Coffee Mug, I find these posts very interesting and hope you continue.

I'm also curious about how the extracellular matrix might be changed by synaptic activity. And how synaptic membrane proteins might be interacting with the extracellular matrix.

Ditto -- if you don't get lots of responses, that's just b/c: 1) no hot mixed race girls figure in the discussion, and 2) most of us don't have much neuro background, beyond basics.

well hopefully i'm providing enough basics and context to understand why the paper was interesting and experiments worth doing..

if i'm not, please let me know. i don't know how many times to reiterate that LTP is a model for memory and explain the basic anatomy of a neuron..

I'm probably not a good person to determine the general readibility of your posts to a non-neuro audience so I'll leave that one alone. As to their informativeness (is that a word?) and fascinatingness (yeah, that ain't a word for sure) suffice it to say that I enjoy them enough to have chased you over here from your other blog

So many profs who teach neuro courses at the undergrad and grad level tend to blow through LTP like it is a done deal and mostly figured out. What I love about many of your article selections is that they show evidence that this isn't the case at all--far from it.

The actin idea is very intriguing, since actin is such an integral part of synaptogenesis and cell motility and transport. Why should it not be important in what is, after all, the morphological/anatomical contribution to LTP. I am especially intrigued by the possible contribution to AMPAr transport to the bilayer.

I'd be interested to see if the family of cadherins (specifically N-cadherin) were at all responsible for some of this stuff, since they have been implicated in dendritic refinement in sensory systems.

I'd also like to see if genetic ablation of particular types of actin (though this would be very painstaking to do without being cell-lethal) stopped LTP or LTD.

Nice post chum.

Good post.