Quick Post That Will Make Sense to Maybe One Person Who Reads This (Or More)

So I've been working on this paper all week, and I was telling everyone the last couple of days that it all made sense so long as psychostimulant sensitization-induced LTD was mediated by a change in AMPAR function rather than endocytosis.

I realized this afternoon that I was wrong, due to something key that I'd forgotten about the Marina Wolf paper I'd been reading on Monday, which I shan't go into right now.

But anyways, I realize that this afternoon and what's the next paper I grab from the pile of stuff I need to read? This:
Nucleus accumbens long-term depression and the expression of behavioral sensitization

The abstract:

Drug-dependent neural plasticity related to drug addiction and schizophrenia can be modeled in animals as behavioral sensitization, which is induced by repeated noncontingent or self-administration of many drugs of abuse. Molecular mechanisms that are critical for behavioral sensitization have yet to be specified. Long-term depression (LTD) of alpha-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid receptor (AMPAR)-mediated synaptic transmission in the brain has been proposed as a cellular substrate for learning and memory. The expression of LTD in the nucleus accumbens (NAc) required clathrin-dependent endocytosis of postsynaptic AMPARs. NAc LTD was blocked by a dynamin-derived peptide that inhibited clathrin-mediated endocytosis or by a GluR2-derived peptide that blocked regulated AMPAR endocytosis. Systemic or intra-NAc infusion of the membrane-permeable GluR2 peptide prevented the expression of amphetamine-induced behavioral sensitization in the rat.

(emphasis mine)

I'm glad I figured that out this afternoon, because otherwise I'd spend this entire paper trying to figure out how they got it wrong. ;-P