-сигналинга.
Оказывается, высокие уровни этого нейромедиатора свойственны людям у которых хорошо развита как мелкая моторика, так и способность воспроизводить движения танца.

Ряд новых идей о шизофрении

Эта неделя оказалась урожайной на новости о генезе шизофрении.


Например, появились вот такие замечательные статьи:

GABAergic interneuron origin of schizophrenia pathophysiology. Nakazawa K, Zsiros V, Jiang Z, Nakao K, Kolata S, Zhang S, Belforte JE.

The viral theory of schizophrenia revisited: Abnormal placental gene expression and structural changes with lack of evidence for H1N1 viral presence in placentae or brains of exposed offspring from infected mice. Fatemi SH, Folsom TD, Rooney RJ, Mori S, Kornfield TE, Reutiman TJ, Kneeland RE, Liesch SB, Hua K, Hsu J, Patel DH.

Schizophrenia and tobacco smoking comorbidity: nAChR agonists in the treatment of schizophrenia-associated cognitive deficits. D'Souza MS, Markou A.

Contributions of the d-serine pathway to schizophrenia. Labrie V, Wong AH, Roder JC.

Behavioral and neurochemical consequences of cortical oxidative stress on parvalbumin-interneuron maturation in rodent models of schizophrenia. Powell SB, Sejnowski TJ, Behrens MM.

Adenosine hypothesis of schizophrenia - opportunities for pharmacotherapy. Boison D, Singer P, Shen HY, Feldon J, Yee BK.

Наслаждайтесь :)

Когнитивные стимуляторы

Обожаю эту девочку. У неё самые весёлые посты о самых интересных веществах. Очередная классная статья - http://scienceblogs.com/neurotopia/2010/07/prozac_ritalin_cognitive_enhan.php. О "улучшителях умственных способностей". Особое внимание уделено Прозаку и Риталину.

О процессах ингибирования в мозгу

Отличная статья на http://www.science20.com/measuring_mind/inhibition_brain_more_simple_game.

Однозначно - за! Лекарства для улучшения работы мозга.

Одна из самых животрепещущих тем - допинг для мозга. Статья на http://blog.wired.com/wiredscience/2008/12/brain-enhancing.html:
If drugs can safely give your brain a boost, why not take them? And if you don't want to, why stop others?

In an era when attention-disorder drugs are regularly — and illegally — being used for off-label purposes by people seeking a better grade or year-end job review, these are timely ethical questions.

The latest answer comes from Nature, where seven prominent ethicists and neuroscientists recently published a paper entitled, "Towards a responsible use of cognitive-enhancing drugs by the healthy."

In short: Legalize 'em.

"Mentally competent adults," they write, "should be able to engage in cognitive enhancement using drugs."

Roughly seven percent of all college students, and up to 20 percent of scientists, have already used Ritalin or Adderall — originally intended to treat attention-deficit disorders — to improve their mental performance.

Some people argue that chemical cognition-enhancement is a form of cheating. Others say that it's unnatural. The Nature authors counter these charges: Brain boosters are only cheating, they say, if prohibited by the rules — which need not be the case. As for the drugs being unnatural, the authors argue, they're no more unnatural than medicine, education and housing.

In many ways, the arguments are compelling. Nobody rejects pasteurized milk or dental anesthesia or central heating because it's unnatural. And whether a brain is altered by drugs, education or healthy eating, it's being altered at the same neurobiological level. Making moral distinctions between them is arbitrary.

But if a few people use cognition-enhancing drugs, might everyone else be forced to follow, whether they want to or not?

If enough people improve their performance, then improvement becomes the status quo. Brain-boosting drug use could become a basic job requirement.

Ritalin and Adderall, now ubiquitous as academic pick-me-ups, are merely the first generation of brain boosters. Next up is Provigil, a "wakefulness promoting agent" that lets people go for days without sleep, and improves memory to boot. More powerful drugs will follow.

As the Nature authors write, "cognitive enhancements affect the most complex and important human organ and the risk of unintended side effects is therefore both high and consequential." But even if their safety could be assured, what happens when workers are expected to be capable of marathon bouts of high-functioning sleeplessness?

Most people I know already work 50 hours a week and struggle to find time for friends, family and the demands of life. None wish to become fully robotic in order to keep their jobs. So I posed the question to Michael Gazzaniga, a University of California, Santa Barbara, psychobiologist and Nature article co-author.

"It is possible to do all of that now with existing drugs," he said. "One has to set their goals and know when to tell their boss to get lost!"

Which is not, perhaps, the most practical career advice these days. And University of Pennsylvania neuroethicist Martha Farah, another of the paper's authors, was a bit less sanguine.

"First the early adopters use the enhancements to get an edge. Then, as more people adopt them, those who don't, feel they must just to stay competitive with what is, in effect, a new higher standard," she said.

Citing the now-normal stresses produced by expectations of round-the-clock worker availability and inhuman powers of multitasking, Farah said, "There is definitely a risk of this dynamic repeating itself with cognition-enhancing drugs."

But people are already using them, she said. Some version of this scenario is inevitable — and the solution, she said, isn't to simply say that cognition enhancement is bad.

Instead we should develop better drugs, understand why people use them, promote alternatives and create sensible policies that minimize their harm.

As Gazzaniga also pointed out, "People might stop research on drugs that may well help memory loss in the elderly" — or cognition problems in the young — "because of concerns over misuse or abuse."

This would certainly be unfortunate collateral damage in the 21st century theater of the War on Drugs — and the question of brain enhancement needs to be seen in the context of this costly and destructive war. As Schedule II substances, Ritalin and Adderall are legally equivalent in the United States to opium or cocaine.

"These laws," write the Nature authors, "should be adjusted to avoid making felons out of those who seek to use safe cognitive enhancements."

After all, according to the law's letter, seven percent of college students and 20 percent of scientists should have done jail time — this journalist, too.

Towards responsible use of cognitive-enhancing drugs by the healthy [Nature]

GABA и контроль веса.

Нейротрансмиттеры - такие загадочные субстанции! Оказывается, GABA может влиять на процессы ожирения и похудения. Прочитала на http://www.scientificblogging.com/news_releases/gaba_neurocircuitry_gets_a_look_in_weight_gain_and_decline и вам советую:

GABA Neurocircuitry Gets A Look In Weight Gain (And Decline)


Submitted by News Staff on 10 August 2008 - 12:00am. Research
Controlling body weight is a complicated process but scientists investigating the brain's intricate neurocircuitry and its role in maintaining energy balance are forming a clearer picture of the myriad events that lead to weight gain ... and weight loss.

Writing in Nature Neuroscience, a study led by scientists at Beth Israel Deaconess Medical Center (BIDMC) identifies another piece of this complex puzzle, demonstrating that the neurotransmitter GABA --one of the master communicators among neurons – plays a role in controlling energy balance.

"Body weight maintenance is made up of three basic stages," explains the paper's senior author Bradford Lowell, MD, PhD, an investigator in the Division of Endocrinology, Diabetes and Metabolism at BIDMC whose laboratory is working to identify the specific neurocircuits responsible for controlling food intake and/or energy through functional neuroanatomical mapping studies.

"In the first stage, the brain receives sensory input from the body [including information provided by circulating hormones such as leptin and ghrelin and from fuels such as glucose and fatty acids]," says Lowell, who is also a Professor of Medicine at Harvard Medical School.

In the second stage, he adds, the brain integrates this sensory information with cues it has received from the environment (such as aromas and other enticements) along with information gathered from the organism's emotional state. Then, in the final stage, the brain's neurocircuitry takes over, enabling the brain to make appropriate alterations in food intake and energy expenditure in order to maintain energy balance – and prevent weight gain and obesity.

Previous work had primarily focused on identifying the neuropeptides involved in this process. And indeed, this group of neurotransmitters often proves essential to maintaining energy balance – but not always.

"It is well known that AgRP [Agouti-related protein] neurons play a critical role in feeding and energy balance regulation," explains Qingchun Tong, PhD, a postdoctoral fellow in the Lowell laboratory and the study's first author. "However, the deletion of AgRP and NPY [two neuropeptides released from the AgRP neurons] produces little metabolic effect."

An alternate theory proposed that release of the GABA neurotransmitter was mediating the function of AgRP neurons, an idea that had long been postulated but never examined.

To test this hypothesis, Tong and his colleagues generated a group of mice with disrupted release of GABA specifically from the AgRP neurons. As predicted, the genetically altered mice exhibited profound metabolic changes.

"The mice with AgRP neuron-specific disruption of GABA release were lean, had higher energy expenditure and showed resistance to diet-induced obesity," says Tong. "We also found that these animals showed reduced food intake response to the hormone ghrelin. This suggests to us that the neurocircuit engaging GABA release from the AgRP neurons mediates at least part of ghrelin's appetite-stimulating action."

A series of studies to examine the function of glutamate and GABA release from other groups of neurons are currently underway as investigators continue to dissect the brain's neurocircuitry.

"As these new findings demonstrate, GABA release is an important component that mediates the function of AgRP neurons," says Tong. "Discoveries such as this will ultimately help us to design an efficient strategy to tackle the current epidemic of obesity and metabolic disease."

This work was funded, in part, by grants from the National Institutes of Health and support from the North American Association for the Study of Obesity.

In addition to Lowell and Tong, coauthors include BIDMC investigators Chian-Ping Ye and Juli Jones and University of Texas Southwestern Medical Center investigator Joel Elmquist.