A recent paper published in Neuron, one of the top neuroscience journals in the world, reveals a new mechanism of action between CBD and epilepsy. The paper was written by a team of researchers with an impressive track record in the field, some of whom have been involved in landmark clinical trials that showed the efficacy of CBD for treatment resistant epilepsy.

The paper describes a new mechanism of how CBD dampens signal transmission between nerve cells by interacting with an endogenous positive feedback loop that regulates neuronal excitability. By modulating this “Rosenberg-Loop”, CBD could potentially reduce seizure frequency and severity.

Cannabinoids show great promise for treatment resistant epilepsy

This discovery has important implications for the development of new therapies for epilepsy based on CBD or other cannabinoids. It also confirms the validity and potential of cannabis as a medicine for various neurological disorders.

At thepineapple, we aim to provide accurate and unbiased information about scientific discoveries related to cannabis and psychedelics. We believe that science should inform public opinion and policy, not belief or ideology. That’s why we aim to let the researchers who actually did the studies tell you in their own words what they have discovered.

In this article, you will find an exclusive interview with Prof. Richard Tsien PhD, Director of the Neuroscience Institute at NYU and his former graduate student Dr. Evan Rosenberg MD PhD, who led the research team behind this groundbreaking paper. They will explain the basic concepts behind the discovery, what it means for epilepsy patients, and what the next steps for further research are.

But don’t worry, reddit, we hear you! This will be as “ELI5” as possible and in no small part thanks to how wonderful of an educator Prof. Tsien is. Before we get into the weeds of the conversation, let me first introduce you to Prof. Richard Tsien, PhD and Evan Rosenberg MD, PhD who were steering the research that we will be discussing down below.

Meet the Researchers

Prof. Richard Tsien, PhD

Prof. Tsien’s scientific career has been both long and consistently accomplished. He has been making major scientific contributions since the 1960s. His work on calcium signaling, neurons, calcium channels and ion channels has dramatically increased humanity’s knowledge of cellular biology.

Starting out at MIT, young Richard Tsien obtained both his Bachelor and Master of Science degrees in electrical engineering. After winning a Rhodes Scholarship, his path took him to the University of Oxford where he acquired a doctorate in biophysics working on “The kinetics of conductance changes in heart cells” in Denis Noble’s lab.

From there he returned to the US where he became an assistant professor and later a full professor in the Department of Physiology at Yale University School of Medicine.

In 1988 he founded Stanford University’s Department of Molecular and Cellular Physiology where he was the “George D. Smith Professor” for 20 years before becoming Co-Director for the Stanford Brain Research Center from 2000 to 2011. For 10 years he was also the “Silvio Conte” Director at the National Institutes of Mental Health Center for Neuroscience Research.

Prof. Tsien served as president of the Society for General Physiologists and as Section Chair of Neurobiology for the United States National Academy of Science, where he has been an elected member since 1997.

He has won numerous prestigious awards and honors, from repeated Kaiser Awards for Outstanding and Innovative Teaching from Stanford University and the Bard Lecture from Johns Hopkins University to the Magnes Prize from Hebrew University in Jerusalem. He is an elected member of the American Academy of Arts and Sciences (AAAS), the National Academy of Sciences (NAS), the Academia Sinica, the Biophysical Society and the United States Institute of Medicine.

Today, Prof. Tsien is the Chair of the Department of Physiology and Neuroscience, the founding Director of the Neuroscience Institute, and Druckenmiller Professor of Neuroscience at NYU Langone Health. He is also a Professor in the Department of Neurology.

One has to admire his dedication and persistence that have driven such a career. Just imagine the collective impact that Prof. Tsien and his students have had on the field of neuroscience over the years. Truly remarkable.

Evan Rosenberg, MD PhD

One of those young researchers Prof. Tsien has trained is Dr. Evan Rosenberg, an up-and-coming researcher with more than 10 years of experience in cellular neuroscience and a strong interest in translational research. Evan’s career goal is to develop novel, cutting-edge therapeutics for neuropsychiatric disorders. His prior expertise includes cellular electrophysiology, in vivo EEG recordings and molecular biology. His PhD research focused on anti-seizure mechanisms underlying cannabidiol.

Evan began his scientific career as an undergraduate researcher at Brandeis University and Children’s Hospital in Boston, where he worked on inhibitory network homeostasis and the functional overlap between epilepsy and autism spectrum disorders, respectively.

In 2012, he joined New York University’s School of Medicine to pursue a dual MD-PhD degree program with a focus on neuroscience. As a graduate student in Prof. Tsien’s lab, he investigated the anti-seizure mechanisms of cannabidiol using multidisciplinary approaches, including electrophysiology, molecular biology and in vivo EEG recordings.

Today he is in the Neurology Residency Program at University of Pennsylvania, where he continues to work on novel therapeutics for neuropsychiatric disorders. We will be following his career with great interest.

The Interview

Alexander Schering, PhD
So, first of all, thank you very much for taking the time to sit down with me. This is very, very great. And I think the first question I should ask is:

Can you please introduce us to your lab and what your overall research objectives are?

Prof. Richard Tsien, PhD

Certainly! Our lab has been interested for some years on how nerve cells communicate with each other, and that involves synaptic transmission, which is the process by which one nerve cell releases a chemical out into the extracellular space outside the neuron. This chemical travels across a very tiny gap, called the synapse, and impinges on protein molecules that respond to that chemical and excite a second cell. This process, called synaptic transmission, is fundamental to how we move and how we think. But it's also fundamental to parts of the brain that are involved in epilepsy.

And just for the fun of it, I'm going to pause and pass the baton on to my co-anchor, Evan Rosenberg, who is an MD PhD graduate now doing his clinical work at the University of Pennsylvania.

Evan Rosenberg, MD PhD

Thanks, Dick. I joined the lab back around 2013, almost exactly a decade ago. I was a graduate student in the lab and then got my PhD. In 2020, I completed my MD PhD at NYU, and since then, I have been in neurology residency at the University of Pennsylvania. I'm specializing in epilepsy with a particular interest in new therapeutic development, specifically for hard-to-treat epilepsy and identifying new targets to treat that.

I have always had a fondness for learning about fundamentals about how the brain works and different mechanisms for plasticity. So it was a nice union when Dick and I met 10 years ago, and it’s still going strong.

Alexander Schering, PhD

So this was your PhD project? 

Evan Rosenberg, MD PhD

Yes, it was my PhD project. And I should mention a third player in our study was Orrin Devinsky. He's an epileptologist at NYU, and he was one of the first people to start the clinical trials looking at cannabidiol in pediatric epilepsy. From the beginning, it was a joint effort, both from the basic science perspective with Dick and the clinical side with Dr. Devinsky, who was just starting this trial about 10 years ago.

It was a really enlightening experience to see things from both ends, looking at the cellular mechanism and early clinical studies which ultimately led to the FDA approval of Epidiolex for epilepsy.

Alexander Schering, PhD

So it's actually interesting that, in this case, the clinical trials really came before the basic science, didn't they? Isn't that unusual? Normally, you would go the other route, right? You would start with the basic science and then go into clinical trials. 

Prof. Richard Tsien, PhD

That's right, partly because of patient need. Parents had children with a very severe form of epilepsy called Dravet syndrome, which is associated with very frequent seizures that are very debilitating for the child. Parents got the idea that there might be some benefit to the use of products of the cannabis plant.

There's a long story that I'm sure one can find in the press about a patient and her parents who persistently tried cannabis oil and even moved to Colorado in order for that to happen.

Alexander Schering, PhD

That is the story of Charlotte Figi you are referring to, isn’t it?

Prof. Richard Tsien, PhD

Right, and her parents deserve a huge amount of credit for being persistent and trying the different products. Now, of course, that's good at an anecdotal level. But not everyone can move to Colorado and do things like that. In order to make a medicine, you need folks who are willing to try and obtain a purified or relatively pure product and then conduct the kinds of systematic and objective trials that involve patients. You also need patients to have the courage to enroll in a trial without knowing whether they're getting the compound or a harmless and apparently innocent substitute known as a placebo, which effectively has no active compound in it.

Charlotte Figi's parents deserve a huge amount of credit

This was done by some very intent and serious clinicians, including Dr. Orrin Devinsky and his colleague in Boston, Dr. Elizabeth Thiele. They had partnered together to do a randomized, placebo-controlled crossover trial that was so strong in its outcome that the FDA was given the opportunity to approve the agent for a narrowly defined indication, namely Dravet Syndrome. Subsequently, the preparation, called Epidiolex, has been approved for other indications. But it all began with Dravet Syndrome and Charlotte's Web and the late Charlotte Figi.

And you're totally right, Alexander, that this is not the expected way of doing things. Very often, a compound seems to have some efficacy, then some basic science is done, and that is part of what leads the FDA to feel comfortable with the approval. Nevertheless, in this circumstance, Evan's work provides a mechanism that greatly enriches the usefulness of the agent because having a mechanism of action helps you understand how this agent might interact with another one that could be used for epilepsy but might not be completely efficacious in the case of a patient.

For example, the other agent could be clobazam, which is an agent used to prevent epilepsy. The mechanisms are not the same, yet they're not completely independent. And having Evan's knowledge about the basic mechanism is greatly helpful in deciding whether, for example, the combination of drugs is a good idea or not a good idea. It also leads one to think about how Epidiolex might be useful for other indications, which involve the balance between excitation and inhibition, excitatory transmission, and inhibitory transmission.

Alexander Schering, PhD

So that brings me to the paper that you just published in NEURON. Could you maybe put the discovery in context for us? Give us the key ideas of what was discovered here? Please keep reddit’s request in mind to “dumb it down”.

Evan Rosenberg, MD PhD

Sure, I can talk about that.—So, the basic idea is that it was previously known that cannabidiol targets a lipid that's produced within our own bodies, which is called LPI. This lipid is naturally produced, and we think that it increases excitability in the brain, meaning that it makes the nerve cells more likely to fire. We discovered that LPI also removes the “brakes” on circuits which can send the system into overdrive. So, there are two separate mechanisms by which we think that this lipid works, and collectively, this makes the brain cells more likely to fire. CBD, by blocking the actions of LPI, reduces the overfiring of the brain, and we think it can reduce seizures.

This one mechanism that cannabidiol uses to reduce seizures is probably one of many. We want to be very clear about what our data shows and what it doesn't show, but in brief, there's a lipid that's produced in the brain that we think cannabidiol opposes, and the overall effect of that is to likely reduce seizures.

Prof. Richard Tsien, PhD

Alexander, I'd like to add another version of that, agreeing with everything that Evan has considered, but in order to better comply with the second request and make it even simpler and maybe more publicly accessible. Okay, so what we're trying to do is be very fair to those who came before us but also be very much teachers. So, one nerve cell gets another nerve cell to fire by delivering two kinds of transmitters, one of which can be likened to an accelerator pedal, and the other which can be likened to a braking pedal. The driving of the second neuron depends on judicious application of the accelerator and the brakes.

CBD calms everything down, dampens the accelerator and doesn't allow the brakes to be removed

The body has its own lipid, which has been described as LPI. And perhaps surprisingly, it has the job of making the accelerator stronger and the brakes weaker. This is useful for getting the nervous system to operate at peak performance, but it's also dangerous because if it is used excessively, then the nervous system can undergo hyperactivity, and perhaps even a seizure. So the body has its own system for making the combination of accelerator and brakes more acute, hyper, and maybe more dangerous. CBD comes along and dampens the effect on the accelerator. This had previously been suggested by a group in London, but Evan's work showed that the more lasting and possibly more important effect is the effect of the LPI on the brakes. In other words, the removal of the brakes is engendered by an endogenous lipid, and CBD blocks that effect.

So the body has ways of auto-regulating both the accelerator and the braking system in a way that makes the nervous system live dangerously. And CBD calms everything down and dampens the effects on the accelerator, and doesn't allow the braking effect to be removed. That was much longer. It wasn't necessarily better. But I think the combination of the two might work.

Evan Rosenberg, MD PhD

I like Dick’s answer better

Alexander Schering PhD

I like them both for different reasons. If you simplify concepts like these too much then at some point they become inaccurate. Finding the right balance is hard.— So, I guess this is kind of a theme for CBD. The endocannabinoid system appears to be involved in so many places where it looks like it regulates homeostasis. In other words, returning cells back to a steady state, but you think there are more pathways involved?

Evan Rosenberg, MD PhD

So, I think I would like to say a few different things on that note. Cannabidiol has many different targets. There are ion receptors, transporters, and enzymes. The protein that we think CBD targets here is called GPR55, a G protein-coupled receptor. However, it is one of many targets, and their relationship to the endocannabinoid system is a really fascinating one that I don't think has been fully explored. But there are endocannabinoids released in the brain too, 2-AG and anandamide are the most well-known ones, and there's a way that the body can shift from those endocannabinoids to this molecule LPI. As you mentioned, endocannabinoids tend to have a homeostatic role where they reduce the firing of the neuron in the circuit, whereas LPI, we showed, is kind of hyping the system up. It may be that they serve two different purposes. Interestingly, they both can be connected and related to the cannabis plant in very different ways.

Prof. Richard Tsien, PhD

It's like Evan means literally inter-converted, that there is an enzyme system that can gradually change endocannabinoids into LPI. So the membrane and the biochemistry of cells are pretty sophisticated in that components of the cell membrane that normally live within the cell membrane can be used to create messages which the nervous system uses to auto-regulate the strength of both excitatory neurotransmission and inhibitory neurotransmission. I think that's actually quite a profound idea. And then put on top of that, this amazing plant, which is generating a compound like CBD. It is not hallucinogenic, does not produce a high, and nevertheless has medicinal effects because it can interfere with, or modulate, or curb the actions of the body's own signaling devices. And just to repeat what you said, Alexander, unlike LPI, which hypes the system up by making the braking weaker and the acceleration stronger, the endocannabinoids have a more homeostatic or a more dampening role in that they dampen both the excitatory and inhibitory effects. So LPI is a much more, if you like, fraught signal. It may be useful for the nervous system to be working at peak performance, but it is more liable to the positive feedback loop that Evan discovered. I actually nicknamed it the “Rosenberg-Loop”. Okay, so we never publicize that because we're modest scientists, more or less (*laughs*), but that was my nickname for it. And Evan reasoned that because living dangerously creates more production of LPI and also increases gene expression of GPR55, both ingredients of that positive feedback loop are regulated by hyperactivity, and that can be dangerous. And so that vicious cycle is inherent in the way the LPI GPR55 system works. And so CBD is particularly strategic in affecting both the accelerator mechanism and the braking mechanism.

Alexander Schering, PhD

For your study you used Epidiolex, remind me, is that a synthetic CBD or extracted from the cannabis plant?

Evan Rosenberg, MD PhD

It’s plant-derived. It’s actually derived from cannabis. It’s not synthetic. GW Pharmaceuticals, which is now owned by Jazz Pharmaceuticals, has a unique process on the isolation of cannabidiol from the cannabis plant. There are other companies that synthesize it, but this is all plant-derived and very highly purified cannabidiol.

Alexander Schering, PhD

Okay, so have you considered trying full spectrum extract in some of your animal models as well, just to see if the effect is still present?—I know a lot of people will be reading this and wondering if they can just take a high-CBD cannabis strain and achieve the same effects. What would you say to those people?

Evan Rosenberg, MD PhD

So yeah, that’s a great question. I think it’s an active area of research. As scientists, we like to be as controlled as possible. There is much variability in the CBD content of “high-CBD” cannabis which can be hard when we are trying to objectively determine benefits of a drug for trials. So when we start mixing THC and cannabidiol and terpenes,  it becomes even more challenging to control our experiments. But clinically, the question is: is cannabidiol in isolation superior to cannabidiol with THC? Or is THC superior to the two of them? What about whole cannabis extract? And I don’t think we really know at this point.

What I can say is the only cannabinoid that’s FDA approved for some forms of pediatric epilepsy is Epidiolex, which is highly purified plant derived cannabidiol. And there’s some research on a 50:50 THC:CBD combination, primarily to combat multiple sclerosis spasticity. And there is ongoing work to answer the relative role of THC or other cannabinoids in multiple neurological disorders. 

We published a review article (Rosenberg, Whalley et al 2017) where we looked at multiple preclinical models of seizures. We looked at the effect of THC, cannabidiol, and synthetic agonists and antagonists of CB1 antagonists, and about 80% of those studies with cannabidiol showed benefit, whereas 20% showed no effect. While with THC, it was a much more mixed effect, where some papers did show a beneficial effect on seizures, some didn’t.

In the literature the effect of THC on epilepsy is inconsistent

So kind of extrapolating that to human data, I would think that cannabidiol seems to have a generally positive experience with seizures or no effect at all. Whereas THC has a mixed effect. It also operates on a different receptor; it operates on the CB1 receptor primarily.

So I think we really need more studies to determine that. And I think the benefit of something like Epidiolex is that it’s highly purified and patients know what they’re getting every time. Whereas if you use a high CBD strain of cannabis, there’s going to be variability in different patients.

Alexander Schering, PhD

So then that leads me to the question of what comes next? What is the next thing you wish to look at, now that you’ve discovered the “Rosenberg loop”?

 Evan Rosenberg, MD PhD

*laughs* I can let the Dick answer that first.

Prof. Richard Tsien, PhD

Well, some of your readership may consider this to be extremely boring, but I think we would like to better understand this control system in the full context of how the nervous system regulates the fundamentals of excitatory and inhibitory transmission. If the LPI and GPR55 system is a way of living dangerously - to tune the nervous system up to Indianapolis 500 Racing standards - then there has to be something else that counters this in a normal situation and keeps things under control in a normal brain. We think there is another lipidic actor in this called LPA. I’m sorry, the initials are confusing. You know, it’s lysophosphatidylinositol (LPI) and lysophosphatidic acid (LPA). There’s a difference of an inositol group. And that inositol is a common biochemical step to distinguish these two. And so LPA acts as a dampening factor for both excitatory and inhibitory transmission, very much like some of the other endocannabinoids. And we think it’s the coordinated use of LPI and LPA that gives the nervous system the ability to dial up whatever ratio of excitation and inhibition it needs. And somehow there have to be thermostats to detect all of that and dial that ratio. So as a scientist interested in how the brain regulates itself, I’m fascinated by that. And I’m willing to take a step back from trying to do things that miraculously cure people of diseases because I believe that understanding the process more fundamentally is going to secure a strategy of lasting importance.

Evan Rosenberg, MD PhD

Yeah, I totally agree with what Dick said. I think the only way that we can learn about some of these therapies is to learn more about the endogenous mechanisms. How is LPI released? What cell is releasing it? Can we modulate it? I think the connection with the endocannabinoids is really fascinating. On a clinical level, I think what would be most interesting based on this study is that we have many patients with treatment-resistant epilepsy. Some of them respond to cannabidiol (CBD) and some don’t. So could we use some of these markers like LPI or GPR55 to stratify patients and predict who might respond to CBD and who wouldn’t? Because our hypothesis is that LPI - the lipid - and GPR55 - the receptor - are probably not the cause of seizures, but they kind of add fuel to the fire through this feedback loop. This then makes patients more prone to seizures. So if patients with chronic seizures have elevated levels of LPI or GPR55, then there’s a possibility that they might be more responsive to CBD. We don’t know that at this point; more studies are needed. But in this study, we were at least able to show proof of principle that we can measure the levels of this lipid in the cerebrospinal fluid and brain tissues of animals. There’s a possibility that this could be used clinically in the future.

Prof. Richard Tsien, PhD

Yeah, and the other payoff in understanding the basic mechanism is the rationale for why a small amount of CBD and a small amount of a modulator of GABA receptors might be reasonable. The receptors that communicate the braking action of the neurotransmitter GABA are called GABA receptors. What CBD does is to keep LPI from taking away the GABA receptors from the membrane surface. By restoring the number of GABA receptors, the potency of an agent that works on each GABA receptor and makes each GABA receptor work better is going to be cooperative, in the same direction, and even multiplicative.

Anecdotal records say that CBD in combination with clobazam work in the clinic. Clobazam is an example of a GABA receptor allosteric agonist. Those are big words, but they mean things that make GABA receptors more effective. And now we have an explanation as to why they work well in the clinic. This will help us design the kind of therapy to take advantage of their synergistic actions. So there’s a possible payoff in terms of clinical understanding, there’s a possible payoff in terms of other agents that affect the conversion from one little bit to another. And we’re just at the beginning of that understanding. So while we know from Charlotte Figi and the work of Devinsky and Thiele that this is an agent that really does work, it’s been defined as working under relatively narrow circumstances. With more insights, we are going to be better able to define the strengths and limitations of this particular therapy.

Alexander Schering, PhD

Let’s switch gears a bit and expand the scope to the rest of the team. What can you tell me about the other people who worked on this paper? 

Prof. Richard Tsien, PhD

We did a lot of extra experiments and collaborated with some wonderful people. These include Dr. Helen Scharfman, an expert on epilepsy, and Prof. Gavin Woodhall, a colleague in the UK who specializes in studying a model of epilepsy that produces chronic epilepsy. The peer-reviewers highly prized these extra dimensions to the work. It was a team effort that we are really proud to be part of. There was also some excellent physiological and anatomical work by people in our own laboratory, including Simon Chamberland, Alejandro Salah, Erica Nebet and Xiaohan Wang. Each person brought different skills. Finally, we were able to measure the level of LPI, thanks to a colleague at NYU named Drew Jones. We don’t want to act as if we produced all of this by ourselves in our own lab!

We had a wonderful team of collaborators, like Ocean's 11 of science

The ideas and the driving force were clearly evident, but we had a lot of help along the way. For future projects, like measuring lipids accurately or developing an optical method to determine LPI locally on a microscopic scale, we will benefit from these colleagues and new technologies that are being developed. For example, a former colleague of ours in China named Yulong Li is currently working on a sensor for LPI. We hope to break through new technological barriers and study this in both greater detail and with exquisite precision.

Alexander Schering, PhD

Every big paper like this has that one experiment that is holding everything up. That one piece of the puzzle that you simply must have but is difficult to achieve. Which one was that for you? 

Evan Rosenberg, MD PhD

I think, like Dick mentioned, isolating this lipid - the LPI - was definitely a challenge. Drew Jones, who was the head of the metabolomics core at NYU, was really instrumental in that. There have been a few papers that have measured it, but it’s very challenging. That kind of was the key to this whole idea of the feedback loop: that the LPI lipid and its receptor molecule go up after seizures. This tied everything together. All the seizure work was done in collaboration with multiple labs at NYU and abroad, such as Helen Scharfman at NYU and Gavin Woodhall and Ben Whalley in the UK. A lot of other people also helped.

Prof. Richard Tsien, PhD

Also, Simon Chamberland did a beautiful experiment to show that the excitatory and inhibitory transmission were both affected with different dynamics and consequences in one recording. There was a very nice fit between the immunocytochemistry that Evan and some talented undergraduates did together and Simon’s work. We really enjoyed the team aspect of this. It was like Ocean’s 11 or  Guns of Navarone, where different people had different skills and they all combined to make a more compelling story. But it also required someone with Evan’s tremendous insight, persistence, and willingness to think outside the box to come up with the positive feedback loop. He deserves an enormous amount of credit. We were excited to have had the chance to work together.

Alexander Schering, PhD

Can you tell me about the undergraduate students who were working with you on this project?

Prof. Richard Tsien, PhD

Erica Nebet was an undergraduate student who joined our lab as a freshman and was trained by Evan and Simon. She has actually appeared on multiple papers. I teased her that her positive and irreverent attitude was always a great tonic for us and made us better scientists. She’s now in medical school in an MD-PhD program, trying to decide what she’s going to do with the rest of her life. But this experience with Evan was instrumental in getting her into medical school and launching her in a career combining medicine and science. We like to do that; we have other undergraduates joining the lab now. And people are interested in different things. Some people love the control system aspect of it, the homeostasis, even the math of a positive feedback loop. And other people are just fascinated by anything that could help a patient like Charlotte Figi.

Alexander Schering, PhD

So really a project like this is a generational project.

Prof. Richard Tsien, PhD

It is! I think it’s a great way to get people interested in science. And you know, it may seem a little bit abstract to understand how the brakes and the accelerator work well together. Why would you have both on at the same time? But in fact, that’s the way the brain works. And understanding the basic principles is greatly motivated by the fact that it has a clinical implication.

Alexander Schering, PhD

Before we end the interview, let me ask you something our readers are probably wondering by now. Have you ever tried cannabis?

Prof. Richard Tsien, PhD

Oh, I definitely tried it! And I inhaled! Unlike my Oxford classmate, Bill Clinton — who was there at the same time and claims he never inhaled — I did, because one wants to try things. And we expect that most people in the younger generation are willing to experiment. Because we’re curious as a species, as people.

Alexander Schering, PhD

Did you enjoy it? Was it a good experience? Or was it stressful?

Prof. Richard Tsien, PhD

It was a good experience, but I think I'd rather have a nice glass of wine.

Alexander Schering, PhD

Finally, as a very much related question, where do you find the best food at NYU?

Evan Rosenberg, MD PhD

On campus? *laughs* Oh, man, I haven’t been to NYU in a while. Tisch Cafeteria is actually very good. It's very fancy. So I would go there often. What else is near there? Dick can help me out here. I've been in Philadelphia for like four years.

Prof. Richard Tsien, PhD

For me Starbucks and Au Bon Pain! My wife loves Indian food at Dhaba.

Alexander Schering, PhD

Thank you very much for sitting down with me and providing me and our readers with this wealth of information. I am sure that people are going to get some insights out of this that they didn’t have before. Everyone appreciates your wonderful contributions!

Prof. Richard Tsien, PhD

I appreciate it. And I also appreciate your love of accuracy and clear communication. So I wish you luck with that. And we will tell the chief science writer for NYU, Greg Williams, that all the practice he gave us was very helpful because he emphasized the point that you can't expect people to know what a synapse is, or an axon, or an excitatory transmitter, and so we're trying our best. Yet Neuroscience could be interesting for everyone.

We would like to end this article by mentioning how instrumental the story of Charlotte Figi has been as the catalyst that gave rise to this entire field of research. Sadly, Charlotte passed away during the COVID-19 pandemic and our hearts go out to her parents. Their efforts were nothing less than legendary and countless children with epilepsy are experiencing relief as a direct consequence of their actions.