Ponto-olivary climbing fibers are the substrate upon which all personal experience is built.
The neonatal period in humans is largely driven by the linking of these fibers to purkinje cells, which form the basis of conscious experience (predictive processing).
The critical period in humans is largely driven by the pruning of connections between these fibers and purkinje cells, which form the basis of cognitive experience.
Under “autism” models, we have two families, four super classes and a bunch of sub classes depending on which units the purkinje cells are primarily connected through.
The first family relates to the connections between the climbing fibers and purkinje cells – Class 1) “Under Links” – individuals with impaired olivo-cerebellar links. These individuals nearly always present with learning disabilities with severity dependent on the paucity of links. The most profoundly disabled individuals fall into this category.
Class 2) “Over Links” – individuals with a high climbing fiber to purkinje ratio. Much, much more mild learning disability to “high” intelligence (for individuals with higher numbers of purkinje cells). An artifact of this is that the linking is often “uneven”, in which some purkinje cells will be over connected to climbing fibers and some functions will have no linking. Group usually presents with high compulsivity for behaviors built on specific purkinje strands (the strand is being overselected).
The second family relates to the pruning of the ponto-olivary intercellular processing pathways (synaptic), including purkinje connections. The focus here has generally been on cortical and limbic effect, but the profound nature means that these effects are likely ponto-cerebellar. We can transfer all the “under/overpruning” work from existing “autism” research and apply them here.
I’m excited because this model is the first time I’ve even had a remotely plausible explanation for why “schizophrenia” type conditions are late onset – they are high connection states with cerebellar overpruning. The effects of this overpruning wont appear until post critical period. We actually should be able to see “schizophrenia” appear in early childhood (grade school) but we aren’t socially sensitive enough to it because childhood processing is still stabilizing. We are only sensitive to a very small fraction of “schizophrenic” phenotypes, much like “autism” phenotypes, it’s a tip of the iceberg kind of thing.
All “theory of mind” type constructs are artifacts of climbing fiber->purkinje construction.
Nearly all amenias and most aphasias are artifacts of purkinje cell insults. Molaison’s memory issues for instance were because the inferior olives no longer had access to the stream (which is what the hippocampal complex constructs) rather than because the hippocampal complex directly instantiates new memory.
Fear is a predictive process, and as such is processed experientially in the cerebellum. The amygdala complex valence weights that fear as feedback to the experience systems in the olivo-ponto circuit.
This pushes the initiation point of salience to the midbrain. Interesting. It should be relatively local to the red nucleus, even in humans.
Lets split this into inferior and superior olivary pathways. Ventral dominant phenotypes, or under the “autism” model, asperger’s would localize to wiring in the inferior olivary pathway. “BAP” and/or dorsal dominant phenotypes would localize to wiring in the superior olivary pathway.
For example, hyper or hypo connection in the superior olivary pathway can lead to auditory processing (and other sensory related) effects, while inferior olivary hyper/hypo connection lead to movement related artifacts (e.g. “clumsiness”). An individual with exceptional audio discrimination should present with hyper connection in the superior ponto-olivary pathways assuming they had the necessary compensation in the associated purkinje chain (or valence weighting). I wonder if we can look at imaging to get a sense of exceptional athletes for sports requiring a lot of fine motor control to look at the inferior ponto-olivary pathways.
Wonder if there are any studies which specifically blockade these pathways, or “lucky” lesions which completely sever the climbing fiber->purkinje cell chain.
Yeah, the mesencephalon (midbrain/tectal region) is developmentally distinct from the olives and cerebellum, which are developed from the rhombencephalon. It seems possible that the olives and DCN are functional equivalents (“inversions”) to the limbic system similar to cerebellar vs. cerebral cortical function.
How much faster is olivo-cerebellar processing than limbic-cerebral processing? Must be significant to make up for the smaller scope of “attention” in olivo-cerebellar schema.
There’s a significant chance I have the strand setup backwards, more climbing fiber->purkinje connections may result in higher inhibition (low external sensitivity – think dorsal “autism” phenotypes (genetic plan) or some “ADHD” phenotypes (environmental response)), while fewer connections result in under-inhibition.