Updating the Map – Cerebellum and DCN edition

Controlling absence seizures from the cerebellar nuclei via activation of the Gq signaling pathway

What does it look like when we tweak the DCN side/Cerebellum side of the equation?

Early Cerebellar Development in Relation to the Trigeminal System

I really wish there was more of this early developmental data available, understanding the developmental priority adds a lot of context to presentation. This one surprised me because it establishes cerebellar circuit connections developing well after cerebral circuit connections to the central integration areas. While this makes sense intuitively, I haven’t seen much data around this. Looking at this this through our “autism” map, we can probably track many of the most significant features of “autism” to dorsal/ventral circuit strength to our integration centers. “Late speech” represents weaker/impaired ventral connections (since actual speech is an artifact of the pons), clumsiness is an artifact of weak dorsal connections (poor motor cortex environment maps). Humans specifically hit developmental milestones as these circuit pairings get established.

In Vivo Localization of the Human Velocity Storage Mechanism and Its Core Cerebellar Networks by Means of Galvanic-Vestibular Afternystagmus and fMRI

So is an example of “external/general” and “internal/specfic” type mechanics looking like synonyms instead of different concepts. We use a very tight calculation to monitor our own head movement, but need to map external head movement. An efficiency trick here is to assume (weight) external head movement will be similar to ours, then we can pseudo model external movement much more quickly. Behaviorally, this would provide a pretty powerful anthromorphic processing bias and might be why children’s content tends to be so heavily anthromorphic.

Increase of vesicular glutamate transporter 2 co-expression in the deep cerebellar nuclei related to skilled reach learning

I’m definitely over biasing here, but this is another example of how this internal/specific vs external/general model works. First, this is REALLY cool in that it establishes that the internal/ventral/specific model itself is largely fixed. It does not modify itself to accept new information, rather it simply reorganizes itself. This is kind of mind blowing as a potential mechanic for “personality” and behavioral adaptation in general. Also as a model for “mental health”, it implies that we are attempting to re-write the construction itself rather than attempting to change the external data. E.g. effective “PTSD” “treatment” is about modifying the self constructs which are being harmed by the stored engrammatic data, rather than addressing the emgrammatic data itself. The takeaway here is that we can possibly selectively target (for good or evil) specific regions which show consistent activation when remodeling the self construct and modify it to produce pretty profound global changes in information processing.

VTA-projecting cerebellar neurons mediate stress-dependent depression-like behaviors

For example…

Electrophysiological alterations of the Purkinje cells and deep cerebellar neurons in a mouse model of Alzheimer disease (electrophysiology on cerebellum of AD mice)

Okay, first it’s annoying that we’re clinging so hard to the concept of individual insults as causal to dementia (plaques, tangles, lewy bodies, etc etc) instead of recognizing that these are circuit issues. It doesn’t matter what’s causing the disruption, the disruption is the issue. This is interesting because it gives a hint at how modifications to DCN output has direct, measurable impact on cortical maps and limbic integration.

Upregulation of Neural Cell Adhesion Molecule 1 and Excessive Migration of Purkinje Cells in Cerebellar Cortex

Another cool peek at the development of cerebellar circuitry if we can deprecate the chemical stuff.

Short Term Memory Impairment

So this was a mild pondering, how can someone have superior memory performance while having awful memory performance at the same time. Are these different working systems altogether? I’ve held the belief for awhile now that our concept of memory is almost certainly completely wrong. This book provides an additional argument that what we actually have are two independent systems which are blended in the hippocampus to generate our “memory” concepts. Our local/self/short term memory should be an analog of ventral stream performance, and long term memory an artifact of dorsal stream strength. This might be a possible null hypothesis for the entire dorsal/ventral internal/external specific/general construct as a whole if I can get this cleaned up. This should be something we can pretty easily test once the mechanics are established.

Ventromedial Thalamus-Projecting DCN Neurons Modulate Associative Sensorimotor Responses in Mice

Thinking about this concept another way, does the DCN provide the search query and the limbic system provide the map/database?

I think my next map update will need to be the globes and olives. I’m suspecting that they are pretty key to the integration puzzle. Perhaps the entire reticulated formation from medulla to big vestibule is one single integration organ?

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