Алкоголизм, наркомания, порнозависимость - а с мозгом что?

Отличная статья о разнице в функционировании мозга при наличии зависимостей разного рода. Алкоголь, никотин, психотропные вещества всяческой природы, еда, порно или азартные игры - всё это приносит удовольствие в момент присутствия и боль при отсутствии. Но много ли общего в формировании звисимостей от разных факторов?
Вот и рассуждения на эту увлекательную тему - https://www.sciencenews.org/blog/scicurious/addiction-showcases-brain-flexibility

Две дофаминовых новости

Дофаминушка опять в новостях. Первое сообщение - о трудоголизме и распределении дофамина в разных участках мозга, а второе - о влиянии этого нейромедиатора на процессы запоминания и забывания информации. 

Наслаждайтесь.

Эффекты разных психоактивных веществ на уровне синапсов

Простенько, но со вкусом.
http://faculty.plattsburgh.edu/donald.slish/DA.html

Допамин в свежих научных новостях

Я очень люблю допамин. Да и как можно его не любить, если именно это чудесное вещество отвечает за нашу мотивацию, удовольствие и другие приятности? В этом блоге достаточно много постов посвящены этому нейромедиатору, поэтому сейчас я хочу поделиться ссылкой на свежайшую статью из авторитетного источника, в которой раскрываются какие-то интересные и не известные до этого, сведения о допамине.

Сообщение на http://www.eurekalert.org/pub_releases/2011-12/osum-ans120111.php гласит, что допамин может быть крайне полезен при лечении опухолей. Оказывается, этот катехоламин способен увеличить эффективность действия противораковых препаратов и радиотерапии! Допамин улучшает приток крови к опухолям и таким образом повышает концентрацию действующих веществ именно в месте потребности, так же увеличивается уровень насыщения этих участков кислородом, что так же способствует борьбе с опухолью. Такие результаты были получены на животных моделях рака груди и кишечника.

Паразит мозг не съест, но химию его изменит...

Сто лет не обновляла этот бложик, пардон.
Вот вам забавная новость. На английском, ага, как обычно.
Некоторые паразиты (токсоплазма, например) в мозгу могут феерически изменять выработку допамина.

Brain parasite directly alters brain chemistry

A research group from the University of Leeds has shown that infection by the brain parasite Toxoplasma gondii, found in 10-20 per cent of the UK's population, directly affects the production of dopamine, a key chemical messenger in the brain.

Their findings are the first to demonstrate that a parasite found in the brain of mammals can affect dopamine levels.

Whilst the work has been carried out with rodents, lead investigator Dr Glenn McConkey of the University's Faculty of Biological Sciences, believes that the findings could ultimately shed new light on treating human neurological disorders that are dopamine-related such as schizophrenia, attention deficit hyperactivity disorder, and Parkinson's disease.

This research may explain how these parasites, remarkably, manipulate rodents' behaviour for their own advantage. Infected mice and rats lose their innate fear of cats, increasing the chances of being caught and eaten, which enables the parasite to return to its main host to complete its life cycle.

In this study, funded by the Stanley Medical Research Institute and Dunhill Medical Trust, the research team found that the parasite causes production and release of many times the normal amount of dopamine in infected brain cells.

Dopamine is a natural chemical which relays messages in the brain controlling aspects of movement, cognition and behaviour. It helps control the brain's reward and pleasure centres and regulates emotional responses such as fear. The presence of a certain kind of dopamine receptor is also associated with sensation-seeking, whereas dopamine deficiency in humans results in Parkinson's disease.

These findings build on earlier studies in which Dr McConkey's group found that the parasite actually encodes the enzyme for producing dopamine in its genome.

"Based on these analyses, it was clear that T. gondii can orchestrate a significant increase in dopamine production in neural cells," says Dr McConkey.

"Humans are accidental hosts to T. gondii and the parasite could end up anywhere in the brain, so human symptoms of toxoplasmosis infection may depend on where parasite ends up. This may explain the observed statistical link between incidences of schizophrenia and toxoplasmosis infection."

Dr McConkey says his next experiments will investigate how the parasite enzyme triggers dopamine production and how this may change behaviour.
http://www.eurekalert.org/pub_releases/2011-11/uol-bpd110411.php

Допаминово-серотониновые новости :)

Пабмед принёс новую пачку статей о допаминергической и серотонинергической системах:

Neuropharmacology. 2011 Apr 12.
Enhanced effects of amphetamine but reduced effects of the hallucinogen, 5-MeO-DMT, on locomotor activity in 5-HT(1A) receptor knockout mice: Implications for schizophrenia.

van den Buuse M, Ruimschotel E, Martin S, Risbrough VB, Halberstadt AL.

Behavioural Neuroscience Laboratory, Mental Health Research Institute, Parkville, Melbourne, Australia; Department of Pharmacology, University of Melbourne, Australia.

Neuropharmacology. 2011 Apr 15.
Possible involvement of serotonin 5-HT2 receptor in the regulation of feeding behavior through the histaminergic system.

Murotani T, Ishizuka T, Isogawa Y, Karashima M, Yamatodani A.

Department of Medical Science and Technology, Division of Health Sciences, Graduate School of Medicine, Osaka University, 1-7 Yamadaoka, Suita, Osaka 565-0871, Japan.

Neuropharmacology. 2011 Apr 17.
Differential effects of cocaine and MDMA self-administration on cortical serotonin transporter availability in monkeys.

Gould RW, Gage HD, Banks ML, Blaylock BL, Czoty PW, Nader MA.

Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC 27157, United States.

Neuropharmacology. 2011 Apr 19.
Dopamine-related drugs act presynaptically to potentiate GABA(A) receptor currents in VTA dopamine neurons.

Michaeli A, Yaka R.

Institute for Drug Research, School of Pharmacy, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.

Neuropharmacology. 2011 Apr 7.
High concentrations of MDMA ('ecstasy') and its metabolite MDA inhibit calcium influx and depolarization-evoked vesicular dopamine release in PC12 cells.

Hondebrink L, Meulenbelt J, Meijer M, van den Berg M, Westerink RH.

Neurotoxicology Research Group, Institute for Risk Assessment Sciences (IRAS), Utrecht University, P.O. Box 80.177, NL-3508 TD Utrecht, The Netherlands; National Poisons Information Centre (NVIC), National Institute for Public Health and the Environment (RIVM), P.O. Box 1, NL-3720 BA, Bilthoven, The Netherlands.

Ряд новых интересностей о допамине :)

Dopamine model could play role in treating schizophrenia and drug addiction


In the brain, dopamine is involved in a number of processes that control the way we behave. If an action results in the substance being released, we are more likely to repeat the action. This applies to actions such as eating, sexual intercourse or winning a competition. However, the same also holds true when individuals take harmful narcotics. Scientists believe that mental illnesses such as schizophrenia can be linked to dopamine imbalances. Дальше на http://www.eurekalert.org/pub_releases/2010-10/uoc-dmc102010.php


Montreal, October 20, 2010 – Daily sleeping and eating patterns are critical to human well-being and health. Now, a new study from Concordia University has demonstrated how the brain chemical dopamine regulates these cycles by altering the activity of the "clock-protein" PER2. Published in the Journal of Neuroscience, these findings may have implications for individuals with Parkinson's Disease with disrupted 24-hour rhythms of activity and sleep. Дальше http://www.eurekalert.org/pub_releases/2010-10/cu-nro102010.php


SEATTLE, Wash. — October 18, 2010 — Researchers at the Allen Institute for Brain Science have found that the same genes have different activity patterns in the brain in individuals with different genetic backgrounds. These findings may help to explain individual differences in the effectiveness and side-effect profiles of therapeutic drugs and thus have implications for personalized medicine. The study is available in this week’s online early edition of the Proceedings of the National Academy of Sciences  Дальше http://scienceblog.com/39433/gene-activity-in-the-brain-depends-on-genetic-background/?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+scienceblogrssfeed+%28Science+Blog%29

Sensation seeking—the urge to do exciting things—has been linked to dopamine, a chemical that carries messages in your brain. For a new study published in Psychological Science, a journal of the Association for Psychological Science, scientists analyzed genes in the dopamine system and found a group of mutations that help predict whether someone is inclined toward sensation seeking. Дальше http://scienceblog.com/39121/a-thirst-for-excitement-is-hidden-in-your-genes/?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+scienceblogrssfeed+%28Science+Blog%29


Glutamate and dopamine: Biological predictors of the transition to psychosis?


Philadelphia, PA, 30 September, 2010 - There is growing evidence that two neurotransmitters - dopamine and glutamate - are abnormal in people with psychotic illness, including schizophrenia. Among many other things, these chemicals play a role in cognitive functions, such as memory, learning, and problem-solving
A new study in Biological Psychiatry is now the first to examine the relationship between these two brain chemicals by measuring both in the same individuals. http://www.eurekalert.org/pub_releases/2010-09/e-gd093010.php


There’s a predictable narrative to a lot of discoveries in molecular biology. The story begins when a scientist discovers that Molecule X causes Phenomenon Y. Perhaps we’re talking about CREB and long-term memory, or serotonin and depression, or cholesterol and heart disease. At first, the data looks really solid – when the gene for Molecule X is knocked out of a mouse, Phenomenon Y disappears! And when patients take a drug that increases/reduces Molecule X, you get a change in Phenomenon Y! The causal relationship seems so simple.


And that’s when things start to get complicated. Time and time again, the neat relationship between Molecule X and Phenomenon Y disintegrates into a knot of feedback loops, enzymatic pathways, environmental interactions and regulatory genes. It’s not that Molecule X doesn’t matter – it’s that it doesn’t exist by itself. Instead, the Molecule exerts its effects by interacting with a byzantine list of other molecules, all of which can also influence the biological outcome. Read More http://www.wired.com/wiredscience/2010/08/sex-is-stressful-but-good-for-you/?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+wiredscience+%28Blog+-+Wired+Science%29

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.

Эндометриальные стволовые клетки и допамин

Информация о возможных способах лечения болезни Паркинсона стволовыми клетками описан на http://www.eurekalert.org/pub_releases/2010-05/nioc-esc050610.php

Endometrial stem cells restore brain dopamine levels

Mouse study may lead to new therapies for Parkinson's Disease

Endometrial stem cells injected into the brains of mice with a laboratory-induced form of Parkinson's disease appeared to take over the functioning of brain cells eradicated by the disease.
The finding raises the possibility that women with Parkinson's disease could serve as their own stem cell donors. Similarly, because endometrial stem cells are readily available and easy to collect, banks of endometrial stem cells could be stored for men and women with Parkinson's disease.
"These early results are encouraging," said Alan E. Guttmacher, M.D., acting director of the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), the NIH Institute that funded the study. "Endometrial stem cells are widely available, easy to access and appear to take on the characteristics of nervous system tissue readily."
Parkinson's disease results from a loss of brain cells that produce the chemical messenger dopamine, which aids the transmission of brain signals that coordinate movement.
This is the first time that researchers have successfully transplanted stem cells derived from the endometrium, or the lining of the uterus, into another kind of tissue (the brain) and shown that these cells can develop into cells with the properties of that tissue.
The findings appear online in the Journal of Cellular and Molecular Medicine.
The study's authors were Erin F. Wolff, Xiao-Bing Gao, Katherine V. Yao, Zane B. Andrews, Hongling Du, John D. Elsworth and Hugh S. Taylor, all of Yale University School of Medicine.
Stem cells retain the capacity to develop into a range of cell types with specific functions. They have been derived from umbilical cord blood, bone marrow, embryonic tissue, and from other tissues with an inherent capacity to develop into specialized cells. Because of their ability to divide into new cells and to develop into a variety of cell types, stem cells are considered promising for the treatment of many diseases in which the body's own cells are damaged or depleted.
In the current study, the researchers generated stem cells using endometrial tissue obtained from nine women who did not have Parkinson's disease and verified that, in laboratory cultures, the unspecialized endometrial stem cells could be transformed into dopamine-producing nerve cells like those in the brain.
The researchers also demonstrated that, when injected directly into the brains of mice with a Parkinson's-like condition, endometrial stem cells would develop into dopamine-producing cells.
Unspecialized stem cells from the endometrial tissue were injected into mouse striatum, a structure deep in the brain that plays a vital role in coordinating balance and movement. When the researchers examined the animals' striata five weeks later, they found that the stem cells had populated the striatum and an adjacent brain region, the substantia nigra. The substantia nigra produces abnormally low levels of dopamine in human Parkinson's disease and the mouse version of the disorder. The researchers confirmed that the stem cells that had migrated to the substantia nigra became dopamine-producing nerve cells and that the animals' dopamine levels were partially restored.
The study did not examine the longer-term effects of the stem cell transplants or evaluate any changes in the ability of the mice to move. The researchers noted that additional research would need to be conducted to evaluate the safety and efficacy of the technique before it could be approved for human use.
According to the researchers, stem cells derived from endometrial tissue appear to be less likely to be rejected than are stem cells from other sources. As expected, the stem cells generated dopamine producing cells when transplanted into the brains of mice with compromised immune systems. However, the transplants also successfully gave rise to dopamine producing cells in the brains of mice with normal immune systems.
According to Dr. Taylor, because women could provide their own donor tissue, there would be no concern that their bodies would reject the implants. Moreover, because endometrial tissue is widely available, banks of stem cells could be established. The stem cells could be matched by tissue type to male recipients with Parkinson's to minimize the chances of rejection.
In addition, Dr. Taylor added that endometrial stem cells might prove to be easier to obtain and easier to use than many other types of stem cells. With each menstrual cycle, women generate new endometrial tissue every month, so the stem cells are readily available. Even after menopause, women taking estrogen supplements are capable of generating new endometrial tissue. Because doctors can gather samples of the endometrial lining in a simple office procedure, it is also easier to collect than other types of adult stem cells, such as those from bone marrow, which must be collected surgically.
"Endometrial tissue is probably the most readily available, safest, most easily attainable source of stem cells that is currently available. We hope the cells we derived are the first of many types that will be used to treat a variety of diseases," said senior author Hugh S. Taylor, M.D., of Yale University. "I think this is just the tip of the iceberg for what we will be able to do with these cells."

###

The NICHD sponsors research on development, before and after birth; maternal, child, and family health; reproductive biology and population issues; and medical rehabilitation. For more information, visit the Institute's Web site at http://www.nichd.nih.gov/.
The National Institutes of Health (NIH) — The Nation's Medical Research Agency — includes 27 Institutes and Centers and is a component of the U. S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical, and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

Об ожидании наслаждения и допамине

Читаем на http://www.scientificblogging.com/news_articles/link_between_dopamine_and_expectation_pleasure_confirmed
Enhancing the effects of dopamine influences how people make life choices by affecting expectations of pleasure, according to new research from the UCL Institute of Neurology.

Published today in Current Biology, the study confirms an important role for dopamine in how human expectations are formed and how people make complex decisions. It also contributes to an understanding of how pleasure expectation can go awry, for example in drug addiction.

The study builds on earlier research which used brain imaging as participants imagined holiday destinations. An area of the brain called the straitum tracked expectations and the
scientists found that they could take that signal and predict what the participants would choose. The authors believed this was dopamine at work and set-up this study to further explore its role.

The research team examined estimated pleasure of future events before and after the administration of a drug called L-DOPA which is known to enhance dopamine function in the brain and is commonly used to treat patients with Parkinson's disease.

The 61 study participants were asked to rate their expectations of happiness if they were to holiday at each of 80 destinations, from Thailand to Greece. They were then given L-DOPA or a placebo and asked to imagine holidaying in those destinations.

The following day participants had to pick between a series of paired destinations that they had initially assigned with equal ratings, one member of the pair was imagined under L-DOPA the day before and the other under placebo. Finally, they rated the full set of 80 destinations again.

Ratings for particular destinations increased after they were imagined under L-DOPA's influence. That increase also affected the participants' selections the following day. Dr Sharot added: "We had reason to believe that dopamine would enhance expectations of pleasure in humans, but were surprised at the strength of this effect. The enhancement lasted at least 24 hours and was evident in almost 80 per cent of the subjects."

Citation: Tali Sharot, Tamara Shiner,Annemarie C. Brown, Judy Fan,Raymond J. Dolan, 'Dopamine Enhances Expectation of Pleasure in Humans', Current Biology Online 2009, doi:10.1016/j.cub.2009.10.025

Новости о влиянии кокаина на допаминовый метаболизм

Очень интересно: http://www.eurekalert.org/pub_releases/2009-05/muhc-cpa051909.php
Contact: Isabelle Klingisabelle.kling@muhc.mcgill.ca514-843-1560McGill University Health Centre
Cocaine: Perceived as a reward by the brain?
Researchers at the MNI and the MUHC open up a new path for cocaine addiction research
This release is available in French.
Montreal, May 19th 2009 - Cocaine is one of the oldest drugs known to humans, and its abuse has become widespread since the end of the 19th century. At the same time, we know rather little about its effects on the human brain or the mechanisms that lead to cocaine addiction. The latest article by Dr. Marco Leyton, of the Montreal Neurological Institute (MNI), McGill University and the McGill University Health Centre, which was published in the journal Biological Psychiatry on May 15, 2009, not only demonstrates a link between cocaine and the reward circuits in the brain but also associates the susceptibility to addiction with these mechanisms.
The results of this study show that sniffing cocaine triggers high levels of dopamine secretion in a central region of the brain called the striatum. Dopamine is known to play a critical role in the brain's response to reward as well as in its response to addictive drugs.
This study was carried out in ten non-addicted users of cocaine, all of whom sniffed cocaine on one test day and placebo powder on another. Participants underwent blood tests before and after taking the drug, and dopamine release in the brain was measured using PET scans.
"The ability of cocaine to activate dopamine release varies markedly from person to person. Our study suggests that this is related to how much of the drug the person consumed in the past," explained Dr. Leyton. The more cocaine someone has used in his or her lifetime, the more the brain will secrete dopamine during subsequent cocaine use. "It's possible therefore that the intensity of the reward-circuit response is related to increased susceptibility to addiction," stated Dr. Leyton.
Although the relationship between the intensity of dopamine secretion and the frequency of drug use has been demonstrated, researchers still do not fully understand its mechanism of action. Is it the repeated stimulation of the reward circuit that leads to addiction, or is it an inherent sensitivity to addiction that leads to the increased secretion of dopamine? This question is not easy to answer, especially since other factors come into play, such as other aspects of the subject's personal history.
Whatever the answer, the relationship between dopamine and cocaine means that this hormone could be a potential target for treatment against addiction. More research is required before treatments are available, but this study opens a new door in this direction.

О допамине и сексуальности :)

Приём агонистов допамина, даже при лечении болезни Паркинсона - влияет на поведенческие характеристики! Читаю на http://www.scientificblogging.com/erin039s_spin/hypersexual_compulsive_gambler_blame_dopamine_only_if_you_have_parkinsons_disease_too
According to a new study published by the Mayo Clinic, patients with Parkinson disease (PD) have another problem to deal with. Researchers have found that one in six patients taking therapeutic doses of
certain prescription drugs for management of PD have developed troubling behavioral symptoms. The most problematic symptoms include compulsive gambling and hypersexuality.

PD is one of the most common degenerative neurological disorders affecting 1.5 million people in the US. PD is characterized by the destruction of neurons responsible for the production of dopamine which allows coordinated function of muscles, movement and signals from the brain. Without dopamine, motor function becomes impaired and other signals from the brain are misinterpreted or not received at all. Tremors, slow movements, stiffness and imbalance are all symptoms of Parkinson’s and can severely impair normal life.

This study, published in the April issue of Mayo Clinic Proceedings, is based upon two previous case series from 2005, report a connection between dopamine agonist medications and the destructive symptoms. Dopamine agonists are compounds that activate dopamine receptors in the absence of dopamine. Dopamine agonists can then act as a dopamine substitute and manage signaling pathways and proper messaging which dopamine is the major mediator.

Dopamine agonists are a significant part of PD treatment and include drugs like pramipexole and ropinirole. In small doses, these drugs have other uses as well, and are also commonly prescribed for Restless Legs Syndrome (RLS). This class of medication stimulates specific brain circuits which are associated with substrates for emotional and reward centers in the brain and can cause an increase in hedonistic behaviors. Too much dopamine substitute may affect a PD patient’s brain chemistry and urge them to do “feel-good” behaviors to an extreme. Thus symptoms such as compulsive gambling and hyper-sexuality can arise.

"The 2005 case series alerted us that something bad was happening to some unfortunate people. This study was done to assess the likelihood that this effect would happen to the average Parkinson's patient treated with these agents," says J. Michael Bostwick, M.D., Mayo Clinic psychiatrist who spearheaded the new study.

Researchers analyzed a group of 267 patients, 66 of which were taking dopamine agonists as their primary medication for management of PD. They found that 7 of the patients experiences new onset of hedonistic behavioral gambling or hypersexuality. They also found that none of the other patients developed these symptoms, which included 28 patients taking lower doses of the dopamine agonists. Mayo physicians suggest that a lower dosage of these dopamine agonists be recommended for susceptible patients to reduce risk of unwanted side effects.

"It is crucial for clinicians prescribing dopamine agonists to apprise patients as well as their spouses or partners about this potential side effect. The onset can be insidious and overlooked until life-altering problems develop," says J. Eric Ahlskog, M.D., Ph.D., Mayo Clinic neurologist and co-author of the 2005 study. "It also is worth noting that the affected patients were all taking therapeutic doses. Very low doses, such as those used to treat restless legs syndrome, carry much less risk."

According to the National Parkinson’s Foundation, the disease affects 1 out of every 100 people over the age of 60. Globally, 2% of the population worldwide will develop Parkinson’s in their lifetime according to projections made by the Mayo Clinic.

References:

Mayo Clinic research

J. Michael Bostwick, Michael J. Frequency of New-Onset Pathologic Compulsive Gambling or Hypersexuality After Drug Treatment of Idiopathic Parkinson Disease." Mayo Clinic Proceedings. 84(4) April 2009. pgs 310-316 doi: 10.4065/84.4.310

О генах и моноаминооксидазе.

Отличная статья. О полиморфизме генов, кодирующих МАОА, и связанных с этим нарушениях поведения. http://www.eurekalert.org/pub_releases/2008-12/ace-aaa120808.php

Contact: Roope Tikkanen, M.D.
roope.tikkanen@helsinki.fi
358-9-471-63760
University of Helsinki

Alcoholism: Clinical & Experimental Research
Alcohol and a polymorphism of the monoamine oxidase A gene predict impulsive violence

The monoamine oxidase A (MAOA) gene is an outer membrane mitochondrial enzyme that breaks down monoamines such as serotonin, noradrenalin and dopamine. A common polymorphism in MAOA results in high- or low-activity MAOA, and both genotypes have been linked to aggression and violence. A Finnish study has found that drinking and high-activity MAOA can predict the risk of impulsive violence, while aging may decrease this risk.

Results will be published in the March issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

"Alcoholism, alcohol consumption and violence are clearly related," said Roope Tikkanen, a researcher in the department of psychiatry at Helsinki University Central Hospital and corresponding author for the study. He noted that crime statistics show that most impulsive homicides occur among adolescent and middle-aged groups rather than among the elderly, and habitually violent-impulsive offenders are often expected to "grow out of their difficulties" with increasing age. "Surprisingly little accurate information, however, is available on this aging-impulsive aggression issue," he said.

Tikkanen and his colleagues decided to look at the MAOA gene, alcohol consumption and aging as predictors for recidivism in impulsive violent behavior among a sample of 174 Finnish alcoholic male offenders originally recruited between 1990 and 1998. Each offender was given a psychiatric assessment; in addition, their alcohol consumption was measured, their violent behavior was assessed, and they were genotyped for polymorphisms of MAOA.

"Increased alcohol consumption and aging seem to predict violence," said Tikkanen, "although these risk factors 'work' in opposite directions, and only concern individuals who have been given by nature a high-activity variant of MAOA." On the other hand, he added, additional research has suggested that individuals with low-activity MAOA seem to be at risk for criminality and violence after exposure to severe childhood maltreatment.

"People react quite differently to acute alcohol exposure," Tikkanen continued. "Most individuals become relaxed and talkative, while some – particularly persons who are introverted while sober – become expansively extroverted and aggressive. A dramatic change from a normally introverted personality to extroverted aggressiveness and uncontrolled behaviors under the influence of alcohol was formerly called 'pathological intoxication' in Finland."

Regarding the decline in impulsive-aggressive behavior with aging among high-activity MAOA offenders, Tikkanen hypothesized that it may be due to a correction of low central serotonin levels in the central nervous system.

Tikkanen cautioned against genetic testing for individuals who may be worried for one reason or another about their risk. "Even though whole genome scans will one day be affordable, the average person probably has very many factors that differ from the violent offenders in the study," he said. "For instance, the average Finnish consumption is two drinks a day or 10 kg pure alcohol per year, whereas the upper 10 percent of violent offenders drink approximately one 0.75 liter bottle of liquor a day or around 100 kg pure alcohol a year."

Tikkanen and his co-authors suggest that high-activity MAOA offenders may be helped to control their violent behaviors by coaching to maintain alcohol abstinence, and possibly by psychopharmacological treatment to increase central serotonin levels.

"In some countries, prison sentences may be very long – even a lifetime or more – and the reason for the sentence may be an accumulation of minor convictions committed in a drunken state," said Tikkanen. "In such cases, it could perhaps benefit all parties to decrease the length of the sentence. Our results suggest that the risk for new violent crimes decreases by 150 percent when high-activity MAOA individuals become 20 years older. Perhaps we could increase the efficacy of addiction rehabilitation by focusing resources particularly on younger heavy-drinking high-activity MAOA individuals."

###

Alcoholism: Clinical & Experimental Research (ACER) is the official journal of the Research Society on Alcoholism and the International Society for Biomedical Research on Alcoholism. Co-authors of the ACER paper, "Effects of MAOA-genotype, Alcohol Consumption, and Ageing on Violent Behavior," were: Richard L. Sjöberg of the Laboratory of Neurogenetics at the National Institute on Alcohol Abuse and Alcoholism, the Center for Clinical Research at Uppsala University in Västerås, Sweden, and the Department of Neurosurgery at University Hospital in Umeå, Sweden; Francesca Ducci of King's College in London; Davie Goldman of the Laboratory of Neurogenetics at the National Institute on Alcohol Abuse and Alcoholism; Matti Holi and Matti Virkkunen of the Department of Psychiatry in the Institute of Clinical Medicine at the University of Helsinki; and Jari Tiihonen of the Department of Forensic Psychiatry and Clinical Physiology at the University of Kuopio, Finland. The study was funded by the National Institute on Alcohol Abuse and Alcoholism, and the Olle Engkvist Byggmästare foundation.

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]

Допаминовые рецепторы и контоль веса.

Вот они какие - мои любимые... :))) Нашла инфу на http://www.scientificblogging.com/news_releases/dopamine_signaling_why_some_like_chocolate_milkshakes_too_much

Dopamine Signaling - Why Some Like Chocolate Milkshakes Too Much
Submitted by News Staff on 16 October 2008 - 2:00am. Neuroscience

Using brain imaging and chocolate milkshakes, scientists have found that women with weakened "reward circuitry" in their brains are at increased risk of weight gain over time and potential obesity. The risk increases even more for women who also have a gene associated with compromised dopamine signaling in the brain.

The results, drawn from two studies using functional magnetic resonance imaging (fMRI) at the University of Oregon's Lewis Center for Neuroimaging, appear in the Oct. 17 issue of the journal Science. The first-of-its-kind approach unveiled blunted activation in the brain's dorsal stratium when subjects were given milkshakes, which may reflect less-than-normal dopamine output.

"Although recent findings suggested that obese individuals may experience less pleasure when eating, and therefore eat more to compensate, this is the first prospective evidence for this relationship," said Eric Stice, lead author and senior researcher at the Oregon Research Institute (ORI) in Eugene. "The evidence of temporal precedence suggests it is a true vulnerability factor that predates obesity onset. In addition, the evidence that this relation is even stronger for individuals at genetic risk for compromised signaling in these brain regions points to an important biological factor that appears to increase risk for obesity onset."

Stice, who has a courtesy appointment in the UO psychology department, has studied eating disorders and obesity for 18 years. He was joined in the new research by ORI colleague Sonja T.P. Spoor, Cara Bohon, a UO doctoral student in clinical psychology, and Dana M. Small of the John B. Pierce Laboratory in New Haven, Conn., and the Yale University School of Medicine.

Dopamine is the primary neurotransmitter in the brain's reward pathways. Food intake is associated with dopamine release, while pleasure from eating correlates with the amount of dopamine release. Previous studies have suggested that obese individuals have fewer dopamine receptors in the brain and have to eat more than lean people to be satisfied.

Using fMRI, Stice's team measured the extent to which the dorsal striatum was activated in response to an individual's receipt of a taste of chocolate milkshake or a tasteless solution.

One study involved 43 female college students ranging in age from 18 to 22 with a mean body mass index (BMI) of 28.6. The second study looked at 33 adolescent girls, ages 14-18, with a mean BMI of 24.3. Most of the participants were tested for the presence of a genetic variation known as the Taq1A1 allele, which is linked to a lower number of dopamine D2 receptors.

Researchers tracked changes in BMI over a year. Results showed that participants with decreased striatal activation in response to receiving milkshake and those with the A1 allele were more likely to gain weight over time.

"I was quite excited by the study itself, as it is the first prospective study to utilize fMRI and genetic data to predict unhealthy weight gain," said Bohon, whose doctoral work is done on both the UO campus and the nearby ORI facility. "The findings suggest that certain biological factors may impact one's risk for weight gain, which is important in order to better understand how we can eventually intervene and prevent obesity."