Very interesting.

”Why should mRNAs get expressed in response to learning anyway? Why involve the nucleus when the action is out at the synapses? I'm convinced that its important, but for my money, local protein synthesis from pre-existing RNAs seems a more specific response to changes in input patterns. Does anyone reading have an explanation for the need to produce new RNAs so far from the locus of plasticity?”

Perhaps the nucleus integrates total neuron signals to control back-propagation of electrical signaling through the dentritic arbol? (First dendritic synapses are stimulated and left in an activated state. When the neuron “decides” that synaptic connections should be strengthened, an electrical signal back-propagates to the dentrites causing the activated synapses to strengthen. The new mRNA’s might temporarily alter the back-propagation signaling.)

chromosome position in the nucleus is also a form of epigenetics, see
http://biology.plosjournals.org/ ...al.pbio.0050081

Many genes are recruited to the nuclear periphery upon transcriptional activation. The mechanism and functional significance of this recruitment is unclear. We find that recruitment of the yeast INO1 and GAL1 genes to the nuclear periphery is rapid and independent of transcription. Surprisingly, these genes remain at the periphery for generations after they are repressed. Localization at the nuclear periphery serves as a form of memory of recent transcriptional activation, promoting reactivation.

but this is mediated by a chromatin modification, so maybe you'd call the modification epigenetic but the positioning something else?

Re. nuclear effects of learning: I expect one thing it does is to prime inhibitory and apototic mechanisms, to prevent a synapse strengthening storm. If so, you would see the same expression changes after epileptic seizure.

"You can attach or detach acetyl groups or methyl groups (or phosphate groups or ubiquitin groups or SUMO groups, histones must look like Katamari Damacy)"

An amusing mental image!

I expect one thing it does is to prime inhibitory and apototic mechanisms, to prevent a synapse strengthening storm.

I like this one especially considering the recently reported role for Arc, one of the most robustly and earliest expressed activity-dependent genes, in homeostasis and reduction of receptor numbers.