Burst as a local learning rule in apical but not basal dendrites

The claustrum is a likely candidate for modulating the GNW.

I am sure claustrum plays a role, but TRN is where you can directly block non-WTA stimuli.
And it’s much smaller / faster / better-connected.

While I’m sure that the brain modulates and does gain control on the GNW, I don’t think you really need a strict WTA competition. Multiple cortical areas can be broadcasting at the same time on the GNW.

My prototype I that I linked to does not use a competition.

Remember that cells (normally) only burst first from apical input if they also spike at least once from their basal & somatic inputs, so local inhibition can prevent burst-firing and control the sparsity (at least within a local area). There is also the inhibitory inter-neuron the Martinotti cell - Wikipedia which targets apical dendrites.


“The entire workspace is globally interconnected in such a way that only one such conscious representation can be active at any given time”

This means that if multiple areas are active at the same time then they all become part of (concatenated into) a single large SDR, as opposed to multiple discrete SDR’s representing different areas. There can only be one representation active in the GNW at a time because there is only one GNW.

HTH

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I don’t see what makes it “one” then. Not everything that happens at the same time in the brain is one representation. Composition of GNW is changing all the time, globally active neurons can become locally active and vice versa?
Also, that “concatenated” SDR probably won’t be in the same dendrite? It’s likely to be multiple concurrently active dendrites, with outputs summed in the soma?

I think the reason why singular consciousness exists, vs. just massively parallel processing in the brain, is a brain-to-body bottleneck, implemented in thalamus. Brain neurons can work in parallel, exploring many scenarios subconsciously. But the body can generally execute only one, even two hands can’t work separately, or two eyes look in different directions.
So these scenarios / threads / motor patterns have to compete for the control of the body, even if that control is imaginary. That requires WTA, and the winning thread becomes conscious.

We like to think about the brain as an information processor, but it evolved for a single purpose: to guide the body. That informs the whole process, even if we are thinking about abstract math.

So I finished reading the OP’s article and I have to say I’m impressed by their model’s faithfulness to biology.
They get a lot of things right, including:

  • The role of burst-firing to signify task relevant / salient information.
  • Dendrites being tuned to respond to burst-firing or single spikes, using short term plasticity.

I think their results are mostly correct, but I still disagree with their interpretation.
They argue that their network approximates back-propagation and solves the credit assignment problem.
And maybe it does, but I think that misses the bigger picture of what apical dendrites are capable of doing?

Regardless, it is interesting to see when other people start with the same information and then come to very different conclusions.

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A bit off-topic wrt OP article, but I think it supports my opinion about WTA in TRN:

" Intrathalamic Inhibition of HO Thalamus

A central regulator of thalamic function is feedback inhibition via thalamic reticular nucleus (TRN), a thin layer of GABAergic neurons partially encapsulating the relay nuclei which project to cortex (Pinault, 2004). As well as TC afferents to cortex, thalamic relay neurons also send thalamoreticular projections to TRN which in turn provide feedback inhibition to relay neurons (Figure 1); the temporal scale of this inhibition is sensitive to spiking patterns (Figure 2), with high-frequency bursts triggering long-lasting IPSCs due to GABA “spillover” to extrasynaptic receptors, while tonic spiking patterns trigger shorter IPSCs (Halassa and Acsady, 2016). A recent pair of milestone studies in the somatosensory thalamus reveal that properties of HO and FO intrathalamic inhibitory circuitry differ significantly: HO nucleus POm excites and is inhibited by a discrete shell population of TRN neurons; furthermore, the synaptic dynamics of POm-TRN connections as well as the intrinsic properties of POm-connected TRN neurons are functionally distinct from those in VP-TRN circuits (Li et al., 2020; Martinez-Garcia et al., 2020). Thus, it may be that the dynamics of intrathalamic inhibition are matched to the distinct signal processing requirements of HO and FO circuits carrying L5tt and sensory information, respectively.

Given its role in gating thalamocortical transmission as well as its positional and physiological properties, the TRN has been implicated in the regulation of attention in the “searchlight hypothesis” (Crick, 1984; Crabtree, 2018). Regions in the TRN show increased activity in response to attentional stimuli, and the specific region in which this response is found is modality-dependent (McAlonan et al., 2000, 2006). Moreover, limbic TRN projections correlate with arousal states, while sensory TRN projections are suppressed by attentional states (Halassa et al., 2014). Work by Halassa et al. (2011) demonstrates TRN-dependent control of thalamocortical firing mode and state regulation, where selective drive of TRN causes a switch from tonic to burst firing and generates state-dependent neocortical spindles (Halassa et al., 2011).

Likewise, there is evidence for an attentional role of HO thalamus. For example, the MD is activated in humans during tasks requiring a rule-dependent shift in attentional allocation (i.e., set-shifting), such as the Wisconsin card-sorting task (Monchi et al., 2001; Halassa and Kastner, 2017). Human and monkey studies also point to a role of the pulvinar in visual attention. Pulvinar lesions in patients result in impairments in filtering distracting information, while pulvinar inactivation in monkey impairs spatial attention (Danziger et al., 2004; Snow et al., 2009; Wilke et al., 2010; Halassa and Kastner, 2017). In addition, Yu et al. (2008) describe the pulvinar’s role in sustained attention, employing the five-choice serial reaction time task to show that half of recorded units in this nucleus were attention-modulated (Yu et al., 2018). However, TRN control of HO thalamus in the context of attention and arousal has yet to be systematically investigated.
"

They are talking about its role in attention, which I think is just a different POV on GNW or working memory: “spotlighted” or globally active areas.

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I much appreciate a new review article! Very interesting, and I see what you mean about WTA in the Thalamus & TRN.

I had a different line of thinking about what the thalamus does, but I think its compatible with yours. My hypothesis is that the thalamus uses some kind of reinforcement learning to control attention and the GNW.


By the way: here is another good review article about the thalamus:

Functioning of Circuits Connecting Thalamus and Cortex
S. Murray Sherman, 2017
DOI: 10.1002/cphy.c160032

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My hypothesis is that the thalamus uses some kind of reinforcement learning to control attention and the GNW.

Thalamus is very complex, so I am sure there is some RL in it. As in any region that gets phasic dopamine. The way I think of it, thalamus is close to a map-reduced brain. And it’s reduced to enable efficient real-time inhibition among competing stimuli and responses, basically a battleground.

That’s in real brain, but brain is a kluge, we need to distinguish functional from biologically plausible.
Most cognitive processes are “hypothetical”, they don’t actually need this real-time WTA for the body. To the extend that they do in the brain, it’s probably just an evolutionary artifact.

So, you may not need WTA in your model, depending on application. But then, you also don’t this binary distinction between globally active GNW and local processes. It will just be a continuous spectrum of activity scope for various co-activated ensembles, Fuster’s “cognits”.

I don’t necessarily disagree, but I don’t think those findings are enough to say anything specific about generic cortex. [9 levels of asterisks about a neuroscience fact in context of generic cortex, yeah I’m cutting the rest of this.]

I vaguely recall the basal ganglia only influences cortex indirectly, mainly by inhibiting thalamus, which would make thalamus a key part of cortical RL.

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It’s speculative, but thalamus does seem to have all the mechanisms needed for map-reduced competition. Which is necessary, considering that only one motor pattern can be implemented by the body at any given time.

Striatum seems to have direct cortical afferents but not efferents. Which is strange, these connections are usually bidirectional.

Agreed. The rules of short term plasticity can be tuned so that synapses respond in arbitrary ways to an input spike, as a function of the recent history of spikes. So there is a lot of wiggle room for different synapses to have different responses based on their particular situation.


I think that both interpretations of the thalamus can be correct:

  • The thalamus does reinforcement learning.
  • The thalamus does a WTA competition.

About WTA in the thalamus:
The winner is going to be the representation of a thing, and that representation is going to be multi-modal and so will show up in many areas of the thalamus.

For example: I have a big ball in each hand and I toss one of them to you and you catch it. Both balls have a representation in your thalamus, but when you go to catch one ball you need to not pay attention to the other ball. This is the WTA in action.

Another example: I experience this one a lot. When playing a first-person-shooter video game (cs:s): two enemy targets appear on my screen at the same time.

  • Sometimes I will focus on one of them and I am able to aim directly at them. In this case I ignore the other enemy; I can see the other and I’m vaguely aware of what they’re doing but I’m incapable of dealing with them until I mentally disengage from my current task of shooting the first enemy that I initially targeted.
  • Othertimes I will focus on both enemies at the same time! This does not work and I usually split the difference and shoot halfway between the two enemies, missing both of them. This could be a failure of WTA inhibition in the thalamus?

And to control the body with a purpose!
The reason I did not like the phrase “WTA” is that in theory: a lot of the cells could be active in the GNW as long as they’re all in agreement about what task you’re doing.

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Yes, if they form an internally self-reinforcing ensemble, then it’s one representation. For each constituent neuron, I think that means multiple SDRs / dendrites active at the same time. If that happens, the neuron should burst?

Well, ideally, if all of the inputs are part of “one representation” then they would form synapses close together on a single dendrite, to enhance detection of the stimulus.

Neurons burst-fire when they are activated by both basal inputs (regular, non GNW inputs) as well as apical inputs (from the GNW).

My problem with that, inputs from different areas are not likely to target the same dendrite. They may or may not turn out to be co-active latter, but even if it’s the former, how do you physically splice / transfer synapses between dendrites?

I think map-reduced competition is an interesting idea. To attend to part of the map, rather than selecting it in the big cortical sheet, it shrinks down to the size of the thalamus’s map, does competition, and then expands back up. It could re-add info lost in the shrinking using direct CC connections or preserve the info by spike patterns or something. That’d be a useful constraint, since it’d mean L5tt cells should be amenable to the loss of info or the means of compression.

That’d require more L5tt cells than TC cells. I couldn’t find cell counts for L5tt in a region and their targeted higher order thalamic nucleus, not that I did an exhaustive search.

I don’t understand the exact connection between those ideas. I know motor patterns need something like global consistency, since there are so many cortical motor outputs (all regions and probably all cortical columns) and that could lead to contradictory motor actions. I don’t think map-reduced competition could do that, because it doesn’t operate on a global scale and wouldn’t work for the motor outputs from primary cortical regions. It’d also be using a lot of the same mechanisms to do things with sensory information (including in higher order thalamic nuclei, because some of those are driven by a mix of L5tt and the same sort of direct sensory input which primary nuclei receive).

Alien hand syndrome is another thing to consider. (For example, someone with it took a cigarette out of their mouth while trying to light it). It results from injuries to the brain, including CC connections (corpus callosum) and some cortical regions. That suggests the thalamus isn’t in charge of motor consistency (although it could be involved or even solely responsible, because damage studies aren’t very clear.)

Which connections? For signals to cortex (i.e. neocortex), my impression is that info-containing signals only go through thalamus. (Maybe olfaction bypasses thalamus, but I think O1 is allocortex and might still go through thalamus to reach neocortex). Modulatory signals (e.g. serotonin) can go straight to cortex, but something like striatum wouldn’t do that because it does something different.

To avoid a potential source of confusion, cortical afferent means cortex sends signals to striatum, right? I’m just not used to the terminology.

There’s attention to things with selected identities but also attention to parts of space (I think parts of reference frames e.g. locations in physical space or the reference frame impacted by hemineglect, as well as parts of the sensor e.g. part of the eye’s field of view). I think WTA in thalamus would be for attention to parts of space since TRN connectivity isn’t very precise. It probably wouldn’t be able to select SDRs, since those are arbitrary sets of cells.

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Hebbian learning. Inputs will target all of the dendrites which they pass near to and whose activity they correlate with.

It’s not like synapses are going to physically up & move from one dendrite to another, but their presynaptic axons will likely pass near enough to multiple dendrites to form synapses in whichever spot seems most advantageous.

Here is an article that discusses the phenomenon:

Electrical Compartmentalization in Neurons
Willem A.M. Wybo,
Benjamin Torben-Nielsen,
Thomas Nevian, Marc-Oliver Gewaltig
2019
DOI: https://doi.org/10.1016/j.celrep.2019.01.074=

Figure 7 shows (their simulation of) the synapses moving dendrites.
IIRC they found that inhibition is critical for prompting synapses to move to different dendrites.


I’m assuming that synapses from TRN to Thalamus are formed using hebbian learning, in which case they are very precise with respect to the activity of the pre & post synaptic cells.

However, the word “precise” has many meanings. Maybe the TRN projections are not topologically precise?
[Edit: I think for many publications discussing the thalamus, topological precision is a big topic because so many of the cells in the thalamus are topologically precise, and its notable that the TRN isn’t]

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Yes, that’s what I meant. Now that I think about it, that doesn’t mean it’s competition on the level of maps because it could just be whichever fires first wins.

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I meant competition among motor patterns, not consistency within each. If you have a fork on the road, you can’t take both. Maybe not directly for primary motor cortices, but those are controlled by higher areas anyway. Which have something like higher-order motor patterns: strategies, etc.

Right. The signal is from higher association cortices: Striatum - Wikipedia
“The largest connection is from the cortex, in terms of cell axons. Many parts of the neocortex innervate the dorsal striatum. The cortical pyramidal neurons projecting to the striatum are located in layers II-VI, with the most dense projections come from layer V”

Thanks, yes, I recollect that extracellular calcium attracts those axons. So a neuron has many SDRs / dendrites, each representing a separate ensemble. My question was, suppose those ensembles are initially unrelated, but then turn out to be coactive under some condition. This will basically combine them into higher-order ensemble. Does that mean some kind of WTA, redirecting coactive presynaptic axons to the strongest SDR, or they can stay where they are because that old SDR is still active, actually the most active if you adjust for the distance from previously associated axons?

Yes! There is a competition among the dendrites. They’re trying to activate, and activity attracts more & stronger synapses, which drives further activation.

And also there is inhibitory input to the dendrites, which is important for controlling this otherwise unchecked positive feedback loop.

Also dendrites have limited space, which limits the total number of synapses they can have. (This fact prevents some run-away positive feedback loops).

IIRC from the article “Electrical Compartmentalization in Neurons”: inhibition effects dendrites by both inhibiting them directly as well as making it more difficult for nearby synapses to cooperate, which has the effect of “breaking” large dendritic segments into many smaller independent segments. Then those small dendrite segments can specialize in detecting very specific things. And when the inhibition goes away, all of those small specialized segments will cooperating again as one big general-purpose segment.

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