Neuroscience

Articles and news from the latest research reports.

Posts tagged binge drinking

219 notes

Stimulating brain cells stops binge drinking, animal study finds
Researchers at the University at Buffalo have found a way to change alcohol drinking behavior in rodents, using the emerging technique of optogenetics, which uses light to stimulate neurons.
Their work could lead to powerful new ways to treat alcoholism, other addictions, and neurological and mental illnesses; it also helps explain the underlying neurochemical basis of drug addiction.
The findings, published in November in Frontiers in Neuroscience, are the first to demonstrate a causal relationship between the release of dopamine in the brain and drinking behaviors of animals. Research like this, which makes it possible to map the neuronal circuits responsible for specific behaviors, is a major focus of President Obama’s Brain Research for Advancing Innovative Neurotechnologies initiative, known as BRAIN.
In the experiments, rats were trained to drink alcohol in a way that mimics human binge-drinking behavior.
First author Caroline E. Bass, PhD, assistant professor of pharmacology and toxicology in the UB School of Medicine and Biomedical Sciences explains:  “By stimulating certain dopamine neurons in a precise pattern, resulting in low but prolonged levels of dopamine release, we could prevent the rats from binging. The rats just flat out stopped drinking,” she says.
Bass’s co-authors are at Wake Forest University, where she worked previously.
Interestingly, the rodents continued to avoid alcohol even after the stimulation of neurons ended, she adds.
“For decades, we have observed that particular brain regions light up or become more active in an alcoholic when he or she drinks or looks at pictures of people drinking, for example, but we didn’t know if those changes in brain activity actually governed the alcoholic’s behavior,” says Bass.
The researchers activated the dopamine neurons through a type of deep brain stimulation, but unlike techniques now used to treat certain neurological disorders, such as severe tremors in Parkinson’s disease patients, this new technique, called optogenetics, uses light instead of electricity to stimulate neurons.
“Electrical stimulation doesn’t discriminate,” Bass explains. “It hits all the neurons, but the brain has many different kinds of neurons, with different neurotransmitters and different functions. Optogenetics allows you to stimulate only one type of neuron at a time.”
Bass specializes in using viral vectors to study the brain in substance abuse. In this study, she used a virus to introduce a gene encoding a light-responsive protein into the animals’ brains. That protein then activated a specific subpopulation of dopamine neurons in the brain’s reward system.
“I created a virus that will make this protein only in dopaminergic neurons,” Bass says.
The neuronal pathways affected in this research are involved in many neurological disorders, she says. For that reason, the results have application not only in understanding and treating alcohol-drinking behaviors in humans, but also in many devastating mental illnesses and neurological diseases that have a dopamine component.
Bass notes that this ability to target genes to dopamine neurons could potentially lead to the use of gene therapy in the brain to mitigate many of these disorders.
“We can target dopamine neurons in a part of the brain called the nigrostriatal pathway, which is what degenerates in Parkinson’s disease,” she says. “If we could infuse a viral vector into that part of the brain, we could target potentially therapeutic genes to the dopamine neurons involved in Parkinson’s. And by infusing the virus into other areas of the brain, we could potentially deliver therapeutic genes to treat other neurological diseases and mental illnesses, including schizophrenia and depression.”

Stimulating brain cells stops binge drinking, animal study finds

Researchers at the University at Buffalo have found a way to change alcohol drinking behavior in rodents, using the emerging technique of optogenetics, which uses light to stimulate neurons.

Their work could lead to powerful new ways to treat alcoholism, other addictions, and neurological and mental illnesses; it also helps explain the underlying neurochemical basis of drug addiction.

The findings, published in November in Frontiers in Neuroscience, are the first to demonstrate a causal relationship between the release of dopamine in the brain and drinking behaviors of animals. Research like this, which makes it possible to map the neuronal circuits responsible for specific behaviors, is a major focus of President Obama’s Brain Research for Advancing Innovative Neurotechnologies initiative, known as BRAIN.

In the experiments, rats were trained to drink alcohol in a way that mimics human binge-drinking behavior.

First author Caroline E. Bass, PhD, assistant professor of pharmacology and toxicology in the UB School of Medicine and Biomedical Sciences explains:  “By stimulating certain dopamine neurons in a precise pattern, resulting in low but prolonged levels of dopamine release, we could prevent the rats from binging. The rats just flat out stopped drinking,” she says.

Bass’s co-authors are at Wake Forest University, where she worked previously.

Interestingly, the rodents continued to avoid alcohol even after the stimulation of neurons ended, she adds.

“For decades, we have observed that particular brain regions light up or become more active in an alcoholic when he or she drinks or looks at pictures of people drinking, for example, but we didn’t know if those changes in brain activity actually governed the alcoholic’s behavior,” says Bass.

The researchers activated the dopamine neurons through a type of deep brain stimulation, but unlike techniques now used to treat certain neurological disorders, such as severe tremors in Parkinson’s disease patients, this new technique, called optogenetics, uses light instead of electricity to stimulate neurons.

“Electrical stimulation doesn’t discriminate,” Bass explains. “It hits all the neurons, but the brain has many different kinds of neurons, with different neurotransmitters and different functions. Optogenetics allows you to stimulate only one type of neuron at a time.”

Bass specializes in using viral vectors to study the brain in substance abuse. In this study, she used a virus to introduce a gene encoding a light-responsive protein into the animals’ brains. That protein then activated a specific subpopulation of dopamine neurons in the brain’s reward system.

“I created a virus that will make this protein only in dopaminergic neurons,” Bass says.

The neuronal pathways affected in this research are involved in many neurological disorders, she says. For that reason, the results have application not only in understanding and treating alcohol-drinking behaviors in humans, but also in many devastating mental illnesses and neurological diseases that have a dopamine component.

Bass notes that this ability to target genes to dopamine neurons could potentially lead to the use of gene therapy in the brain to mitigate many of these disorders.

“We can target dopamine neurons in a part of the brain called the nigrostriatal pathway, which is what degenerates in Parkinson’s disease,” she says. “If we could infuse a viral vector into that part of the brain, we could target potentially therapeutic genes to the dopamine neurons involved in Parkinson’s. And by infusing the virus into other areas of the brain, we could potentially deliver therapeutic genes to treat other neurological diseases and mental illnesses, including schizophrenia and depression.”

Filed under binge drinking alcohol optogenetics deep brain stimulation neurons neuroscience science

68 notes

A brain protein called vimentin can indicate damage to the hippocampus following binge drinking

Chronic drinking is known to have detrimental health effects such as cardiac and liver problems, cognitive impairments, and brain damage. Binge drinking in particular is known to increase the risk of developing dementia and/or brain damage, yet little is known about an exact threshold for the damaging effects of alcohol. A study using rodents to examine various markers of neurodegeneration has found that brain damage can occur with as little as 24 hours of binge-like alcohol exposure.

Results will be published in the March 2013 issue of Alcoholism: Clinical & Experimental Research and are currently available at Early View.

"We know that the extent of damage following alcohol exposure depends heavily on the manner in which it is consumed," said Kimberly Nixon, associate professor of pharmaceutical sciences at The University of Kentucky as well as corresponding author for the study. "Human studies suggest that binge-pattern drinking is more closely associated with brain damage. One study, for example, reported that binge drinking at least once per month in adulthood significantly increases the risk of developing dementia later in life. Animal models help provide the critical information that binge drinking, which produces high blood alcohol levels, directly causes damage."

"The exact threshold for the damaging effects of alcohol on the brain is unclear," commented Fulton T. Crews, John Andrews Distinguished Professor and director of the Center for Alcohol Studies at the University of North Carolina. "It is likely that the higher the blood alcohol level the greater the damage, however, this manuscript only studies binge drinking, using vimentin and flurojade B as markers of neurotoxicity."

"People hear from multiple sources that low-moderate alcohol consumption can be beneficial, and then we come along and say that heavy alcohol use leads to detrimental outcomes," said Nixon. "People then want to know what the line is between beneficial and detrimental Unfortunately, we don’t know exactly. However, our study suggests that it may be even less than previously thought."

Nixon and her colleagues administered a nutritionally complete liquid diet to adult male Sprague-Dawley rats that additionally contained either alcohol (25% w/v) or isocaloric dextrose every eight hours for either one or two days. The rodents were sacrificed immediately following, two days after, or seven days after alcohol exposure and their brain tissues were examined.

"This was really a simple study that took advantage of some new ‘tools’ to look for evidence of brain damage," explained Nixon. "In other words, we didn’t look for dying cells themselves, but we looked at more indirect indices of damage by looking at what happens to astroglia, one of the ‘supporting’ cells for neurons. Astroglia react to brain damage by expressing several proteins that they do not normally express under healthy, happy conditions, one of which is an intermediate filament protein called vimentin. We saw a remarkable number of cells expressing this marker It is one of those ‘here is your brain, here is your brain on drugs’ kind of findings where the expression was obvious to the naked eye in many brains with as little as 24 hours of high blood alcohol levels."

Nixon added that, because rodents metabolize alcohol significantly faster than humans do, it is important to look at the actual concentration of alcohol in the blood in order to translate this to the human condition. “These rats had blood alcohol levels that were more than four times the legal driving limit, which for humans would require excessive drinking in the nature of a 12-pack of beer, a couple bottles of wine, or half of fifth of whisky. Unfortunately, drinking self-reports and blood alcohol level data from emergency rooms confirm that this level of drinking is common in those with alcohol use disorders.”

"Rodent brain damage can model human damage," noted Crews. "Vimentin seems to be a good marker of glial activation that shows that one day of binge drinking can cause some brain damage that persists and grows after a week of abstinence. However, both rodent and human brain damage generally require long-term alcohol consumption that models alcoholism and not the acute responses studied in this manuscript."

Nixon agreed. “The lack of overt neuronal deterioration suggests that a single, short-term, high-level binge probably does not result in functional changes and/or cognitive deficits,” she said. “However, since alcoholics experience multiple binges throughout their lifetime, it is important to consider that each successive binge, starting with the very first one, affords some level of damage to the brain. Therefore, theoretically, with multiple binges comes a cumulative detrimental effect where pronounced cognitive, behavioral, and structural effects are observed.”

Nixon said this study demonstrates that new discoveries are always possible. “You have to know where and when to look for some of these effects,” she said. “The reason why this discovery wasn’t made previously is merely due to groups, ourselves included, not taking the time to thoroughly investigate these lower threshold doses with some pretty specific time points. Chasing down a threshold is not a sexy topic and it was actually fairly risky in that it was possible that we would have had all negative effects. Nonetheless, the take-home message of our data is that even one short-duration binge-alcohol experience – which is unfortunately similar to what young adults may experience during spring break or weekend partying - may start a cascade that leads to brain damage.”

(Source: eurekalert.org)

Filed under alcohol binge drinking brain cognitive impairment brain damage vimentin science

115 notes

Excessive alcohol when you’re young could have lasting impacts on your brain
Alcohol misuse in young people causes significant changes in their brain function and structure. This and other findings were recently reviewed by Dr Daniel Hermens from the University of Sydney’s Brain and Mind Research Institute in the journal Cortex.
"Young people are particularly vulnerable to the damaging effects of alcohol misuse," said Dr Hermens.
Most people have their first alcoholic drink during adolescence and while they drink less frequently than adults, they tend to drink more on each occasion - binge drinking.
The early functional signs of brain damage from alcohol misuse are visual, learning, memory and executive function impairments. These functions are controlled by the hippocampus and frontal structures of the brain, which are not fully mature until around 25 years of age.
Structural signs of alcohol misuse include shrinking of the brain and significant changes to white matter.
In his review, Dr Hermens notes that changes in a young person’s brain caused by alcohol misuse could either represent a predisposition (genetic or environmental) to alcohol misuse, or a marker for future risk of ongoing misuse. Whichever it is, there is no doubt that the more frequent the alcohol misuse, the greater the damage and the less likely the brain is to recover from that damage.
"When the toxicity of alcohol stops your brain from laying down new memories, you experience a blackout," said Dr Hermens. Young people who binge drink may only drink once a week, but on a massive night out they may have three to four blackouts, which begins to cause serious damage to their brain.
One of the best predictors of a person having problems with alcohol is their earliest age of first use. But changing the legal drinking age is not the answer. In Australia the legal drinking age is 18, three years earlier than in the US. Despite the difference in legal drinking age, the age of first use is the same between the two countries.
Another key factor affecting young people who drink is mental health, “poor mental health more than doubles a young person’s risk of alcohol and other substance misuse” says Dr Hermens.
The solution lies in education, treatment and prevention. Dr Hermens and his team have been working with NSW Health to prepare a set of guidelines for health carers to identify and respond to early stages of brain impairment in young people resulting from alcohol misuse. They are currently working on a set of educational charts that inform young people of the risks of irresponsible drinking.
It may be possible to use cognitive remediation to change the drinking habits of young drinkers and prevent relapse. At the same time, vitamin supplements or other medicines may effectively treat some of the structural changes, and it may be possible to develop protective agents that can prevent young brains from the damaging effects of alcohol.
"More work needs to be done in this area. Excessive alcohol use accounts for 4 percent of the global burden of disease. We would save a lot of money and improve the quality of life for millions of people if we could prevent the mental and physical problems associated with alcohol misuse" said Dr Hermens.

Excessive alcohol when you’re young could have lasting impacts on your brain

Alcohol misuse in young people causes significant changes in their brain function and structure. This and other findings were recently reviewed by Dr Daniel Hermens from the University of Sydney’s Brain and Mind Research Institute in the journal Cortex.

"Young people are particularly vulnerable to the damaging effects of alcohol misuse," said Dr Hermens.

Most people have their first alcoholic drink during adolescence and while they drink less frequently than adults, they tend to drink more on each occasion - binge drinking.

The early functional signs of brain damage from alcohol misuse are visual, learning, memory and executive function impairments. These functions are controlled by the hippocampus and frontal structures of the brain, which are not fully mature until around 25 years of age.

Structural signs of alcohol misuse include shrinking of the brain and significant changes to white matter.

In his review, Dr Hermens notes that changes in a young person’s brain caused by alcohol misuse could either represent a predisposition (genetic or environmental) to alcohol misuse, or a marker for future risk of ongoing misuse. Whichever it is, there is no doubt that the more frequent the alcohol misuse, the greater the damage and the less likely the brain is to recover from that damage.

"When the toxicity of alcohol stops your brain from laying down new memories, you experience a blackout," said Dr Hermens. Young people who binge drink may only drink once a week, but on a massive night out they may have three to four blackouts, which begins to cause serious damage to their brain.

One of the best predictors of a person having problems with alcohol is their earliest age of first use. But changing the legal drinking age is not the answer. In Australia the legal drinking age is 18, three years earlier than in the US. Despite the difference in legal drinking age, the age of first use is the same between the two countries.

Another key factor affecting young people who drink is mental health, “poor mental health more than doubles a young person’s risk of alcohol and other substance misuse” says Dr Hermens.

The solution lies in education, treatment and prevention. Dr Hermens and his team have been working with NSW Health to prepare a set of guidelines for health carers to identify and respond to early stages of brain impairment in young people resulting from alcohol misuse. They are currently working on a set of educational charts that inform young people of the risks of irresponsible drinking.

It may be possible to use cognitive remediation to change the drinking habits of young drinkers and prevent relapse. At the same time, vitamin supplements or other medicines may effectively treat some of the structural changes, and it may be possible to develop protective agents that can prevent young brains from the damaging effects of alcohol.

"More work needs to be done in this area. Excessive alcohol use accounts for 4 percent of the global burden of disease. We would save a lot of money and improve the quality of life for millions of people if we could prevent the mental and physical problems associated with alcohol misuse" said Dr Hermens.

Filed under binge drinking alcohol alcohol misuse brain function brain white matter neuroscience science

46 notes


Alcohol Drinking Behavior Reduced By Inhibiting Brain Protein in Rodents
Decreasing the level of a key brain protein led to significantly less drinking and alcohol-seeking behavior in rats and mice that had been trained to drink, according to a study by researchers at the Ernest Gallo Clinic and Research Center at UCSF.
The scientists identified the protein, known as H-Ras, as a promising target for development of new medications to treat alcohol abuse disorders in humans.
The study, which was published on Nov. 7 in the Journal of Neuroscience, was recommended as being of special significance in its field by the Faculty of 1000, an online service that identifies great peer-reviewed biomedical research.
The researchers, led by Gallo investigator Dorit Ron, PhD, first demonstrated that alcohol intake significantly increased H-Ras activity in the animals’ nucleus accumbens, a brain region that in both rodents and humans is part of the reward system that affects craving for alcohol and other addictive substances.
They then showed that suppressing H-Ras levels in the nucleus accumbens with a targeted virus reduced alcohol consumption among mice that had been trained to seek out and drink alcohol in an animal model of binge drinking.
The researchers then administered FTI-276, an experimental compound that has been shown to inhibit H-Ras production, to binge-drinking rats. They observed a significant reduction in alcohol consumption after the compound was given.
The scientists also found that H-Ras inhibition reduced alcohol-seeking behavior among rats that had been trained to receive a drink of alcohol when they pressed a lever. When alcohol was withheld, rats that had received FTI-276 discontinued pressing the lever significantly sooner than rats that did not receive the compound.
Importantly, the rodents’ consumption of water, sugar solution, saccharine solution and quinine was not reduced when H-Ras was inhibited, indicating that H-Ras activity is specific to alcohol.

Alcohol Drinking Behavior Reduced By Inhibiting Brain Protein in Rodents

Decreasing the level of a key brain protein led to significantly less drinking and alcohol-seeking behavior in rats and mice that had been trained to drink, according to a study by researchers at the Ernest Gallo Clinic and Research Center at UCSF.

The scientists identified the protein, known as H-Ras, as a promising target for development of new medications to treat alcohol abuse disorders in humans.

The study, which was published on Nov. 7 in the Journal of Neuroscience, was recommended as being of special significance in its field by the Faculty of 1000, an online service that identifies great peer-reviewed biomedical research.

The researchers, led by Gallo investigator Dorit Ron, PhD, first demonstrated that alcohol intake significantly increased H-Ras activity in the animals’ nucleus accumbens, a brain region that in both rodents and humans is part of the reward system that affects craving for alcohol and other addictive substances.

They then showed that suppressing H-Ras levels in the nucleus accumbens with a targeted virus reduced alcohol consumption among mice that had been trained to seek out and drink alcohol in an animal model of binge drinking.

The researchers then administered FTI-276, an experimental compound that has been shown to inhibit H-Ras production, to binge-drinking rats. They observed a significant reduction in alcohol consumption after the compound was given.

The scientists also found that H-Ras inhibition reduced alcohol-seeking behavior among rats that had been trained to receive a drink of alcohol when they pressed a lever. When alcohol was withheld, rats that had received FTI-276 discontinued pressing the lever significantly sooner than rats that did not receive the compound.

Importantly, the rodents’ consumption of water, sugar solution, saccharine solution and quinine was not reduced when H-Ras was inhibited, indicating that H-Ras activity is specific to alcohol.

Filed under brain brain protein binge drinking alcohol abuse reward system neuroscience science

138 notes


Research shows binge drinking inhibits brain development
Teenagers who binge drink risk inhibiting part of their brain’s development and many are laying the groundwork for alcoholism down the track a Queensland University of Technology (QUT) researcher has found.
Professor Selena Bartlett, from QUT’s Institute for Health and Biomedical Innovation (IHBI), studied the effect excessive binge drinking during adolescence had on a particular receptor in the brain and discovered teen bingeing altered it irreversibly, keeping the brain in an adolescent state.
"The human brain doesn’t fully develop until around age 25 and bingeing during adolescence modifies its circuits, preventing the brain from reaching maturity," she said.
"During adolescence, the brain undergoes massive changes in the prefrontal cortex and areas linked to drug reward but alcohol disrupts this.
"The research, which was carried out on rats, suggests that during ageing, the brain’s delta opioid peptide receptor (DOP-R) activity turns down, but binge drinking causes the receptors to stay on, keeping it in an adolescent stage.
"The younger a child or teenager starts binge drinking and the more they drink, the worse the possible outcome for them."
Professor Bartlett said recent trends to mix high-caffeine drinks such as Red Bull with alcohol were making the binge drinking problem worse.

Research shows binge drinking inhibits brain development

Teenagers who binge drink risk inhibiting part of their brain’s development and many are laying the groundwork for alcoholism down the track a Queensland University of Technology (QUT) researcher has found.

Professor Selena Bartlett, from QUT’s Institute for Health and Biomedical Innovation (IHBI), studied the effect excessive binge drinking during adolescence had on a particular receptor in the brain and discovered teen bingeing altered it irreversibly, keeping the brain in an adolescent state.

"The human brain doesn’t fully develop until around age 25 and bingeing during adolescence modifies its circuits, preventing the brain from reaching maturity," she said.

"During adolescence, the brain undergoes massive changes in the prefrontal cortex and areas linked to drug reward but alcohol disrupts this.

"The research, which was carried out on rats, suggests that during ageing, the brain’s delta opioid peptide receptor (DOP-R) activity turns down, but binge drinking causes the receptors to stay on, keeping it in an adolescent stage.

"The younger a child or teenager starts binge drinking and the more they drink, the worse the possible outcome for them."

Professor Bartlett said recent trends to mix high-caffeine drinks such as Red Bull with alcohol were making the binge drinking problem worse.

Filed under binge drinking adolescents brain prefrontal cortex alcohol neuroscience psychology science

42 notes

Rutgers Researchers Say Daily Drinking Can Be Risky

Study finds moderate consumption decreases number of new brain cells

Drinking a couple of glasses of wine each day has generally been considered a good way to promote cardiovascular and brain health. But a new Rutgers University study indicates that there is a fine line between moderate and binge drinking – a risky behavior that can decrease the making of adult brain cells by as much as 40 percent.

In a study posted online and scheduled to be published in the journal Neuroscience on November 8, lead author Megan Anderson, a graduate student working with Tracey J. Shors, Professor II in Behavioral and Systems Neuroscience in the Department of Psychology, reported that moderate to binge drinking – drinking less during the week and more on the weekends – significantly reduces the structural integrity of the adult brain.

“Moderate drinking can become binge drinking without the person realizing it,” said Anderson.“In the short term there may not be any noticeable motor skills or overall functioning problems, but in the long term this type of behavior could have an adverse effect on learning and memory.”

(Source: news.rutgers.edu)

Filed under brain brain cells alcohol binge drinking neuroscience psychology science

free counters