Here actually read what the research is telling us and you’ll understand that you aren’t afraid of butterflies because your ancestors were attacked by a swarm of butterflies in the past. That just sounds ridiculous doesn’t it?
Just wanted to make this into it’s own post. Sorry to do this again, wildcat2030, but there’s just so many people commenting saying this explains their fear of (insert noun) and they need to know what’s actually going on. Original discussion here.
Phobias may be memories passed down in genes from ancestors
Memories may be passed down through generations in DNA in a process that may be the underlying cause of phobias
Memories can be passed down to later generations through genetic switches that allow offspring to inherit the experience of their ancestors, according to new research that may explain how phobias can develop. Scientists have long assumed that memories and learned experiences built up during a lifetime must be passed on by teaching later generations or through personal experience. However, new research has shown that it is possible for some information to be inherited biologically through chemical changes that occur in DNA. Researchers at the Emory University School of Medicine, in Atlanta, found that mice can pass on learned information about traumatic or stressful experiences – in this case a fear of the smell of cherry blossom – to subsequent generations. The results may help to explain why people suffer from seemingly irrational phobias – it may be based on the inherited experiences of their ancestors. (via Phobias may be memories passed down in genes from ancestors - Telegraph)
This post is really misleading and explains it in a way that’s far from the truth about what’s really (possibly) happening. The future generations aren’t getting “memories”, but rather, an inherited sensitivity of sorts.
Note: In the quote below, F1 refers to the first generation of offspring from the parent taught to fear the smell, and F2 is the second generation.
from National Geographic:
The scientists then looked at the F1 and F2 animals’ brains. When the grandparent generation is trained to fear acetophenone, the F1 and F2 generations’ noses end up with more “M71 neurons,” which contain a receptor that detects acetophenone. Their brains also have larger “M71 glomeruli,” a region of the olfactory bulb that responds to this smell.
This is far from a memory.
We’ve identified a few forms of epigenetic inheritance—primarily chemical modifications of DNA—that can be changed during the life of an organism but can still be passed down to its progeny.
Mice can be taught to fear the smell of a specific odorant simply by giving them electric shocks whenever they’re exposed to it. It’s then simple to read out the strength of this through a startle response. When they hear a loud noise, mice tend to freeze for a short period of time. If you hit them with both a loud noise and the odor they fear, they’ll freeze for even longer.
Rather than testing the mice themselves, however, the researchers decided to test their offspring. And they found that mice in the next generation, as well as the generation after that, also showed an enhanced startle effect when exposed to the same chemical. They ruled out the simplest explanation for this—researcher bias—by making sure that the person measuring the response was blinded to whether the mouse they were testing was an experimental animal or a control.
And, in an even more concise way to say it’s not a memory, nor is it a phobia per se,
In other words, the parental exposure and training seemed to prime offspring to be able to perceive the odor much more easily.
So, yes, while this is an amazing scientific discovery—if further research confirms these findings—it’s a far more subtle biological change that’s occurring. The results show that it’s sensory sensitivity to a stimulus that’s being passed down, and that’s a pretty big leap from memories, phobias and “inherited experiences of their ancestors.”
This is what I was thinking too. The mice were just being trained to be more sensitive to the odors, by up-regulating certain odor-receptors, allowing them to have a better/faster reaction to what they perceived to be a ‘bad smell’. Like how we humans do not like the smell of rotten eggs, or Hydrogen Sulfide, because we have a sensitivity to it since it is toxic.
Very far from Assassin’s Creed (so stop with that AC-hype BS) and really any phobias like fear of clowns or spiders and some people were saying it explained Islamophobia (ridiculous!). Those are a result of the brain interpreting visual stimulus and gene regulation has very little influence in something like that. — Your eyes can’t tell the difference between a photon that bounced off a spider or an Islamic person. — Those phobias are more a result of your childhood upbringing and how society framed them for you, causing certain neural pathways to be reinforced, leading to the phobia.
Dysfunction in dopamine signaling profoundly changes the activity level of about 2,000 genes in the brain’s prefrontal cortex and may be an underlying cause of certain complex neuropsychiatric disorders, such as schizophrenia, according to UC Irvine scientists.
This epigenetic alteration of gene activity in brain cells that receive this neurotransmitter showed for the first time that dopamine deficiencies can affect a variety of behavioral and physiological functions regulated in the prefrontal cortex.
The study, led by Emiliana Borrelli, a UCI professor of microbiology & molecular genetics, appears online in the journal Molecular Psychiatry.
K Brami-Cherrier, A Anzalone, M Ramos, I Forne, F Macciardi, A Imhof, E Borrelli. Epigenetic reprogramming of cortical neurons through alteration of dopaminergic circuits. Molecular Psychiatry, 2014; DOI: 10.1038/mp.2014.67
Image via Resverlogix
It’s long been known that many species of worms have the remarkable ability to grow back body and even specific organs when they’ve been cut off. But new research by a pair of scientists from Tufts University has revealed that planarians—small creatures, often called flatworms, that can live in water or on land—are capable of regenerating something even more amazing.
The researchers, Tal Shomrat and Michael Levin, trained flatworms to travel across a rough surface to access food, then removed their heads. Two weeks later, after the heads grew back, the worms somehow regained their tendency to navigate across rough terrain, as the researchers recently documented in the Journal of Experimental Biology.
Interest in flatworm memories dates to the 1950s, when a series of strange experiments by Michigan biologist James McConnell indicated that worms could gain the ability to navigate a maze by being fed the ground-up remains of other flatworms that had been trained to run through the same maze. McConnell speculated that a type of genetic material called “memory RNA” was responsible for this phenomenon, and could be transferred between the organisms.
Subsequent research into planarian memory RNA exploited the fact that the worms could easily regenerate heads after decapitation. In some studies, the worms’ heads were cut off and then regenerated while they swam in RNA solutions; in others, as the Field of Science blog points out, worms that had already been trained to navigate a maze were tested after they were decapitated and their heads grew back.
Unfortunately, McConnell’s findings were largely discredited—critics pointed to sloppy research methods, and some even charged that planarians had no capacity for long-term memory—and research in this area lay dormant. Recently, though, Shomrat and Levin developed automated systems to train and test the worms, which would enable standardized and rigorous measures of how the organisms acquired and retained memories over time. And though memory RNA is still believed to be a myth, their recent research has confirmed that these worms’ memories do work in astoundingly bizarre ways.
The researchers’ computerized system dealt with the worms, from the species Dugesia japonica, in two groups of 72 each. One group was conditioned to live in a rough-bottomed petri dish, with the other in a smooth-bottomed one, for ten days. Both dishes were stocked with ample worm food (small pieces of beef liver), so each group was conditioned to learn that their particular surface meant “food is nearby.”
Next, each group was separately put into a rough-bottomed petri dish with food located only in one quadrant, along with a bright blue LED. Flatworms typically avoid light, so spending time in that quadrant meant that their expectation of food nearby trumped their aversion to light.
As a result of their conditioning, the worms who’d lived in rough containers were much quicker to flock to the lit quadrant. The researchers had the automated system’s video cameras track how long it took for the worms to spend three straight minutes under the lights, and those reared in the rough dishes took an average of six minutes to pass this number, compared to about seven and a half minutes for the other group. This difference showed that the former group had been conditioned to associate rough surfaces with food, and explored these surfaces more readily.
Afterward, all worms were fully decapitated (every bit of brain was removed) and left alone to regrow their heads over the course of the next two weeks. When they were put back in the chamber with the rough surface, the group that had previously lived in the rough dishes—that is, their previous heads had lived in the rough dishes—were still willing to venture into the lit quadrant of the rough dish and spend an extended period of time there more than a minute faster than the other group.
Incredible as it seems, some lingering memories of the rough-surface conditioning seem to have lived on in the bodies of these worms, even after their heads were chopped off. The biological explanation for this is unclear, as The Verge blog notes. Previous research confirmed that the worms’ behavior is controlled by their brains, but it’s possible that some of their memories may have been stored in their bodies, or that the training given to their initial heads somehow modified other parts of their nervous systems, which then altered how their new brains grew.
There’s also another sort of explanation. The researchers speculate that epigenetics—changes to an organism’s DNA structure that alter the expression of genes—could play a role, perhaps encoding the memory (“rough floors = food”) permanently in the worms’s DNA.
In that case, this strange experiment would provide yet another surprising outcome. There may not be such a thing as “memory RNA” per se, but in speculating on the role of genetic material in the retention of these worms’ memories, McConnell may have been on the right track after all.
Scientists Discover Parts of Our Bodies Age at Different Rates
Some people age faster than others, but the discovery of a DNA body clock by UCLA researchers now shows that different parts of our bodies age faster than others. The discovery offers important insights into the aging process — and what we might be able to do about it.
This isn’t the first time that biologists have developed a mechanism for assessing age. Earlier “biological clocks” have been derived from data drawn from saliva and hormones. More crucially, there are our telomeres to consider — those fraying tips of our chromosomes that have been linked to cellular expiry dates, and by virtue, our individual rates of aging.
Genetics vs. Epigenetics
From “Hidden Switches in the Mind” by Eric J. Nestler, in Scientific American 305, 76 - 83 (November 2011)
SOURCE: Scientific American @ Nature
This week struck me as a particularly exhausting one when it came to that certain brand of provocatively-headlined-but-probably-not-what-you-think-it-is science news that we know and
As usual, it’s the science media click-machine that’s to blame, which is a polite way of saying that…
Gerty Theresa Cori (1896 – 1957) was an American biochemist who became the third woman—and first American woman—to win a Nobel Prize in science, and the first woman to be awarded the Nobel Prize in Physiology or Medicine.
Cori was born in Prague. She was admitted to medical school there, where she met her future husband Carl Ferdinand Cori. After graduation, they married and emigrated to America in 1922. Gerty continued her early interest in medical research, collaborating in the laboratory with Carl. She published research findings coauthored with her husband, as well as publishing singly. Unlike her husband, she had difficulty securing research positions, and the ones she obtained provided meager pay. Her husband insisted on continuing their collaboration, though he was discouraged from doing so by institutions that employed him.
Gerty and her husband jointly received the Nobel Prize in 1947 for the discovery of the mechanism by which glycogen—a derivative of glucose—is broken down in muscle tissue into lactic acid and then resynthesized in the body and stored as a source of energy (known as the Cori cycle).
In 1957, Gerty Cori died after a ten-year struggle with myelosclerosis. She remained active in the research laboratory until the end. She received recognition for her achievements through multiple awards and honors. The Cori crater on the Moon and the Cori crater on Venus are named after her.