Is beauty in the eye of the beholder or the neurobiology of the brain? The answer to this question might surprise you. As a marketer, you have an opportunity to create an immediate connection with your audience and that starts with the look and feel of your marketing assets. This is because your audiences brain responds favorably to aesthetically pleasing stimuli. And yes, that includes emails, print ads, web pages, social media posts, digital ads and more.

The aesthetic experience starts the moment your audience looks at your ad. At this moment, your audiences brain begins to process visual content quickly. In fact, the processing of visual information happens so quickly that your audience is unaware of what the eyes see, at least initially. Put more succinctly, the brain processes visual stimuli before consciousness is even possible.

When it comes to creating an aesthetic experience, the visual strength of your imagery is key for creating an immediate connection. According to Anjan Chatterjee, Professor of Neurology at the University of Pennsylvania, the brain responds automatically to beauty. In other words, beautiful imagery, whether in the form of a print ad or a social media post, is critical for creating positive associations with your brand automatically.

An aesthetic experience stirs activity in different regions in the brain, including areas associated with emotion, reward and decision-making. Importantly, the experience extends across multiple sensory modalities and happens to occur regardless of whether a person is viewing a painting, listening to music or admiring a perfectly constructed math equation. Remarkably, you can quantify the experience.

Researchers across multiple studies directed subjects to view artwork and state the extent to which each image was considered beautiful all while measuring activity in the brain. As Semir Zeki, Professor of Neuroaesthetics at University College London, observes, activity in a key area of the brain, the medial orbitofrontal cortex, was proportional to the declared intensity of the aesthetic experience.

When it comes to viewing attractive faces, the experience becomes even more profound. In a 2019 study, Chatterjee demonstrated how an aesthetic experience can actually activate the motor parts of the brain to compel people to move physically towards attractive faces. In the study, a computer monitor displayed a number at the bottom of the screen and two numbers at the top. The task was simple. Click on the number that was closest to the number on the bottom.

Simple enough, right? But to see if attractiveness affects motor behavior, the researchers paired the top numbers with faces, one attractive and the other unattractive. Incredibly, researchers discovered the mouse would drift toward the attractive face even if the number was incorrect. In other words, the aesthetic response to an attractive face was so powerful that it affected hand movement!

As you think about the look and feel of your marketing assets, you might want to consider these key takeaways:

Given that your audiences brain responds automatically to beauty on a subconscious level, one of your goals as a marketer should be to facilitate approach-behavior on a subconscious level. In other words, get your audience to become drawn toward your marketing asset. As a skilled marketer, however, you already know thats only part of the story. Once you engage your audiences brain on a subconscious level, you must present the appropriate message, which taps into individual preferences within a culture-appropriate framework. As such, you must create content that resonates with your audience since triggering aesthetic appreciation is only a starting point.

In your role, youre often presented with obstacles from less informed persons. Have you worked for a client or reported to a CEO who was uninterested in what your marketing content looked like? Are you told that your audience doesnt care what your marketing collateral looks like? The problem is that your audiences brain is attracted to aesthetically pleasing stimuli whether they know it or not. Now you can make a science-based argument on why you must create good-looking marketing content.

The most important takeaway is to understand that visually appealing content matters. Since brain regions that are associated with emotion and reward become active when viewing aesthetically appealing content, its important to create marketing assets that tap into the circuitry thats involved in the aesthetic experience. When youre able to do that, youll find that beauty is not only in the eye of the beholder but also in the neurobiology of the brain.

Opinions expressed in this article are those of the guest author and not necessarily MarTech Today. Staff authors are listed here.

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Neuroscience and beauty: How to create an immediate connection with your audience - MarTech Today

The room is pitch black. Every light, from the power button on the computer to the box controlling the microscope, is covered with electrical tape. I feel a gush of air as the high-powered AC kicks on, offsetting the heat emitted from the microscopes lasers.

I take my mouse out of its cage and get ready to image its brain. Im wearing a red headlamp so I can see, but it is still quite dim. I peer closely at my lab notebook and note the two positions: 1, +2. I recite them repeatedly in a hushed tone, so I dont forget; it is 1 A.M., after all. I hook the mouse up to the stage of the microscope and then use my handy toothpick to make sure its head position is correct.

While there are many unsung heroes of scienceveterinarians, lab technicians, graduate students (I might be a bit biased with this one!)these arent the ones Im talking about. Im talking about a toothpick that played a significant role in my research project.

I am lucky enough to have access to a cutting-edge microscope and several other pieces of expensive equipment in my lab. But can also find things you might never guess were used in science: red-light headlamps, black electrical tape, and toothpicks.

Using the microscope, I can take a picture of a mouses living, working brain through a literal window: a piece of glass that replaces a small piece of the animals skull.

To image the mouse, we affix a plastic bar on the front of its head and then secure the bar to a head-mounting device on the stage under the microscope lens. Using this mount, we can precisely position the head up and down and right to left.

This is where our problem starts.

As neuroscience advances, weve grown to appreciate how each individual brain cell plays a vital role in the larger organ. A lot of the nuance is lost, however, when we cant see whats happening in each individual cell. But with this specialized setup, we can image the same cells in the brain across several days, allowing us to follow each ones activity over time.

We did one round of experiments, and though we thought we were imaging the same cells each time, the analysis revealed that was not the case. Using this technique was new in our lab, and while there are scientific papers with instructions, some of the little details were lost in translation. When the next round of animals was ready, we needed to think of a solution fast. Thats when the idea to track the mouses head tilt came in.

We made a crude scale from 4 to +4 in both the up-down and left-right directions on the head mount, but we needed a way to indicate what position the mouses head was in. We needed something easy and fast that we use to track the position. Then the idea struck: a toothpick would be perfect. We would create two mini protractors (one for up-down and one for left-right), with the toothpick serving as the position tracker. We broke the toothpick in half and stuck the rough edge to the head mount. The pointy end would point to a position on our scale, one for up-down and one for left-right. And just like that with a toothpick and a bit of superglue, our problem was solved.

Now I can record the toothpick position, then go back and put the mouses head in an identical position day after day. Over a four-day experiment we have to go back into the darkroom every six hours, and the handy toothpick allows me to collect the data I need for my next insight into the ever-complex biology of the brain.

Walk into any molecular biology lab, and you may see something similar: an everyday object as humble as a toothpick next to (or even attached to) a very expensive piece of equipment. These are the labs where we learn about the types of cells that allow us to think, which proteins cause which diseases and how our genetic code can be targeted to improve our health. The environment where we make these lifesaving discoveries may seem utterly exotic, but we sometimes have to improvise with whatever we can findjust like anyone else. I know I will always have a toothpick at the ready from now on.

And keep in mind, next time you need a quick fix, there are probably some tiny, pointy wooden sticks in a drawer near youor something equally commonthat can turn failure into success.

The possibilities are endless.

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The Toothpick That Saved a Neuroscience Experiment - Scientific American

Psychedelic drugs have long been exiled to the fringes of medicine, dismissed as recreational drugs with limited therapeutic potential. That all changed with the breakthrough therapy status granted last year to psilocybin, the active compound found in psychedelic mushrooms, for its ability to rapidly reverse treatment-resistant depression. This has led to an explosion of interest in the field, with new institutes opening and new disorders identified as targets for psychedelic therapy. In our latest interview series, we discuss the potential of psychedelics to revolutionize clinical neuroscience with thought leaders in the field.When you think about psychedelics, 3,4-Methylenedioxymethamphetamine (MDMA), also known as Ecstasy, isnt what first comes to mind. Whilst this commonly used party drugs status as a psychedelic is still debated by some in the field, MDMA has, alongside more traditional psychedelics, become a hot topic in neuropharmacological research, and received its own Breakthrough Therapy status from the FDA for treatment of post-traumatic stress disorder (PTSD). Its therapeutic potential for neurological disorders has attracted attention from researchers and ravers alike. In this first interview of our series exploring the Neuroscience of Psychedelics, we talk to Johns Hopkins Associate Professor Gul Dlen, who has spent years exploring the effects of MDMA on the mammalian (and more recently, cephalopod) brain.

Ruairi Mackenzie (RM): In a recent paper, you exposed octopuses to MDMA. Could you tell us why?Gul Dlen(GD): Years ago, people had started to suspect that psychedelic drugs might be acting on the serotonergic system and specifically MDMA had been shown to be interacting with a protein called the serotonin transporter or SERT. Most people have heard of this transporter by another name because theyve heard of drugs like Prozac, which is a blocker of the serotonin transporter. Prozac makes serotonin available in the synapse by preventing the serotonin transporter from vacuuming extra serotonin from the synapse. Because Prozac blocks that action it makes more serotonin available.

What MDMA does is it reverses the direction of the serotonin transporter. Instead of vacuuming up the serotonin, it is spewing it out into the synapse. Its not just making more serotonin available, but its actually pushing more serotonin into the synapse. That was the main mechanism that people had focused on for the last couple of decades. When we studied the octopus we just wanted to know whether an animal which is evolutionarily so distant from humans our last common ancestor was over 515 million years ago would have the same serotonin transporter, similar enough that if we gave the animals MDMA it would cause the animals to behave in a way that is recognizable to the way that we know MDMA makes humans and other mammals behave.

What was super exciting for us was that when we gave MDMA to the octopuses, they spent more time in the social chamber of the three-chambered tank that we had built for them. This was exactly what happens when we do the same experiment in mice, for example. That was both a little bit exciting and surprising because octopuses arent normally social. It was amazing to us that MDMA could encourage social behaviors in an animal that doesnt normally exhibit social behaviors at all, much less increase social behaviors. What it suggests is that the neural circuitry that enables social behavior exists in an octopus brain but then outside the reproductive period, when they would be socially tolerant, it just gets turned off. What MDMA is doing is releasing that circuitry to act the way that they would when theyre mating, for example.

RM: You also conducted research exposing mice to MDMA what did you learn from these experiments?GD: The mouse study had more novel mechanistic details. The way we started studying MDMA really was that firstly we had discovered a brand-new critical period in mouse behavior. Critical periods are familiar to most people because they are aware of the adage you cant teach an old dog new tricks. Anybody whos tried to learn a second language when they were an adult knows that its much harder to do. When youre a child you pick up languages without even being aware of the effort of learning them but as an adult, when you try and learn a language its difficult. The reason for that is the brain is less able to learn information when its older than when its younger because it has less plasticity. Different parts of the brain have different windows of time when they are most plastic. Those different windows of time support learning and memory of different types of behaviors.

Theres a critical period for language and for vision. What we discovered is that theres also a critical period for social behaviors and forming social attachments. We think that this critical period for social reward learning is the reason why, for example, kids are so much more susceptible to peer pressure and why they have 400 friends, and theyre always on their iPhones.

Theyre insatiably social, whereas most adults relish their alone time and after a week of conferencing for example you need to have some quiet time when youre not interacting quite so much. What we wondered is whether or not we could reopen that [social] critical period in adulthood. We thought this might be important in certain clinical situations where, for example, a person was socially injured during their childhood, which was leading to all kinds of maladaptive behaviors in adulthood: addiction or PTSD.

There are some theories out there that these are the consequence of social injury during earlier parts of life. If we could reopen that critical period and have them relearn those social interactions under optimized conditions, that might have some therapeutic value. When we were working on the critical period for social reward learning one of the mechanisms that we focused on was the developmental regulation of the receptor for [love hormone] oxytocin in a brain region called the nucleus accumbens. In mammals, the nucleus accumbens is one of those nodes of the brain thats knowing for sex, drugs, and rock and roll and is the pleasure center of the brain. In previous work I had done when I was a post-doc, we had shown that oxytocin acting in that nucleus accumbens node of the reward circuit was really important for encoding the reward value of social interactions.

What we figured out in this more recent paper is that the oxytocin receptor protein that senses the oxytocin in the nucleus accumbens is developmentally downregulated. This downregulation of the receptor corresponds to the time in the animals life when social interactions behaviorally become less important for helping them learn new things. We had identified this mechanism, but we knew that targeting it to reopen the critical period would be difficult because despite what you may have heard about intranasal oxytocin, it actually doesnt get into the brain when you squirt it up your nose.

But then we thought of this psychedelic drug, MDMA. Everybody knows when people take it at parties, they get extremely social and they want to hug everybody. They form these cuddle puddles! So wouldnt it be cool if MDMA could somehow interact with our neural circuits to reopen the critical period? Basically, thats what we found that it does. It causes the oxytocin synaptic plasticity mechanisms to come back online and make the adult brain socially plastic again, the way that it was when the animal was a juvenile. We think that this property of MDMA to reopen this critical period is going to be really useful in explaining why this drug works so well for treating things like PTSD. It also gives us some hints about where we might go next; understanding the mechanism helps us to build up other potential applications and figure out how else we might tweak this critical period for therapeutic benefit.

RM: So, should we be giving out MDMA at conferences?GD: I dont know about you, but for me, being a teenager was difficult. Its not without an energetic cost to care what people think about you. I think the great thing about being an adult is not having to care quite so much. I find that to be quite nice. I think a lot of people have a first knee jerk reaction of Great, I can make my brain young again! I want to make myself young in every way, why not my brain too? I think that its adaptive to devote your emotional energies to other things as you mature, once your group membership is stabilized. If you have a problem that youre trying to fix, then maybe you want to be able to selectively target this one critical period, open it, fix your problem and then have it closed back up again.

RM: Is there therapeutic potential for disorders with social deficits?GD: I think that there are a lot of other diseases that we dont necessarily think of as being social in their ideology but actually are. Theres a lot of evidence that people who become addicts have social injury in their past. A huge percentage of female heroin addicts have been sexually abused when they were children. For those types of illnesses where there is a social injury component, I think theres an obvious potential therapeutic link.

Even if there is no social injury per se, I think that there is something useful about being able to reopen the social critical period. Being able to reopen the critical period and reform a therapeutic alliance with your therapist, for example, and being able to trust somebody and tell them everything that has been festering because its so horrifying you havent been able to look at it. I think thats another way that we can think about how MDMA might be working therapeutically in the context of a critical period for social learning.

RM: These drugs are very heavily regulated in research. Is the regulation proportionate to the risk?GD: Very soon, I suspect, the FDA will reconsider their scheduling of these drugs. MDMA and psilocybin are both what we call Schedule 1 drugs in the United States. Cocaine, for example, is Schedule 2 and the reason that they have decided to schedule them that way is because cocaine has some therapeutic uses, I believe in dentistry as a numbing agent. Theres no known therapeutic use for psychedelic drugs but given that the FDA has just given both the psychedelics MDMA and psilocybin breakthrough therapy status, which is encouraging clinical trials for these drugs, that rationale for making them Schedule 1 will go away.

The other rationale for making them Schedule 1 is that they are highly addictive. There is to my knowledge no evidence that these drugs are addictive at all. Most people who take psilocybin take it once and they need a rest, theyre not really interested in taking another dose for months. It doesnt have a profile of a drug that is addictive in any way. I think both of those reasons mean that these drugs will be rescheduled shortly. I hope.

RM: What does Schedule 1 classification mean in terms of access to these drugs in research?GD: It takes a long time to get a license. You need a separate license for Schedule 1 drugs. Its different from the license that you need for Schedule 2 drugs. It took our lab roughly eight months or something to get the Schedule 1 license. The FDA has to send people out here and make sure the building is secure and we have the proper locks and safes and double locks and logs and that people who are using it are properly trained in how to handle it and dispose of it and log the amount that we use every time we use it.

Its involved, and for a lot of science, before you can devote the resources to studying something you want to test it quickly. Just to do a quick pilot study and if it works then you can devote a full-time post-doc to it, put the resources in. When a drug is Schedule 1, and you dont have a Schedule 1 license, doing that pilot experiment is not feasible.

A lot of crazy ideas just dont get done because its not worth it to invest eight months of paperwork to test one crazy idea that probably wont work anyway.

RM: Theyre often the best ideas.GD: I think so, yes. With our octopus MDMA idea, we would never have started with MDMA and an octopus if it hadnt been for the fact that we were already licensed to use it in the PTSD and critical period for social behavior studies. I think a lot of science comes from those one-off, crazy, wouldnt it be cool if, kind of experiments, that just dont get done if you have to fill out too much paperwork.

Interviews have been edited for length and clarity

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The Neuroscience of Psychedelic Drugs: Octopuses, MDMA and Healing Social Injury - Technology Networks

Graduate students host 'Ouch: Neuroscience of Pain' event to showcase research in the field  The Daily Pennsylvanian

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Graduate students host 'Ouch: Neuroscience of Pain' event to showcase research in the field - The Daily Pennsylvanian

Teens who bully their peers tend to display a different pattern of brain activity in response to certain facial expressions, according to new research published in Social Cognitive and Affective Neuroscience. The findings shed light on the neurological underpinnings of bullying behaviors and could help lead to new interventions to combat bullying.

Bullying is fairly common during adolescence, with about 25-50% of teenagers in the U.S. reporting that they have bullied or been a victim of bullying, said study author Johnna R. Swartz, an assistant professor at the University of California, Davis.

We also know that being a bully or victim of bullying is associated with poor mental health. I was interested in examining how measures of brain function relate to bullying or being a victim of bullying so we could better understand which factors may contribute to higher likelihood of these outcomes.

Swartz and her colleagues were particularly interested in a brain region known as the amygdala, which plays a key role in emotional processing and responding to threats.

The researchers used functional magnetic resonance imaging to examine amygdala activity in 49 adolescents as they completed an emotional face matching task.

They found that adolescents who reported engaging in more relational bullying behaviors (such as purposefully excluding a peer or spreading rumors) tended to display higher amygdala activity in response to angry faces and lower amygdala activity in response to fearful faces.

Higher amygdala activity to angry faces could suggest that these teens are more sensitive to signals of anger from other people, while lower amygdala activity to fearful faces could suggest that their brains are less responsive to signals of distress, which could lead to lower empathy when bullying victims, Swartz told PsyPost.

The higher amygdala activity to angry faces could also lead teens to perceive more hostility in their social interactions, whereas the lower amygdala activity to fearful faces could lead to lower empathy, and this combination seems to be associated with more bullying behavior. These results can help us to understand what may make some teens more likely to bully their peers.

The researchers also found that lower amygdala activity in response to angry faces and lower amygdala activity in response to fearful faces were both associated with lower levels of victimization.

But the study like all research includes some limitations.

A major caveat of this study is that the design was cross-sectional, meaning that amygdala activity and the measures of bullying behavior were collected at the same point in time. This means it is unclear whether these patterns of brain activity may have led to increased likelihood of bullying, or whether being a bully leads to these changes in brain activity, Swartz said.

Future research could use longitudinal designs with measures across several occasions to test whether these patterns of brain activity predict bullying behavior, or whether engaging in more bullying behavior predicts changes in these patterns of brain activity over time.

If longitudinal research confirms that these patterns of brain activity predict increases in bullying behavior over time, results from this study could have implications for new ways to reduce bullying behavior in the future, Swartz explained.

For example, the finding that higher amygdala activity to angry faces predicts more bullying behavior suggests that training teens attention away from angry faces or teaching teens to interpret ambiguous facial expressions in less hostile ways could be potential methods for reducing bullying.

The more we understand about how patterns of brain activity and the way we process social cues relates to bullying and victimization, the better we will be able to intervene to reduce bullying and victimization in teens, Swartz added.

The study, Amygdala activity to angry and fearful faces relates to bullying and victimization in adolescents, was authored by Johnna R. Swartz, Angelica F. Carranza, and Annchen R. Knodt.

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Neuroscience study finds amygdala activity is related to bullying behaviors in adolescents - PsyPost