It's been too long. Still, another attempt to revive the blog. I am at the SfN at this moment and I have to say that the environment is very inspiring. Inspiring for my research and inspiring for blogging.
There are a lot of gaps in our current understanding of the neurosystem. One particular issue concerning the cerebellum is how it fits into the rest of the nervous system. Just ask any cerebellar scientist what the cerebellum does and how it does that. You'll get very diverse answers. Also, nobody knows exactly how the cerebellum codes signals and how the code is composed coming from the cerebellar nuclei. What is the influence of the cerebellar nuclei on the thalamus, on the red nucleus, on motor nuclei in the brainstem? Are there projections from the cerebellar nuclei directly to the cerebral cortex, or to the hippocampus? All these questions have only been very slightly touched upon in the sixties and seventies of the twentieth century using tracing techniques and some basic electrophysiology. Only recently a few papers came out from David McCormick's lab and Dieter Jaeger's lab on how the cerebellar neurons relate to EEG signals from the cerebral cortex. Many scientists I have spoken to are anxious to start and discover how the cerebellum ties in with the rest of the nervous system.
Today I saw three posters from the Detlef Heck's lab that shed some light on how the dentate influences the thalamic and the reticulo-tegmental nuclear pathways to the prefrontal cortex. Apparently, when Purkinje cell input to the dentate nucleus stops (for example due to PC loss in Lurcher mice) the balance between RTN and thalamic pathways shift towards more input from the thalamus to the prefrontal cortex. This shift is probably only visible on longer timescales, so acute pharmacological interventions won't show this shift. The posters were written from the standpoint of an autism model. I find that a bit of a long shot; I had never considered Lurcher mice an autism model. However, the same effects were seen in Fragile X mice making the claim somewhat more believable. Still, all mutants used were global mutants, so no cell specificity here, so the results are quite hard to interpret.
It seems that the cerebellar cortex has a direct effect on the cerebral cortex, but how and what influence this is, is completely unknown. We know the pathways, we know a bit about coding in the cerebellum and frontal neocortex. Let's hope we can find answers to these questions in the coming years. The first steps have been taken, now we need to find the details.