Thanks for being patient enough to go through and clarify your confusion!
About the pyramidal cells—I should have been more specific and said that prefrontal cortex [as opposed to primary motor cortex] - AFAIK does not have output pyramidal cells in Layer V. Those are Betz cells and basically only the primary motor cortex has them, although Wikipedia (on Betz cells and pyramidal cells) tells me the PFC has any neurons that qualify as “pyramidal neurons”, too; it looks like their role in processing is markedly different from the giant pyramidal neurons found in the primary motor cortex’s Layer 5.
Pyramidal neurons in the prefrontal cortex are implicated in cognitive ability. In mammals, the complexity of pyramidal cells increases from posterior to anterior brain regions. The degree of complexity of pyramidal neurons is likely linked to the cognitive capabilities of different anthropoid species. Pyramidal cells within the prefrontal cortex appear to be responsible for processing input from the primary auditory cortex, primary somatosensory cortex, and primary visual cortex, all of which process sensory modalities.[21] These cells might also play a critical role in complex object recognition within the visual processing areas of the cortex.[3] Relative to other species, the larger cell size and complexity of pyramidal neurons, along with certain patterns of cellular organization and function, correlates with the evolution of human cognition. [22]
This is technically compatible with “pyramidal neurons” playing a role in schizophrenic hallucinations, but it’s not clear how there’s any correspondence with the A vs B [vs C] ratio concept.
Maybe I slightly misunderstood your original theory, if you are not trying to say here, in general, that there is an “action-origination” signal that originates from one region of cortex, and in schizophrenics the major data packet [“B”] and the warning signal [“C”] experience different delays getting to the target.
If you are postulating a priori that the brain has a capability to begin the “B” and “C” signals in different regions of cortex at the same time, then how can you propose to explain schizophrenia based on intra-brain communication delay differentials at all? And if it’s just signal strength, rather than signal speed, why bring “A” into it, why not just have “B” and “C”?
My own view is: Antipsychotics block dopamine receptors. I think you’re right that they reduce a ratio that’s something like your B/A ratio. But I can’t draw a simple wiring diagram about it based on any few tracts. I would call it a Q/P ratio—a ratio of “quasi-volition”, based on dopamine signaling originating with the frontal cortex and basal ganglia, and perception, originating in the back half of the cortex and not relying on dopamine.
Illustration of how the Q/P idea is compatible with antipsychotics reducing something like a B/A ratio in the motor case: Antipsychotics cause “extrapyramidal” symptoms, which are stereotyped motions of the extremities caused by neurons external to the pyramidal [corticospinal] tract. As I understand it, this is because one effect of blocking dopamine receptors in the frontal lobe is to inhibit the activity of Betz cells.
I don’t think time-delays are important at all here.
The part where I wrote “we gradually increase the “volume” of a part of cortex…” is trying to pedagogically explain something; I wasn’t literally saying that the “volume” actually increases “gradually” in the brain.
I have now rewritten that paragraph to avoid all mention of time (i.e. “first” and “second”). I also added a new diagram. Hope that’s clearer now, for you and anyone else who reads this going forward! Sorry for any confusion and thanks for feedback.
I still think you’re wrong about various aspects of pyramidal cells, but maybe we’ll have to agree to disagree on some of the issues here. :)
Thanks for clarifying. The point where I’m at now is, as I said in my previous comment,
if it’s just signal strength, rather than signal speed, why bring “A” [cortico-cortical connections] into it, why not just have “B” [“quasi-volitional” connections] and “C” [“perceptual” connections]?
Hmm, this seems really obvious to me, so maybe we’re talking past each other somehow.
In this oversimplified picture, we’re supposing that somatosensory cortex is tasked with trying to figure out exactly where and how the arm will be moving in the immediate future.
How does the somatosensory cortex do that? Well, it takes whatever input data it has access to, and builds a (very-short-term) predictive model that leverages that data.
The input data is critical. In general, in life, you can’t make predictions if you have absolutely nothing to go on. If you ask me to predict who’s going to win the football match, but don’t tell me which teams are playing, then all I can do is guess randomly. If you tell me the teams, I can do a bit better; if you tell me their records so far this season, I can do even better; if you tell me which players are injured today, then I can do better yet; etc. More relevant input data enables better predictions.
Anyway, what’s the input data that the somatosensory cortex can use for its predictions? Well, visual data is helpful—maybe you see that your hand is heading towards a wall. Proprioceptive data is obviously helpful—for example, if the arm is already fully extended then you can be confident that it won’t extend further. And then there’s data from all sorts of random slow interoceptive fibers, like muscle strain sensors or whatever. All that data and more is good and helpful for the somatosensory cortex to issue accurate predictions of exactly where and how the arm will be moving in the immediate future.
…But those predictions are still going to be way off if the somatosensory cortex isn’t getting any data indicating what motor cortex is up to. Like, let’s say some part of motor cortex decides it’s a good time to move my arm, and then starts sending appropriate signals to motoneuron pools or whatever. But also assume there’s no data going from motor cortex to somatosensory cortex. Then obviously the somatosensory cortex would have no idea what the motor cortex is up to, and would issue very bad predictions regarding how my arm is about to move. Right?
I agree that the somatosensory cortex [in the case of arm movements, actually mostly the parietal cortex, but also somewhat the somatosensory] needs to be getting information from the motor cortex [actually mostly the DLPFC, but also somewhat the motor] about what to expect the arm to do!
This necessary predictive-processing “attenuate your sensory input!” feedback signal, could be framed as “A [C]”, such that “weak A [C]” might start giving you hallucinations.
However, in order for the somatosensory cortex to notice a prediction error and start hallucinating, it has to be receiving a stronger [let’s say “D”] signal, from the arm, signifying that the arm is moving, than the “weak A [C]” signal signifiying that we moved the arm.
I don’t think your theory predicts this or accounts for this anyhow?
My “Q/P” theory does.
[ “B” in your theory maps to my “quasi-volition”, ie anterior cortex, or top-down cortical infrastructure.
Every other letter in your theory—the “A”, “C”, and “D”—all map to my “perception”, ie posterior cortex, or bottom-up cortical infrastructure. ]
Thanks for being patient enough to go through and clarify your confusion!
About the pyramidal cells—I should have been more specific and said that prefrontal cortex [as opposed to primary motor cortex] - AFAIK does not have output pyramidal cells in Layer V. Those are Betz cells and basically only the primary motor cortex has them, although Wikipedia (on Betz cells and pyramidal cells) tells me the PFC has any neurons that qualify as “pyramidal neurons”, too; it looks like their role in processing is markedly different from the giant pyramidal neurons found in the primary motor cortex’s Layer 5.
This is technically compatible with “pyramidal neurons” playing a role in schizophrenic hallucinations, but it’s not clear how there’s any correspondence with the A vs B [vs C] ratio concept.
Maybe I slightly misunderstood your original theory, if you are not trying to say here, in general, that there is an “action-origination” signal that originates from one region of cortex, and in schizophrenics the major data packet [“B”] and the warning signal [“C”] experience different delays getting to the target.
If you are postulating a priori that the brain has a capability to begin the “B” and “C” signals in different regions of cortex at the same time, then how can you propose to explain schizophrenia based on intra-brain communication delay differentials at all? And if it’s just signal strength, rather than signal speed, why bring “A” into it, why not just have “B” and “C”?
My own view is: Antipsychotics block dopamine receptors. I think you’re right that they reduce a ratio that’s something like your B/A ratio. But I can’t draw a simple wiring diagram about it based on any few tracts. I would call it a Q/P ratio—a ratio of “quasi-volition”, based on dopamine signaling originating with the frontal cortex and basal ganglia, and perception, originating in the back half of the cortex and not relying on dopamine.
Illustration of how the Q/P idea is compatible with antipsychotics reducing something like a B/A ratio in the motor case: Antipsychotics cause “extrapyramidal” symptoms, which are stereotyped motions of the extremities caused by neurons external to the pyramidal [corticospinal] tract. As I understand it, this is because one effect of blocking dopamine receptors in the frontal lobe is to inhibit the activity of Betz cells.
I don’t think time-delays are important at all here.
The part where I wrote “we gradually increase the “volume” of a part of cortex…” is trying to pedagogically explain something; I wasn’t literally saying that the “volume” actually increases “gradually” in the brain.
I have now rewritten that paragraph to avoid all mention of time (i.e. “first” and “second”). I also added a new diagram. Hope that’s clearer now, for you and anyone else who reads this going forward! Sorry for any confusion and thanks for feedback.
I still think you’re wrong about various aspects of pyramidal cells, but maybe we’ll have to agree to disagree on some of the issues here. :)
Thanks for clarifying. The point where I’m at now is, as I said in my previous comment,
Hmm, this seems really obvious to me, so maybe we’re talking past each other somehow.
In this oversimplified picture, we’re supposing that somatosensory cortex is tasked with trying to figure out exactly where and how the arm will be moving in the immediate future.
How does the somatosensory cortex do that? Well, it takes whatever input data it has access to, and builds a (very-short-term) predictive model that leverages that data.
The input data is critical. In general, in life, you can’t make predictions if you have absolutely nothing to go on. If you ask me to predict who’s going to win the football match, but don’t tell me which teams are playing, then all I can do is guess randomly. If you tell me the teams, I can do a bit better; if you tell me their records so far this season, I can do even better; if you tell me which players are injured today, then I can do better yet; etc. More relevant input data enables better predictions.
Anyway, what’s the input data that the somatosensory cortex can use for its predictions? Well, visual data is helpful—maybe you see that your hand is heading towards a wall. Proprioceptive data is obviously helpful—for example, if the arm is already fully extended then you can be confident that it won’t extend further. And then there’s data from all sorts of random slow interoceptive fibers, like muscle strain sensors or whatever. All that data and more is good and helpful for the somatosensory cortex to issue accurate predictions of exactly where and how the arm will be moving in the immediate future.
…But those predictions are still going to be way off if the somatosensory cortex isn’t getting any data indicating what motor cortex is up to. Like, let’s say some part of motor cortex decides it’s a good time to move my arm, and then starts sending appropriate signals to motoneuron pools or whatever. But also assume there’s no data going from motor cortex to somatosensory cortex. Then obviously the somatosensory cortex would have no idea what the motor cortex is up to, and would issue very bad predictions regarding how my arm is about to move. Right?
I agree that the somatosensory cortex [in the case of arm movements, actually mostly the parietal cortex, but also somewhat the somatosensory] needs to be getting information from the motor cortex [actually mostly the DLPFC, but also somewhat the motor] about what to expect the arm to do!
This necessary predictive-processing “attenuate your sensory input!” feedback signal, could be framed as “A [C]”, such that “weak A [C]” might start giving you hallucinations.
However, in order for the somatosensory cortex to notice a prediction error and start hallucinating, it has to be receiving a stronger [let’s say “D”] signal, from the arm, signifying that the arm is moving, than the “weak A [C]” signal signifiying that we moved the arm.
I don’t think your theory predicts this or accounts for this anyhow?
My “Q/P” theory does.
[ “B” in your theory maps to my “quasi-volition”, ie anterior cortex, or top-down cortical infrastructure.
Every other letter in your theory—the “A”, “C”, and “D”—all map to my “perception”, ie posterior cortex, or bottom-up cortical infrastructure. ]