This is a copy of an article in Naturel News Certain fears can be inherited through the generations, a provocative study of mouse reports1.
The authors suggest that a similar phenomenon may influence anxiety and addiction in humans.
But some researchers are skeptical of the findings because a biological mechanism that explains the phenomenon has not been identified.
According to the convention, the genetic sequences contained in DNA are the only way to transmit biological information across generations.
Random DNA mutations, when beneficial, allow organisms to adapt to changing conditions, but this process occurs slowly over many generations.
But some studies have suggested that environmental factors can affect biology more quickly through 'epigenetic' modifications, which change the expression of genes but not their actual nucleotide sequence.
For example, children raised during a severe wartime emergency in the Netherlands in the 1940s are at increased risk of diabetes, heart disease and other conditions – possibly due to epigenetic changes to genes involved in these diseases2.
Although epigenetic modifications are known to be important for processes such as the development and inactivation of one copy of the X chromosome in females, their role in the inheritance of behavior remains controversial.
Kerry Ressler, a neurobiologist and psychiatrist at Emory University in Atlanta, Georgia, and co-author of the latest study became interested in epigenetic inheritance after working with poor people living in inner cities, where the cycles of drug addiction, neuropsychiatric illness and other problems seems to recur often in parents and their children.
"There are many anecdotes that suggest there is a general transfer of risk and that it is difficult to break that cycle," he says.
Hereditary characteristics It would be difficult to study the biological basis of these effects in humans.
So Ressler and his colleague Brian Dias chose to study the inheritance of epigoneris in laboratory mice trained to fear the smell of acetophenone, a substance whose scent has been compared to cherries and almonds.
He and Dias wafted the scent around a small chamber while giving small electric shocks to male mice.
The animals eventually learned to associate the scent with pain, shivering in the presence of acetophenone even without a shock. This response was carried over to their pups, Dias and Ressler report today in Nature Neuroscience1.
Despite never having experienced acetophenone in their lives, the offspring showed increased sensitivity when introduced to the odor, shadowing more markedly in its presence compared to the offspring of mice that had been conditioned to be startled by another odor or which had not gone through the condition.
A third generation of mice - the "grandchildren" - also inherited this reaction, just as mice were conceived by in vitro fertilization with sperm from men sensitized to acetophenone.
Similar experiments showed that the response can also be transmitted from the mother.
These responses were paired with changes in brain structures that process smells.
The mice sensitive to acetophenone, as well as their offspring, had more neurons that produce a receptor protein known to detect the odor compared to control mice and their offspring.
Structures that receive signals from the acetophenone-detecting neurons and transmit odor signals to others parts of the brain (such as those involved in processing fear) were also larger.
The researchers suggest that DNA methylation - a reversible chemical modification of DNA that typically blocks transcription of a gene without changing its sequence - explains the inherited effect. In the fearful mice, the acetophenone-sensing gene of sperm had fewer methylation marks, which could have led to greater expression of the odor receptor gene during development.
But how the association of smell with pain affects sperm is a mystery.
Ressler notes that sperm cells themselves express odorant receptor proteins, and that some odorants find their way into the bloodstream, offering a potential mechanism, as do small blood-borne fragments of RNA known as microRNAs that control gene expression.
Content-rich results Predictably, the study has divided researchers.
"The overwhelming response has been 'Wow! But how the hell does that happen? "Says Dias.
David Sweatt, a neurobiologist at the University of Alabama at Birmingham who was not involved in the work, calls it
"the most rigorous and convincing set of studies yet published demonstrating acquired transgenic rational epigenetic effects in a laboratory model" .
However, Timothy Bestor, a molecular biologist at Columbia University in New York who studies epigenetic modifications, is incredulous.
DNA methylation is unlikely to affect the production of the protein that detects acetophenone, he says. Most genes known to be controlled by methylation have these modifications in a region called the promoter, which precedes the gene in the DNA sequence.
But the acetophenone-detecting gene does not contain nucleotides in this region that can be methylated, Bestor says.
"The claims they are making are so extreme that they violate the principle that extraordinary claims require extraordinary proof," he adds.
Tracy Bale, a neuroscientist at the University of Pennsylvania in Philadelphia, says that researchers need to
"determine the piece that connects experience with the specific signals that are able to produce changes in epigenetic marks in the germ cell and how these are maintained".
"It's quite disheartening to think that our germ cells can be so plastic and dynamic in response to changes in the environment," she says.
Humans inherit epigenetic changes that affect behavior, Ressler also suspected.
A parent's anxiety, he speculates, could affect later generations through epigenetic modifications of receptors for stress hormones.
But Ressler and Dias aren't sure how to prove the case, and they plan to focus on lab animals for now.
The researchers now want to determine how many generations the sensitivity to acetophenone lasts and whether this response can be removed.
Skepticism that the inheritance mechanism is real is likely to persist, Ressler says,
"until someone can really explain it in a molecular way," says Ressler.
"Unfortunately, it will probably be complicated and it will probably take a while."
Translation from Google
Source Nature News
