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Researchers block damage to fetal brain following maternal alcohol consumption
August 11, 2008In a study on fetal alcohol syndrome, researchers were able to prevent the damage that alcohol causes to cells in a key area of the fetal brain by blocking acid sensitive potassium channels and preventing the acidic environment that alcohol produces. The cerebellum, the portion of the brain that is responsible for balance and muscle coordination, is particularly vulnerable to injury from alcohol during development.
The researchers also found that although alcohol lowers the amount of oxygen in the blood of the mother, it is not the lack of oxygen that damages the fetal cerebellum, but the drop in pH.
The study with sheep, published in the August issue of the American Journal of Physiology, demonstrated that the damage can be prevented by blocking acid sensitive potassium channels, known as TASK channels, that lead into the Purkinje cells. The study, "Acid Sensitive Channel Inhibition Prevents Fetal Alcohol Spectrum Disorders Cerebellar Purkinje Cell Loss," was carried out by Jayanth Ramadoss, Emilie R. Lunde, Nengtai Ouyang, Wei-Jung A. Chen and Timothy A. Cudd. The research was done at Texas A&M University.
Fetal Alcohol Syndrome
Fetal alcohol syndrome is a condition in which maternal drinking during pregnancy injures the brain of the developing fetus. Alcohol is the most common cause of injury to the fetal brain. Children born with fetal alcohol syndrome may have cognitive impairments and difficulty regulating their behavior. They often have difficulty in school and exhibit behavioral problems, such as impulsiveness, later in life.
The syndrome is estimated to occur in approximately one in every 1,000 births in Western countries. Milder forms of the condition, known as fetal alcohol spectrum disorders, occur more frequently.
Maternal drinking lowers the blood pH of both the mother and the fetus, making the blood more acidic. The researchers hypothesized that this acidity damages the Purkinje cells of the fetal cerebellum. Using 56 pregnant sheep, they induced the change in pH in some sheep using alcohol, while in others they manipulated the extracellular pH. This approach allowed them to test their hypothesis that it was the fall in pH that created the damage, not the alcohol, per se.
Alcohol produced a 45% reduction in Purkinje cells of the fetal cerebellum, while the pH changes alone produced a 24% decrease. A drop in the number of Purkinje cells in the cerebellum is a measure of damage.
However, when the researchers used a drug, doxapram, to block the TASK channels leading into the Purkinje cells, they prevented the change in pH in the fetal cerebellar cells and prevented any reduction in the number of these cells.
"This study demonstrates that direct pharmacological blockade of TASK 1 and TASK 3 channels protects the most sensitive target of fetal alcohol exposure, cerebellar Purkinje cells," the authors concluded.
Finding adds to growing body of work
This study complements work by other researchers who have found success with supplements such as choline, a precursor for the neurotransmitter acetylcholine. These supplements may work on the same mechanism that Dr. Cudd's lab has been researching.
American Physiological Society
Fetal Alcohol Syndrome
Fetal alcohol syndrome is a condition in which maternal drinking during pregnancy injures the brain of the developing fetus. Alcohol is the most common cause of injury to the fetal brain. Children born with fetal alcohol syndrome may have cognitive impairments and difficulty regulating their behavior. They often have difficulty in school and exhibit behavioral problems, such as impulsiveness, later in life.
The syndrome is estimated to occur in approximately one in every 1,000 births in Western countries. Milder forms of the condition, known as fetal alcohol spectrum disorders, occur more frequently.
Maternal drinking lowers the blood pH of both the mother and the fetus, making the blood more acidic. The researchers hypothesized that this acidity damages the Purkinje cells of the fetal cerebellum. Using 56 pregnant sheep, they induced the change in pH in some sheep using alcohol, while in others they manipulated the extracellular pH. This approach allowed them to test their hypothesis that it was the fall in pH that created the damage, not the alcohol, per se.
Alcohol produced a 45% reduction in Purkinje cells of the fetal cerebellum, while the pH changes alone produced a 24% decrease. A drop in the number of Purkinje cells in the cerebellum is a measure of damage.
However, when the researchers used a drug, doxapram, to block the TASK channels leading into the Purkinje cells, they prevented the change in pH in the fetal cerebellar cells and prevented any reduction in the number of these cells.
"This study demonstrates that direct pharmacological blockade of TASK 1 and TASK 3 channels protects the most sensitive target of fetal alcohol exposure, cerebellar Purkinje cells," the authors concluded.
Finding adds to growing body of work
This study complements work by other researchers who have found success with supplements such as choline, a precursor for the neurotransmitter acetylcholine. These supplements may work on the same mechanism that Dr. Cudd's lab has been researching.
American Physiological Society
Fetal Alcohol Syndrome Current Events and Fetal Alcohol Syndrome News RSSFrogs reveal clues about the effects of alcohol during development
Fetal alcohol spectrum disorder (FASD) and Fetal alcohol syndrome (FAS) cause malformations in babies, including facial defects, short stature, and mental and behavioral abnormalities.
Prenatal alcohol exposure damages white matter, the brain's connective network
One part of the prenatal brain that may be particularly sensitive to alcohol's effects is white matter, nerve fibers through which information is exchanged between different areas of the central nervous system. A recent study has demonstrated that alcohol consumption during pregnancy can alter the microstructural integrity of developing fetal cerebral white matter in the frontal and occipital lobes of the brain.
Alcohol consumption can cause too much cell death, fetal abnormalities
The initial signs of fetal alcohol syndrome are slight but classic: facial malformations such as a flat and high upper lip, small eye openings and a short nose.
Prenatal drinking, environmental enrichment: effects on neurotrophins are independent of each other
Prenatal alcohol exposure may be particularly destructive for neurotrophins, a family of peptides that influence the growth, development and functional plasticity of the fetal brain.
Study suggests new way to screen infants for fetal alcohol syndrome
Children who have been diagnosed with Fetal Alcohol Syndrome (FAS) are more likely to have serious psychiatric and behavioral problems later in life, including a higher risk for dropping out of school, unemployment, and criminal behavior.
Eye blinks may help to identify children prenatally exposed to alcohol
While children with fetal alcohol syndrome (FAS) have identifiable craniofacial abnormalities, children with alcohol-related neurodevelopmental disorder (ARND) can have significant cognitive impairments without facial anomalies.
Research Reveals Secrets of Alcohol's Effect on Brain Cells
Alcohol triggers the activation of a variety of genes that can influence the health and activity of brain cells, and new research from Weill Cornell Medical College in New York City sheds light on how that process occurs.
Little evidence that binge drinking while pregnant seriously harms fetus
There is little substantive evidence that binge drinking while pregnant seriously harms the developing fetus, finds a study in the Journal of Epidemiology and Community Health.
Study reveals possible genetic risk for fetal alcohol disorders
New research in primates suggests that infants and children who carry a certain gene variant may be more vulnerable to the ill effects of fetal alcohol exposure.
Prenatal alcohol exposure alters brain activity in the frontal-striatal areas
Heavy prenatal alcohol exposure does not always lead to fetal alcohol syndrome (FAS); sometimes it can lead to cognitive and behavioral deficits in the absence of craniofacial features needed to make an FAS diagnosis.
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