From Our Neurons to Yours

The cannabinoids within: how marijuana hijacks an ancient signaling system in the brain | Ivan Soltesz

• Wu Tsai Neurosciences Institute at Stanford University, Nicholas Weiler, Ivan Soltesz • Season 6 • Episode 3

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Given the widespread legalization of cannabis for medical and recreational uses, you'd think we'd have a better understanding of how it works. But ask a neuroscientist exactly how cannabinoid compounds like THC and CBD alter our perceptions or lead to potential medical benefits, and you'll soon learn just how little we know.

We know that these molecules hijack an ancient signaling system in the brain called the "endocannabinoid" system (translation: the "cannabinoids within"). These somewhat exotic signaling molecules (made of fatty lipids and traveling "backwards" compared to other transmitters) have been deeply mysterious until recently, when new tools made it possible to visualize their activity directly in the brain.

So what is the "day job" of the endocannabinoid system — and how does it connect to the dramatic highs that come with taking THC or the medical benefits of CBD? 

To unpack all this, we're talking this week with neuroscientist Ivan Soltesz, the James Doty Professor of Neurosurgery and Neuroscience at Stanford, and a leading expert on the endocannabinoid system.

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Nicholas Weiler:

Hey there, Nicholas Weiler here. Before we get started with today's episode, we have just a couple of notes. First, we are very excited that this show has been nominated for a prestigious Signal Award. We are very honored to be a finalist among some other excellent shows. And if you're a fan of this show, you can participate by voting for us in the Listener's Choice category.

Second, we're doing some listener research to help us make this show even better. We want to hear from you to get your input, from your neurons to ours. Send us a note if you'd be willing to help out, and we'll be in touch with some follow-up questions. You can reach us at neuronspodcast@stanford.edu, and you can find that address in the show notes. Thanks so much. Now let's get to today's episode.

This is From Our Neurons to Yours, a podcast from the Wu Tsai Neurosciences Institute at Stanford University, bringing you to the frontiers of brain science. Today, our brain's cannabinoid system.

In recent years, there's been a push here in the US to decriminalize marijuana. It's now possible to buy marijuana for recreational use in almost half of US states. At the same time, there's been an explosion of CBD products derived from the marijuana plant that purport to address a wide variety of medical concerns.

But in terms of how the various cannabinoid molecules in the marijuana plant actually affect our brains, the truth is there's still a lot neuroscientists are just beginning to unpack. It turns out the plant mimics an ancient signaling system in the brain that's used for fundamental tweaking of neural signal processing. These natural chemical signals are called endocannabinoids. While these molecules are named after the cannabis plant, we're actually talking about an unrelated system that evolved millions of years ago and is found across vertebrate brains. Endocannabinoids are part of a fundamental, if slightly weird, signal processing system that's part of the everyday operations of our brains. For example, one recent study finds that disabling endocannabinoids tanks the sensitivity of our internal navigation system, the GPS of the brain that we've discussed on a previous episode with Lisa Giocomo.

So how does endocannabinoid's day job, enhancing signal processing, connect to the dramatic highs that come with taking THC or the medical benefits of CBD? It's only in the past five years that new research tools are making it possible to see how these endocannabinoid signaling molecules work in the living brain. So to unpack all this, we're bringing in an expert who's at the cutting edge of studying the endocannabinoid system.

Ivan Soltesz:

My name is Ivan Soltesz, and I'm a professor in the Department of Neurosurgery at Stanford University, and I'm interested in the cellular synaptic communication that takes place in the brain. In particular, I'm interested in the endocannabinoid system, how neurons use these compounds to communicate with each other and how this system malfunctions in neurological and psychiatric disorders, as well as how they are modulated in response to marijuana-derived compounds.

Nicholas Weiler:

I know that you are very focused on the endocannabinoid system, the system that is affected by cannabis when we ingest it, and that's something I want to spend a lot of our conversation on. But first, I wonder if we could just spend a little time thinking about the things that happen particularly in the brain when people take cannabis. I'm interested in understanding what's going on in the brain and when you come down to it, cannabis and its main derivatives, THC and CBD, are affecting a pretty complex set of things.

I mean, from the research I was doing coming into this conversation, people report cannabis heightening sensory experience, colors, smells, maybe eighties movies, building a sense of meaningfulness. There can be euphoria, potentially some giggles. It changes people's appetite. People get the munchies.

And it has negative effects too. People get forgetful or spacey. People can be clumsy. People can feel anxiety or paranoia. Then there are all kinds of other things like dry mouth and red eyes and effects on the immune system. So that's a whole lot of effects for one plant to have. What do we know at a high level about how compounds like THC and CBD and cannabis are affecting the brain?

Ivan Soltesz:

So let's talk about THC and CBD separately because THC is a agonist of a receptor. That means that it actually acts on a specific molecular entity in the brain. So THC when we inhale it or ingest it and it goes to the brain, it will act on these receptors, and these receptors are basically everywhere in the brain. And that's fundamentally the reason why you can get all kinds of effects that you mentioned.

People who use marijuana, the psychoactive effects are due to the THC part of the marijuana compounds. And as you said, you can feel euphoric, relaxed, and you can also get the munchies. Let's just stop there. Why is that? Well, basically because these diversity of effects involve different brain centers that can modulate a feeling of being rewarded, hunger, cognition, memory, and a variety of other things.

CBD is what we call the non-psychoactive part of the marijuana plant. So CBD on its own is not really changing cognition much. You can think of it as a molecule that attenuates or decreases the THC effects.

Nicholas Weiler:

So they have somewhat opposite effects?

Ivan Soltesz:

Somewhat opposite. It pushes back gently against the THC effects. So for example, why THC may impair learning, CBD in general can enhance learning. The same with anxiety. THC can increase anxiety. It all depends on the dose and the individual, but it can in some individuals increase anxiety. CBD has anti-anxiety effects. So these two compounds, THC and CBD together shape what users experience as euphoria and hunger and being relaxed or amused and so on, both the positive and negative effects, and what the user experiences will heavily depend on the ratio of these two compounds.

Nicholas Weiler:

Interesting. And is this because THC and CBD are acting on different kinds of receptors on different targets throughout the brain?

Ivan Soltesz:

Yes. So THC is molecularly acting on this one receptor, what we call the CB1 receptor. That receptor is the THC's sole target.

CBD is much more promiscuous. CBD acts on no less than 65 different molecular targets. So one can get confused extremely fast once one digs into the literature and tries to understand which one of these may be more important than the other for CBD targets, molecular targets in the brain. But perhaps that's the feature of CBD. It's not a bug that it acts on many things a little bit. And does it act specifically on the CB1 receptor the THC itself targets? There are reports, quite a number, that actually CBD can indeed even at the CB1 receptor level push back against THC activation of the CB1 receptor, but that's controversial like many, many things about CBD.

Nicholas Weiler:

Well, it seems like this field has been really burgeoning in recent years. As more has been learned, there's presumably been more access and more availability to make it possible to study, but it seems like we're still in pretty early days in understanding these brain systems that cannabis is acting on.

Ivan Soltesz:

Absolutely. The brain has these, for example, the CB1 receptors, not because it's waiting for you to smoke marijuana, right?

Nicholas Weiler:

Right.

Ivan Soltesz:

So evolution developed these CB1 receptors for a reason. And the main reason is that the CB1 receptor is waiting there in the specific points in the nervous system to be activated, not by THC necessarily, but some compounds that the brain itself generates. We refer to these compounds that the brain itself generates endocannabinoids.

Nicholas Weiler:

Meaning the cannabinoids from within.

Ivan Soltesz:

Cannabinoids for within, exactly. That's a very good way of putting it, yes.

Nicholas Weiler:

So the endocannabinoids is one of the things that has been the main focus of your research for a number of years. I mean, as we learn more, it seems increasingly clear that cannabis has opened this window onto what seems to me like a very strange and exotic piece of the brain, this endocannabinoid system. It doesn't seem to work like other aspects of brain signaling that we are used to thinking about. Hopefully listeners will join us to geek out a little bit on what is this endocannabinoid system, what do we know about it, and how does it work?

Actually, let me expand on that a little bit. I want to flag two things that stuck out to me, and I hope you'll correct me if I get any of this wrong. So first of all, they're lipids, as in the fatty stuff that our cell membranes are made of. And just to remind listeners, most of the neurotransmitters we think of in the brain, like glutamate or serotonin or dopamine, are the building blocks of proteins. They're amino acids or derived from amino acids. But endocannabinoids are pretty unique as a lipid-based neurotransmitter. There aren't other lipids that the brain uses for signaling as far as we know.

Ivan Soltesz:

Right. So definitely the endocannabinoids are by far the biggest part of these what we call lipid messengers. And that's interesting in itself because the brain, if you take a brain and you just break it down, how much nucleic acid do I have? How much proteins do I have? How much lipids do I have in the brain? Well, actually most of the brain is made of lipids. But as you said, much of the lipids is used to make cell membranes or wrapping around the neuronal processes like an insulation on a cable to make the signals go faster.

But in terms of molecules that are being used to signal between nerve cells, and we can talk about exactly how that happens, that's really the endocannabinoid molecules that do that.

Nicholas Weiler:

Okay. So we've got first on the one hand they're lipids, which is an unusual choice for a signaling molecule. And then the second thing that's unusual about endocannabinoids is that they work backwards compared to other neurotransmitters. Most neurotransmitters send signals from cell A to cell B through a synapse traditionally thought of as a one-way information channel. But endocannabinoids are released by the receiving end of the synapse by cell B in response to an incoming signal from cell A and they go backwards or to other nearby cells. So this suggests that endocannabinoids may work in ways that are pretty different from most of the neurotransmitters we're accustomed to thinking about.

Ivan Soltesz:

That's absolutely correct. So it was around the early 1990s where people noticed that traditionally neuron A would talk to neuron B, but B wouldn't talk to neuron A. And people noticed that, oh, in fact, there is something that happens when neuron B is activated. It's firing spikes. It's electrically active, and something comes out of that cell that goes backward and affects cell A at the synapse.

Nicholas Weiler:

I want to stick with this retrograde signaling bit for a moment because we'll come back to it in the example of epilepsy, which you've also studied. So you had a recent study just earlier this year that helped me conceptualize, and I think probably has helped the field conceptualize, what this retrograde signaling may be doing, at least in some cases.

So it touched on place cells in the hippocampus, which is something we've talked about before on the show with Lisa Giocomo and others, the brain's GPS system in the hippocampus. And your study revealed something fundamental about how endocannabinoids may be changing how information is processed in this circuit. Can you tell us a little bit about what you found there?

Ivan Soltesz:

Yes. So let's go back to our little example about cell A influencing cell B. What cannabinoids do is that they actually signal back from cell B towards cell A. So what we showed was that, and this was a big question in the field, what amount of activity that hypothetical cell B need to have in order to produce these endocannabinoids? That was the big question. What triggers it? Because the way people studied retrograde signaling by endocannabinoids was not in the living brain. They extracted parts of the brain, put it in a dish, and then studied these kind of signalings in a dish.

There, neuron B, in our example, we would make it fire a lot and then you would see these effects, the retrograde signaling effects, but whether that kind of activity was anywhere near realistic was not known. So we now have tools that we could show that in the part of the brain that you refer to as the brain's GPS system, these neurons, what we call place cells that tells you where you are in space or tells the mouse where it is in space, they signal, oh, I'm in this part of the space, this little GPS cell is going off, and that relatively small amount and totally natural activity is enough indeed to generate endocannabinoids that then cross the synapse and modulate neurotransmitter release.

Nicholas Weiler:

Huh. So it's not an extreme situation thing. It's a everyday function. At least in this case, whenever these neurons are sending signals, they're getting feedback, in a sense. The synapse is getting feedback-

Ivan Soltesz:

Exactly, exactly.

Nicholas Weiler:

...through the endocannabinoid system.

Ivan Soltesz:

That was the major insight in our paper, that completely normal activity is sufficient to generate these endocannabinoid substances. And we also showed that they indeed signal back to cell A, and cell A's ability to influence cell B is reduced as a result of endocannabinoid retrograde action. And all of this is in a living animal, and it happens every time you, for example, walk around, your brain, your GPS system is going off I'm in this part of my room now. I'm in the middle of the room. Now I'm in the corner. Each of those little positions, different cells will be active in your neuronal GPS. This little activity, neuronal activity is enough to generate the endocannabinoids and modulate the input to those neurons.

Nicholas Weiler:

I just wanted to go back to that for a moment and make sure I understood. So did you say that the endocannabinoid system is reducing the signaling from cell A to cell B? I had read that as it's increasing the signal-to-noise ratio, but maybe I'm misunderstanding.

Ivan Soltesz:

No, you did not. So cell B is essentially saying, you can imagine perhaps this is the best way of putting it, that when cell B is active in your GPS, cell B is saying I'm in the middle of the room, for example, and what it does in a sense is that it's telling all the other cells in your GPS, "I am talking now. You should reduce the signals that you are sending to the rest of the brain because I am the one who is saying something important," which is that you are in the middle of the room. So yes, in that sense, it does enhance a signal-to-noise ratio. That's how we conceptualize it.

So the fundamental idea here is that when a neuron is naturally active because it signals something, it makes sense to tell the other cells in the vicinity and the other communicating cells in the network that, "Hey, I'm talking now. Listen to me. I'm saying something important." And that's what we mean by this signal-to-noise enhancing capability of the CB1 receptor-dependent, the endocannabinoid system.

And indeed, when we remove CB1 receptors from synapses using genetic means, we can show that the ability of the GPS neurons to signal precisely the space where the mouse is located is decreased. In other words, the CB1 receptors that are located on the terminals, axon terminals of cell A, actually do something very important so that when cell B is active and releases endocannabinoids, and these endocannabinoids go back and tell cell A through these CB1 receptors on its terminals that you shouldn't be talking as much, that actually is important.

And once again, how do we know that? Because if we essentially block this signaling by removing the CB1 receptors so the endocannabinoids now just float away, they can't bind into anything, then the whole GPS system becomes a little bit less precise.

Nicholas Weiler:

A little bit noisier. It reminds me a little bit of the cocktail party problem where there's so many voices going on that you need to be able to focus in on just one voice. My recollection of neuroscience classes from back in the day says it's by reducing the input of other voices and increasing the volume of the voice you're trying to listen to.

Ivan Soltesz:

Exactly.

Nicholas Weiler:

So I know that this was recent work. Does this imply to you that this may be how the endocannabinoid system is working across the brain through this signal enhancing property, or do you think this is just one of many ways that the endocannabinoid system is affecting the brain?

Ivan Soltesz:

We mentioned at the beginning of our conversation that the CB1 receptors are really in most places in the brain, really throughout. And by the way, not just in the brain, they're also in the spinal cord, so they are really all across the central nervous system. It is in the brain's GPS system, what we call the hippocampus, where we actually understand this to the level that we can even track these molecules in real time using new molecular tools in the living brain. So we have a really high-level understanding of what goes on with these endocannabinoid signaling systems in the hippocampus, the GPS part of the brain.

But we do know that the CB1 receptors are there in other parts of the brain, the reward center, the appetite stimulating center, and so on. And we know that fundamentally this kind of backward signaling occurs in all of these parts of the brain.

And so now that we have these wonderful new tools that made our study possible, indeed scientists can go and study the endocannabinoid system in the living brain in all of these parts of the brain. There is now no technical reason why we couldn't actually do this and ask the question, okay, how does precisely hunger, why does it occur in that part of the brain when people excite cannabinoid receptors?

Nicholas Weiler:

That's exciting. It's just striking me, and it may be striking listeners. I'd love to get your take on this. This is a bit of a speculation, but in my mind, one of the commonalities between different effects of THC is that it seems to both amplify a lot of things, food seems tastier, your ideas seem smarter, but also muddy the waters where different things may feel connected that normally wouldn't feel connected. Do you see any potential connection here between this very circuit-oriented, how is the brain processing information and some of those higher level experiences, or is that pretty uncharted territory at this point?

Ivan Soltesz:

I think it's a little uncharted in the sense that now again, we have these tools where we could track not just the endocannabinoids, but also THC itself. Since THC will activate the CB1 receptor, we can actually track that too. It hasn't been done really to any great degree, but that's technically possible.

But going back to your question, so the fundamental difference between when an endocannabinoid gets generated by the natural brain activity and when we inhale THC and activate the same receptors, is that in the first case, in the natural case, it's cell B that's active and it is telling the other cells to be quiet, essentially. Don't talk to me now. I'm talking. Don't disturb me with what you have to say because I'm talking.

In the case of THC when people inhale it or apply it to the brain, it's essentially acting on, as far as we can tell, on many, many brain centers on many neurons, not just in this case, neuron A, but it's also acting on neuron B. And so the problem is that you essentially flood the brain with what we call an exo-cannabinoid, which just means we applied it ourselves from the outside world, we inhaled THC. As opposed to the endocannabinoid system that signals in an extremely specific manner in space, but also in time because the signal that goes from B to A is very short-lived, is only there for a couple of seconds at the most.

And that's a very important thing because when you're in the middle of the room and your hypothetical neuron B is saying, "I'm talking now," and you generate these endocannabinoids that suppress the noise around it, if you want, you don't want that to happen when you moved on to the other room because now that cell has to be active that represents the other room or the corner of the room.

So the way the GPS system can function with high precision through this mechanism is that this retrograde signal that is mediated by the endocannabinoid system has to be very, very short-lived because if it would be lasting for half an hour, then you couldn't really use this system for helping you with precise navigation in space.

Nicholas Weiler:

Right, and it's also very, very local within the circuit. It's just that cell talking to its immediate neighbors.

Ivan Soltesz:

Exactly. So both in space and time, it is very precise when it's endocannabinoid-mediated. But when it's THC, which is of course coming from the outside, from the marijuana plant, then this precision is lost both in space and in time. The THC is going to be around for a while. Users know that. And so therefore, that is going to, in difficult to predict ways, but it's going to influence the endocannabinoid system, not just in the hippocampus, the GPS of the brain, but also in all the other centers, the reward center, the cognition center, the memory centers, pain centers and all that.

Nicholas Weiler:

Interesting. So if the endocannabinoid system is providing this fundamental feedback and signal-to-noise control in regular brain signaling, then flooding the brain with that signal is going to essentially, I imagine, make all the neurons be trying to quiet each other down at the same time and over a long period of time.

Ivan Soltesz:

Exactly.

Nicholas Weiler:

Which would have unpredictable results. It's changing the entire signaling paradigm of the brain, which maybe explains why it has such psychoactive effects. It's just going to change the way that cells are talking to each other.

Ivan Soltesz:

That's exactly right. And that's why THC is going to have effects that can go from very, very nice effects, euphoria, being amused and all that, feeling giggly to psychosis-like effects and increase in anxiety and impaired learning. It all depends on exactly how it's smudging that system, smearing the precision in brain communication. And it can have a variety of positive effects, but also a variety of potentially negative effects.

Nicholas Weiler:

Well, speaking of negative effects, so that brings me to one of the last things I wanted to talk about. You've been studying the connection between these endocannabinoid signaling systems in the brain and epilepsy, and I know that there's interest in potential uses of CBD as a potential treatment for some forms of epilepsy, but what is the connection between the endocannabinoid system and epilepsy?

Ivan Soltesz:

Yes. So the endocannabinoid system, as we just said, normally acts in this very highly spatially and temporally specific manner. And what our research shows is that during seizures, neurons are of course hyperactive. They show too much activity. And frequently that activity is synchronous, so many neurons fire at the same time. That's what we see as a seizure-like event or a seizure event.

And during this excessive activity, the endocannabinoid system is essentially put into overdrive. That excessive neural activity now generates too much endocannabinoids. And a little bit like what we just discussed with THC, this overproduction of the endocannabinoid molecules during seizures leads to a loss of that precision in signaling. And we can see that with our new sensors in that, oh, huge amounts of endocannabinoids are being generated by seizures. Now, this large wave of endocannabinoids then spreads across the neuronal network and basically causes the loss of precision signaling that is normally mediated by the endocannabinoids.

So there's a loss in both spatial and temporal precision. And what our research also showed that a large wave of endocannabinoids that are being generated during the seizure actually also leads to all kinds of not-so-good downstream effects. For example, it can get actually converted to a class of compounds that can generate brain inflammation and can also result in the constriction of blood vessels causing a decrease in the blood supply to the brain.

So the seizures really lead to both an immediate effect in that the endocannabinoid production as a result of the excessive neural activity leads to the loss of precision in endocannabinoid signaling, but it also causes medium and long-term effects through conversion of the endocannabinoid molecules that are normally broken down really fast in small amounts.

Now, this breakdown occurs later, and there is, of course, then a corresponding wave of byproducts from the enzymatic breakdown of the endocannabinoids leading to all these effects, like I mentioned, constriction of blood supply, and longer term we believe can also lead to brain inflammation.

Nicholas Weiler:

So from your description, it sounds a little bit like the effects of epilepsy or of a seizure on the endocannabinoid system are in some ways pretty similar to what you would expect to see with THC. Am I hearing that right, or are there some distinctions there that would be worth highlighting?

Ivan Soltesz:

That's basically correct. So I would say that during a seizure, it's typically still, at least at the beginning of the seizure, what we call in the case of focal seizures, they're called focal because they don't engage the entirety of the brain. And many of the seizures that people experience are this type, that is they are focal. So they still only if you want flood only a part of the brain. Whereas THC that people inhale is typically flooding many, many centers in the brain. But again, it's all a question of what type of epilepsy we talk about, and also how much THC is there in the marijuana that a particular individual may be smoking, for example.

Nicholas Weiler:

So given that there are these new tools now available for studying the activity and then the function of these endocannabinoids, and presumably also the effects of exo-cannabinoids like cannabis derivatives, I imagine that listeners who have been following the burgeoning cannabis industry who are interested in the more medical applications with seizures, or whether CBD can have various beneficial effects. I know that this is all in some ways very early stage and there's a lot to be learned. What do you think people should be paying attention to? What are some of the big questions that you think may be answered or at least answerable in the next few years to help people better understand what this system reveals about the brain?

Ivan Soltesz:

I think that it's definitely good news that CBD alone can have beneficial effects in, for example, a group of children with severe forms of developmental epilepsy. That's really good news. And that was actually the first drug in 2018 that the Federal Drug Administration approved CBD as a marijuana extract to be used in the treatment of these severe forms of childhood epilepsies.

But it should be said that not every child is benefiting from this or reacting to this positively, to this drug. And even those where it's positive, they can still have side effects, all kinds of side effects. So clearly where we can go more in terms of the research is to better understand the endocannabinoid system and related systems so we're using these novel tools, for example, the sensor where we can pick up endocannabinoids and exo-cannabinoids or our ability to track the CB1 receptors.

We didn't mention this, but also we have now beautiful new tools where we can resolve individual CB1 receptors in the microscope and see how that CB1 receptor moves when it's exposed for a long time for hours to THC, for example. That's also pretty revolutionary and new. We can manipulate neurons using new techniques and manipulate what level of activity is needed in neuron A and neuron B's communication to engage this network and how these kind of things differ between brain centers from the reward center to cognition and memory and all that.

So I would say just generally, the time is really ripe now. We have the right tools at multiple levels to for the first time track molecular signaling mediated by the endocannabinoid system and its engagement by the exo-cannabinoid system in the living brain, whether it's in response to natural brain activity or in response to seizures or in response to being exposed to THC or CBD at various combinations.

So I would say that all of these technical breakthroughs make it really exciting to study the cannabinoid system. And I think our listeners will hear a lot in the news about neuroscience is really advancing this field really, really rapidly.

And of course, the regulation controlling the availability of THC and CBD for researchers is also changing. And it's a very good thing because I can tell you that in my lab, we spent untold days filling out forms and asking for permission to use a minute amount of THC, whereas you can go down in Palo Alto and buy marijuana in a shop. So I'm very pleased to say that these things are changing now.

Nicholas Weiler:

It's exciting to hear how many ways this field is accelerating to teach us about the brain to help us understand these compounds that people take for entertainment or for medical purposes. And it brings back a theme that's come up often on the show, that as our knowledge increases as we get more and more precise, we can understand exactly what is happening in which circuit of the brain and which molecule and which receptor and so on.

You could imagine a future where if someone is a chemotherapy patient that needs to have their appetite increased, that we could really focally target some of these hunger-related systems. If someone really just wants the entertainment value and we're trying to get rid of~ you could imagine ways to reduce some of the potentially negative side effects, like understanding these things is really going to help understand not only our own brains, but also what these compounds that people ingest are doing. So thank you so much for giving us so much to think about and for joining us on the show.

Ivan Soltesz:

My pleasure. It was great talking to you. Thank you.

Nicholas Weiler:

Thanks again so much to our guest, Ivan Soltesz. Ivan Soltesz is the James R. Doty professor of neurosurgery at Stanford University School of Medicine. To read more about his work, check out the links in the show notes.

If you're enjoying the show, please subscribe and share with your friends. It helps us grow as a show and bring more listeners to the frontiers of Neuroscience.

As we mentioned at the top, we'd love to hear from you. Tell us what you love or what you hate in a comment on your favorite podcast platform, or send us an email at neuronspodcast@stanford.edu. From Our Neurons to Yours is produced by Michael Osborne at 14th Street Studios, with production assistance from Morgan Honaker. I'm Nicholas Weiler, until next time.