Haven’t been on here in a while. I happen to have a pretty good understanding of HTM theory and some knowledge of neuroscience. I’ve got my own ideas on how it might interact with the cortex. Maybe if I’m not completely wrong, I can help point you guys in the right direction, or at least bring up some interesting talking points.
So on the BG:
A Few Things I Know:
- The basal ganglia mainly consists of the striatum, globus pallidus (internal and external parts), and a few other small nuclei.
- The striatum gets a lot of input from the cortex (from an occulomotor area in the occipital lobe, and from pretty much the entire frontal lobe).
- The striatum also gets inputs from a few dopaminergic nuclei. It then sends outputs along two different pathways; one excited by the dopamine, one inhibited by it. The excitatory pathway (called the direct pathway) outputs directly to the Internal Globus Pallidus (GPi), and the inhibitory pathway (the indirect pathway) outputs to the External Globus Pallidus (GPe), which then outputs to the GPi. The GPi then outputs to the thalamus, which relays signals back the the cortex.
- GPi and GPe only produce inhibitory outputs and don’t appear to do any learning. The inhibitory outputs (including those to the thalamus) end up being disinhibitory, meaning that an inhibitory signal from one area in the basal ganglia to another ends up leading to an excitatory signal being sent somewhere else. For example, an inhibitory signal from teh GPi to the thalamus ends up sending an excitatory signal to the cortex.
- There are a few other minor pathways, but those are the main two.
- The frontal lobe is structured in a hierarchy (limbic system at the base, motor at the top, and various prefrontal areas in the middle, which feature a lot of connections to non-frontal areas), and each part has an associated part of the basal ganglia it communicates with. The output from the thalamus back to the cortex feeds back into the same part of the cortex that the input originated from, forming a loop.
- The striatum is known to be active in learning, the other areas of the basal ganglia, not so much. The dopaminergic inputs to it are very strongly connected to the limbic system.
- Damage to the basal ganglia tends to have few immediate effects, but in the long term leads to erratic behavior. For example, Parkinson’s and Huntington’s diseases.
- Motor output appears to be based on population coding; i.e, a large number of neurons control the same muscle, and the more neurons that fire, the more the muscle contracts.
What I Don’t Know:
- How exactly does the striatum learn? Does it use some form of sequence memory? Something related to spatial pooling? Something else?
- How precise are these loops (Cortex -> Striatum -> GP -> Thalamus -> Cortex)? Does the thalamus excite the same group of neurons that triggered it (my guess is yes)? If so, is it the same column? Same minicolumn? Same neuron?
What I Think is Going On
This won’t be everything I think is going on; just a basic summary of the most important ideas.
The frontal lobe is structured in a hierarchy. The base of the hierarchy consists of various areas of the cingulate cortex, which gets inputs primarily from the limbic system and control high-level goals (stay happy, avoid pain, etc.). The next level up appears to be the orbitofrontal cortex, which gets inputs from the cingulate cortex, as well as the amygdala and a couple other areas. It’s known to be involved in moral decision making. The next couple levels are various prefrontal areas, such as the dorsolateral prefrontal cortex. These areas have very strong connections to pretty much every other area of the brain, especially high-level areas in the temporal and parietal lobes. It’s known to be where the Where/What sensory pathways in the cortex seem to converge. These areas are known to be very involved in abstract thinking, decision making, working memory (they’re strongly connected to the hippocampus too), and strategic thinking. They then feed into the premotor areas (which are very strongly connected to the high-level somatosensory cortex), and then into the motor areas (strongly connected to the low-level somatosensory cortex).
Every level of the hierarchy I just mentioned has strong connections with the basal ganglia.
What I think is going on in the frontal lobe is that abstract goals originate in or near the limbic system, and the higher levels of the frontal hierarchy work to convert them into increasingly specific and flexible goals, gradually incorporating information from sensory regions as appropriate.
So what is the basal ganglia doing? Reinforcement learning.
What I think is going on is that the limbic system is constantly determining if the inputs are producing results that meet the goals (be happy, avoid pain, etc). If they are, they send positive reinforcement to the striatum, and if not, negative reinforcement. However, I believe the striatum is learning two representations of the output of the cortex; one that represents patterns associated with positive reinforcement, and one that learns patterns associated with negative reinforcement. The positive patterns output to the direct pathway, and the negative to the indirect pathway. The output is a pair of SDRs, each likely a subset of some high-level activity in the cortex.
The globus pallidus then appears to run the biological equivalent to a bitwise AND operation on the SDRs, with the input from the indirect pathway inverted. Essentially, it only allows bits through that are associated with positive reinforcement, and not associated with negative reinforcement (as it’s conceivable that a bit in the SDR could be associated with both). Because of how the logic works, a negative of this SDR is sent to the thalamus, and the thalamus then inverts it, and sends the signals to the cortex as a bias signal.
TL;DR : The cortex sends an SDR to the striatum. The striatum splits it into two SDRs; one featuring only the bits associated with positive reinforcement, and one featuring only the bits associated with negative reinforcement. The basal ganglia does some bitwise operations on the SDRs and the Thalamus sends it back to the cortex to bias activity in columns (or minicolumns, etc… Not sure about the granularity) associated with positive behavior, cancelling out any that have been associated with negative behavior.
An interesting side effect of all of this is that this should mean that there will be a large number of patterns that the frontal lobe is biased to avoid learning. That, and the higher levels of this hierarchy likely become organized to be closely associated with the motor map. If you remove this bias, it seems as though the cortex would no longer have anything keeping it from learning these patterns, as well as nothing to keep it organized. Seeing as neurons in HTM associate themselves with patterns randomly, this would suggest that damage to the basal ganglia would over time lead to very erratic output, and the brain would eventually begin to lose fine control over the body. Very much like what you see in diseases of the basal ganglia, like Parkinson’s and Huntington’s.
Any feedback would be appreciated! I’d love to work with you guys if I had time; HTM theory really interests me. Unfortunately I’m pretty busy right now. I’ve got a compiler I’m working on for a really ambitious programming language, and I’m working at a startup that’s just getting into the prototyping phase. Hopefully I’ll have some time soon. Maybe I’ll write an HTM implementation to test the compiler at some point. We’ll see.