The big idea
As fruit fly larvae age, their neurons shift from a highly adaptable state to a stable state and lose their ability to change. During this process, support cells in the brain – called astrocytes – envelop the parts of the neurons that send and receive electrical information. When my team removed the astrocytes, the neurons in the fruit fly larvae remained plastic longer, hinting that somehow astrocytes suppress a neuron's ability to change. We then discovered two specific proteins that regulate neuroplasticity.
Sarah DeGenova Ackerman, CC BY-ND
Why it matters
The human brain is made up of billions of neurons that form complex connections with one another. Flexibility at these connections is a major driver of learning and memory, but things can go wrong if it isn't tightly regulated. For example, in people, too much plasticity at the wrong time is linked to brain disorders such as epilepsy and Alzheimer's disease. Additionally, reduced levels of the two neuroplasticity-controlling proteins we identified are linked to increased susceptibility to autism and schizophrenia.
Similarly, in our fruit flies, removing the cellular brakes on plasticity permanently impaired their crawling behavior. While fruit flies are of course different from humans, their brains work in very similar ways to the human brain and can offer valuable insight.
One obvious benefit of discovering the effect of these proteins is the potential to treat some neurological diseases. But since a neuron's flexibility is closely tied to learning and memory, in theory, researchers might be able to boost plasticity in a controlled way to enhance cognition in adults. This could, for example, allow people to more easily learn a new language or musical instrument.
In this image showing a developing fruit fly brain on the right and the attached nerve cord on the left, the astrocytes are labeled in different colors showing their wide distribution among neurons.Sarah DeGenova Ackerman, CC BY-ND
How we did the work
My colleagues and I focused our experiments on a specific type of neurons called motor neurons. These control movements like crawling and flying in fruit flies. To figure out how astrocytes controlled neuroplasticity, we used genetic tools to turn off specific proteins in the astrocytes one by one and then measured the effect on motor neuron structure. We found that astrocytes and motor neurons communicate with one another using a specific pair of proteins called neuroligins and neurexins. These proteins essentially function as an off button for motor neuron plasticity.
What still isn't known
My team discovered that two proteins can control neuroplasticity, but we don't know how these cues from astrocytes cause neurons to lose their ability to change.
Additionally, researchers still know very little about why neuroplasticity is so strong in younger animals and relatively weak in adulthood. In our study, we showed that prolonging plasticity beyond development can sometimes be harmful to behavior, but we don't yet know why that is, either.
What's next
I want to explore why longer periods of neuroplasticity can be harmful. Fruit flies are great study organisms for this research because it is very easy to modify the neural connections in their brains. In my team's next project, we hope to determine how changes in neuroplasticity during development can lead to long–term changes in behavior.
There is so much more work to be done, but our research is a first step toward treatments that use astrocytes to influence how neurons change in the mature brain. If researchers can understand the basic mechanisms that control neuroplasticity, they will be one step closer to developing therapies to treat a variety of neurological disorders.
Sarah DeGenova Ackerman, Postdoctoral Fellow, UO Institute of Neuroscience and Howard Hughes Medical Institute, University of Oregon
This article is republished from The Conversation under a Creative Commons license. Read the original article.
It's called the Proust effect after a story in the author's "Remembrance of Things Past: Swann's Way." When a character dipped a madeleine, a sweet, buttery French cake, into some lime-blossom tea, the scent suddenly transported him back in time to the moment his aunt had served him that same combination:
"Immediately the old grey house upon the street, where her room was, rose up like the scenery of a theatre to attach itself to the little pavilion, opening on to the garden, which had been built out behind it for my parents… and with the house the town, from morning to night and in all weathers, the Square where I was sent before luncheon, the streets along which I used to run errands, the country roads we took when it was fine."
Nothing conjures up a memory so viscerally as the scent with which you associate it. While it's been understood for some time that our olfactory system has a unique ability to vividly summon memories, the mechanism behind the phenomenon has net been well-understood. Now a study by researchers from Northwestern University's Feinberg School of Medicine may have solved the puzzle. The olfactory system has an unusually direct connection to the brain's hippocampus, believed to play an important role in memory.
The study's published in the journal Progress in Neurobiology.
A lasting connection
Credit: schankz/Adobe Stock
Previous neuroimaging and intracranial electrophysiology investigations have revealed that our senses are functionally connected to the hippocampus, if not directly. However, the new research, for which the principle investigator is Christina Zelano, is the first rigorous comparison of the strength of those connections.
It turns out that our primary olfactory cortex is a sense that's still directly connected to the hippocampus.
"This has been an enduring mystery of human experience," Zelano tells Medical Xpress. "Nearly everyone has been transported by a whiff of an odor to another time and place, an experience that sights or sounds rarely evoke. Yet, we haven't known why. The study found the olfactory parts of the brain connect more strongly to the memory parts than other senses. This is a major piece of the puzzle, a striking finding in humans. We believe our results will help future research solve this mystery."
It's believed that during evolution, the hippocampus' role shifted away from its original strong relationship to the sensory cortexes and toward connections with higher association cortexes. (In rodents, for example, the hippocampus maintains a powerful connection to all sensory cortexes.) It now appears that as this occurred, the olfactory cortex alone continued to be directly wired to the hippocampus.
"Humans experienced a profound expansion of the neocortex that re-organized access to memory networks," explains Zelano. "Vision, hearing and touch all re-routed in the brain as the neocortex expanded, connecting with the hippocampus through an intermediary-association cortex-rather than directly. Our data suggests olfaction did not undergo this re-routing, and instead retained direct access to the hippocampus."
The importance of smell
It's known that people who experience a loss of smell, or "anosmia," often develop depression. "Loss of the sense of smell is underestimated in its impact," says Zelano. "It has profound negative effects of quality of life, and many people underestimate that until they experience it. Smell loss is highly correlated with depression and poor quality of life."
Anosmia is also associated with COVID-19. "The COVID-19 epidemic," says Zelano, "has brought a renewed focus and urgency to olfactory research." Lead author Guangyu Zhou agrees: "There is an urgent need to better understand the olfactory system in order to better understand the reason for COVID-related smell loss, diagnose the severity of the loss and to develop treatments."
"Most people who lose their smell to COVID regain it," notes Zelano, "but the time frame varies widely, and some have had what appears to be permanent loss. Understanding smell loss, in turn, requires research into the basic neural operations of this under-studied sensory system."
She notes that, "While our study doesn't address COVID smell loss directly, it does speak to an important aspect of why olfaction is important to our lives: Smells are a profound part of memory, and odors connect us to especially important memories in our lives, often connected to loved ones."
If the heavens vanished, they wondered, would time continue to pass? If existence were distinct from essence, would that mean that existence itself must exist? Can God turn your household servant into a horse, so that you come back home to find it has urinated all over your books?
But the most famous is the so-called 'flying man' thought experiment, devised by the most influential philosopher of the Islamic world, Avicenna (in Arabic, Ibn Sīnā, who lived from 980 to 1037 CE). Imagine, he says, that a person is created by God in mid-air, in good condition but with his sight veiled and his limbs outstretched so that he is touching nothing, not even his own body. This person has no memories, having only just been created. Will his mind be a blank, devoid as it is of past or present sensory experience? No, says Avicenna. He will be aware of his own existence.
Three questions immediately arise. First, when Douglas Adams, the author of The Hitchhiker's Guide to the Galaxy (1978), imagined a whale popping into existence in mid-air above an alien planet, had he been reading Avicenna? I have no idea, but I like to think so.
Second, is Avicenna right that the 'flying man' would be self-aware? Well, it's important to realise that Avicenna does not attempt to argue that the flying man would know that he exists. Rather, he takes it as obvious. In one version, he even tells readers that we should imagine ourselves being so created. If we put ourselves in the flying man's dangling shoes, we should just see that we would be self-aware. Indeed, this turns out to be a fundamental idea in Avicenna's philosophy. He thinks that we are all always self-aware, even when we're asleep or focusing hard on something other than ourselves. Paradoxically, we're often not aware of being self-aware: it is the non-interruptive background music of human psychology, something we notice only when our attention is called to it, a pre-reflective awareness of self. The flying man thought experiment is itself one way to call attention to this self-awareness: Avicenna calls it a tanbīh, meaning a 'pointer' to something.
Our self-awareness is a foundation for our first-person perspective on things. It's a sign of this that when I see, imagine or think something, I can immediately apprehend that I am seeing, imagining or thinking about that thing. Any other form of cognition – any awareness of other things – presupposes awareness of oneself.
Incidentally, you might object that the flying man would have certain forms of bodily awareness despite his lack of vision, hearing and so on. Wouldn't he at least sense the location of his limbs by another form of sensation, namely proprioception? Imagine you are in total darkness and your arm is not resting on anything: proprioception is the sense that tells you where it is. This is indeed a problem for the thought experiment as Avicenna sets it up, but it isn't really philosophically decisive. One can just modify the scenario by adding that God blocks the man's ability to use proprioception, or that the flying man's proprioceptive faculty happens to be defective. Avicenna's claim will then be that, even under these circumstances, the flying man would be aware of himself.
Now for the third, and hardest, question: what does the flying man thought experiment prove? Avicenna draws a surprising conclusion: it shows that we are not identical with our bodies. Just consider. The flying man is aware of himself; he knows that he exists. But he is not aware of his body; he doesn't know that his body exists, nor indeed that any body exists. And if I am aware of one thing but not another, how can those two things be identical?
This sounds pretty persuasive, until you reflect that one can be conscious of a thing without being conscious of everything about it. You, for example, have been aware of reading this article for the past few minutes, but you haven't been aware of reading something written while Dixieland jazz was playing. It would be a mistake to conclude from this that the article is not something written with Dixieland jazz playing. In fact, that is exactly what it is. To put it another way, the flying man could be aware of his self without realising that his self is a body. Contemporary philosophers would say that Avicenna is mistakenly moving from a 'transparent' to an 'opaque' context, which is basically a fancy way of saying what I just said.
Efforts have been made to spare Avicenna from this mistake. One possible way to rescue the argument would go like this. Avicenna is trying to criticise another way of thinking about the soul, one that goes back to Aristotle. According to the theory he rejects, the soul is so closely associated with the body that it can only be understood as an aspect or organising principle of the body, which Aristotle called the body's 'form'. The thought experiment is designed to show that this is wrong. It does so by calling to our attention that we have a means of access to our souls apart from bodily sensation, namely self-awareness.
How would this refute Aristotle? Well, consider again just why it is that the flying man is not aware of his body. It is because he is not currently using his senses and has never done so (he only just started existing, remember), and sense perception is, Avicenna assumes, the only way to become aware of any body. If this is right, then anything that the flying man grasps without using sense perception is not a body, not material. Since he does grasp his soul without using sense perception, his soul is therefore not a body.
On this reading, Avicenna would be helping himself to a pretty big assumption, which is that bodies can be discovered only by the senses. You can see, hear, touch, taste or smell them, but otherwise you can never so much as know that they exist. Since for Aristotle the soul was a form of the body, if you couldn't experience the body, you would not, on his account, have access to the soul; and yet, Avicenna claims, the falling man would have access to his soul.
I suspect this is (at least in part) what he had in mind in creating this thought experiment. But that's not to say that I'm convinced. All Avicenna has really done is to throw down a challenge to his materialist opponents: show me how a body could be aware of itself without using sensation to do so.
Philosophy in the Islamic World by Peter Adamson is out now through Oxford University Press.
Peter Adamson
This article was originally published at Aeon and has been republished under Creative Commons. Read the original article.
Escapism is one of the imagination's great joys. Through fantastic literature, we can explore the vast stretches Arrakis's deserts or the forests of Middle Earth alongside Gandalf the Grey. We can embark on vacations weeks in advance and enjoy a sunny beach while at our desks. We can relive a cherished memory with a favorite relative in an instant, and, of course, always rely on our flock of trusty sheep to lull us to sleep.
We manage this through what is colloquially called "the mind's eye," our ability to generate psychological images without sensory input. However, such escapism is not possible for people with the rare, and only recently identified, condition aphantasia. People with aphantasia cannot conjure mental images—original or from memory. Instead, their minds' eyes produce dark, blank canvases that cannot be painted in. As Wilma Bainbridge, an assistant professor of psychology at the University of Chicago, told UChicago News:
"Some individuals with aphantasia have reported that they don't understand what it means to 'count sheep' before going to bed. They thought it was merely an expression, and had never realized until adulthood that other people could actually visualize sheep without seeing them."
For such individuals, literature may produce facts but not visual representations. Arrakis isn't a planet of vast deserts but vast emptiness, Gandalf the Grey a colorless, featureless blob. Sunny beaches can't be visited in their imaginations but must remain on the office calendar until summer vacation. And while memories exist, they cannot be visually recalled except between scrapbook cellophane.
Scientists don't yet know what causes aphantasia, whether it's a distinct psychological condition, or, indeed, if we are simply jarring against language's limited ability to accurately describe our internal realities. But a burgeoning body of research—among it a new study led by Bainbridge and published in Cortex last month—suggests the condition is more than misfiring expressions.
Changing our understanding of the mind's eye
Francis Galton was the first to describe a condition that would today be recognized as aphantasia.
Though no long-term studies have focused on aphantasia, its history stretches back more than a century. Francis Galton first described people with "no power of visualising" in 1880, an observation made during his breakfast-table survey. At that time, however, the science of psychology was still in its infancy, and Galton's observation was shelved like so many other early-day curios—brought down and dusted off by the occasional psychologist but given little attention before being shelved again.
That changed in 2003 when neurologist Adam Zeman was contacted by a 65-year-old man who claimed his mind's eye went blind. During a coronary angioplasty, the man suffered a small stroke that damaged his brain. Afterward, he lost his ability to render psychological imagery.
"He had vivid imagery previously," Zeman told Science Focus. "He used to get himself to sleep by imagining friends and family. Following the cardiac procedure, he couldn't visualise anything, his dreams became avisual, [and] he said that reading was different because previously he used to enter a visual world and that no longer happened. We were intrigued."
Zeman and his colleagues began a case study into the man's condition. Tests found he could describe objects and their color but could not visualize them. (He claimed he simply knew the answer.) He could rotate three-dimensional images in his mind, but it took him longer to manage than controls. And brain imaging showed brain regions associated with visualization to be dark when he tried to imagine images.
Zeman published his case study, and it was subsequently featured in Discover magazine. After the story's publication, more people reached out to Zeman. They too claimed their minds' eyes were blind, but unlike Zeman's original subject, many of these people had lived with the condition their entire lives. They only became aware of their condition later in life when, as Bainbridge mentions above, they realized that the mental worlds described by friends and family were based on more than fanciful expressions.
While some managed to live normal, even thriving, lives without visual memory, others found the condition distressing. As one subject told Zeman and his coauthors: "After the passing of my mother, I was extremely distraught in that I could not reminisce on the memories we had together. I can remember factually the things we did together, but never an image. After seven years, I hardly remember her."
Zeman published another case study focusing on 21 of these individuals in 2015. It was here that he coined the phrase* "aphantasia," from the Greek phantasia meaning "imagination." Since then, Zemen has connected with thousands of people claiming to have the condition, and his studies have raised intriguing questions for researchers interested in memory and the mind.
Visualizing the difference
On the left, an aphantastic participant's recreation of a photo from memory. On the right, the participant's recreation when the photo was available for reference.
Bainbridge is one such researcher. Her previous work has focused on perception and memory, both their underlying mechanics and how this content is stored. In her latest study, she and her co-authors aimed to not only tease out the distinctions between object and spatial memory but also deepen our understanding of aphantasia.
To do this, they invited 61 people with aphantasia and a group of controls to participate in their experiment. They showed each participant a photo of a room and then asked them to draw it in as much detail as possible. For one test, the participants were allowed to keep the photo for reference. For the next test, however, they had to draw the room from memory. Bainbridge and her coauthors then put the drawings online to be quantified by nearly 3,000 online assessors, who were asked to score both sets of test images for object and spatial details.
The results showed the aphantastic participants had difficulty with the memory experiment. They produced reproductions with fewer objects, less color, and fewer details than their control peers. Many leaned on verbal scaffolding in lieu of visual details—for example, one participant drew a rudimentary box with the word "window" rather than a window with a frame and panes of glass.
Although the aphantastic patients drew rooms with fewer objects, they were very accurate in their placement of those objects. They also made fewer errors than the controls and avoided incorporating features and furniture absent in the original images. The researchers write that this suggests high spatial accuracy despite a lack of visualization.
"One possible explanation could be that because aphantasics have trouble with this task, they rely on other strategies like verbal-coding of the space," Bainbridge told UChicago News. "Their verbal representations and other compensatory strategies might actually make them better at avoiding false memories."
The online assessors found no significant differences between the aphantastic participants and the controls when the original photo was available for reference. In fact, some of the aphantastic participants produced stunningly accurate and artistic recreations during this test.
Bainbridge and her coauthors suggest that these results not only support the idea that object and spatial information is store in separate neural networks. They also provide "experimental validation" for aphantasia as a valid psychological phenomenon.
Discovering a new reality in aphantasia?
And Bainbridge's study has joined an ever-growing panoply. A 2018 study, also published in Cortex, measured the binocular rivalry—the visual phenomenon in which awareness fluctuates when different images are presented to each eye—of participants with and without aphantasia. When primed beforehand, control participants choose the primed stimuli more often than not. Meanwhile, aphantastic participants showed no such favoritism, whether primed or not. Like Bainbridge's study, these results suggest a physiological underpinning for aphantasia.
Another critical factor is growing awareness. As more studies and stories are published, more and more people are realizing they aren't alone. Such a realization can empower others to come forward and share their experiences, which in turn spurs researchers with new questions and experiences to study and hypothesize over.
Yet, there's still much work to be done. Because this psychological phenomenon has only recently been identified—Galton's observation notwithstanding—there has been sparingly little research on the condition and what research has been done has relied on participants who self-report as having aphantasia. While researchers have used the Vividness of Visual Imagery Quiz to test for aphantasia, there is currently no universal method for diagnosing the condition. And, of course, there is the ever-vexing question of how one can assess one mind's experiences from another.
"Skeptics could claim that aphantasia is itself a mere fantasy: describing our inner lives is difficult and undoubtedly liable to error," Zeman and his co-authors wrote in their 2015 case study. "We suspect, however, that aphantasia will prove to be a variant of neuropsychological functioning akin to synesthesia [a neurological condition in which one sense is experienced as another] and to congenital prosopagnosia [the inability to recognize faces or learn new ones]."
Time and further research will tell. But scientists need phenomenon to test and questions to experiment on. Thanks to researchers like Zeman and Bainbridge, alongside the many people who came forward to discuss their experiences, they now have both when it comes to aphantasia.
* Zeman also coined the term "hyperphantasia" to describe the condition in which people's psychological imagery is incredibly vivid and well-defined.
