Dr. Terry Sejnowski

Yeah, auditory hallucinations, paranoia, very, very advanced. You'd say that, my God, this person here has become a schizophrenic. And this is really, like you say, the symptoms are the same. However, if you isolate them for a couple of days, they'll come back. Right?

Yeah, auditory hallucinations, paranoia, very, very advanced. You'd say that, my God, this person here has become a schizophrenic. And this is really, like you say, the symptoms are the same. However, if you isolate them for a couple of days, they'll come back. Right?

Yeah, auditory hallucinations, paranoia, very, very advanced. You'd say that, my God, this person here has become a schizophrenic. And this is really, like you say, the symptoms are the same. However, if you isolate them for a couple of days, they'll come back. Right?

So it means that schizophrenia can induce, I'm sorry, ketamine can induce a form of schizophrenia, psychosis, temporarily, not permanently fortunately. Okay, so what does it attack? Okay, and there's another literature on this. It turns out that it binds to a form of receptor, a glutamate receptor called NMDA receptors, which are very important by way for learning and memory.

So it means that schizophrenia can induce, I'm sorry, ketamine can induce a form of schizophrenia, psychosis, temporarily, not permanently fortunately. Okay, so what does it attack? Okay, and there's another literature on this. It turns out that it binds to a form of receptor, a glutamate receptor called NMDA receptors, which are very important by way for learning and memory.

So it means that schizophrenia can induce, I'm sorry, ketamine can induce a form of schizophrenia, psychosis, temporarily, not permanently fortunately. Okay, so what does it attack? Okay, and there's another literature on this. It turns out that it binds to a form of receptor, a glutamate receptor called NMDA receptors, which are very important by way for learning and memory.

But we know the target, and we also know what the acute outcome is that it... reduces the strength of the inhibitory circuit, the interneurons that use inhibitory transmitters. The enzyme that creates the inhibitory transmitter is downregulated. And what does that do? It means that there's more excitation. And what does that mean when there's more excitation?

But we know the target, and we also know what the acute outcome is that it... reduces the strength of the inhibitory circuit, the interneurons that use inhibitory transmitters. The enzyme that creates the inhibitory transmitter is downregulated. And what does that do? It means that there's more excitation. And what does that mean when there's more excitation?

But we know the target, and we also know what the acute outcome is that it... reduces the strength of the inhibitory circuit, the interneurons that use inhibitory transmitters. The enzyme that creates the inhibitory transmitter is downregulated. And what does that do? It means that there's more excitation. And what does that mean when there's more excitation?

It means that there's more activity in the cortex, and there's actually much more vigor, and you start becoming crazy, right, if it's too much activity. So this is interesting. So this is telling us, I think, that we should be thinking about – and now there's a whole field now in psychiatry that has to do with the glutamate hypothesis for the first – where the actual – imbalance first occurs.

It means that there's more activity in the cortex, and there's actually much more vigor, and you start becoming crazy, right, if it's too much activity. So this is interesting. So this is telling us, I think, that we should be thinking about – and now there's a whole field now in psychiatry that has to do with the glutamate hypothesis for the first – where the actual – imbalance first occurs.

It means that there's more activity in the cortex, and there's actually much more vigor, and you start becoming crazy, right, if it's too much activity. So this is interesting. So this is telling us, I think, that we should be thinking about – and now there's a whole field now in psychiatry that has to do with the glutamate hypothesis for the first – where the actual – imbalance first occurs.

It's an imbalance between the excitatory-inhibitory systems that are in the cortex that keep you in balance.

It's an imbalance between the excitatory-inhibitory systems that are in the cortex that keep you in balance.

It's an imbalance between the excitatory-inhibitory systems that are in the cortex that keep you in balance.

That's one class. That's right. Okay, so now... Here is a hypothesis for why ketamine might be good for depression. People are taking it now who are depressed, right? So here you have a drug that causes overexcitation, and here you have a person who is underexcited. Depression is associated with lower excitatory activity in some parts of the cortex.

That's one class. That's right. Okay, so now... Here is a hypothesis for why ketamine might be good for depression. People are taking it now who are depressed, right? So here you have a drug that causes overexcitation, and here you have a person who is underexcited. Depression is associated with lower excitatory activity in some parts of the cortex.

That's one class. That's right. Okay, so now... Here is a hypothesis for why ketamine might be good for depression. People are taking it now who are depressed, right? So here you have a drug that causes overexcitation, and here you have a person who is underexcited. Depression is associated with lower excitatory activity in some parts of the cortex.

Well, if you titrate it, you can come back into balance, right? So what you do is you fight depression with schizophrenia, a touch of schizophrenia. Now, you have to keep giving. I think once every three weeks, they have to have a new dose of ketamine. But it's helped an enormous number of people with very, very severe clinical depression.

Well, if you titrate it, you can come back into balance, right? So what you do is you fight depression with schizophrenia, a touch of schizophrenia. Now, you have to keep giving. I think once every three weeks, they have to have a new dose of ketamine. But it's helped an enormous number of people with very, very severe clinical depression.