Is this redundant? This was mentioned in the section on non-neuronal plasticity and perhaps should merely be elaborated more in that section there are two studies that might be discussed in more detail either in that section or here. Tj's ensheathment paper fits in this discussion. The point of putting it here is by way of a segue into a discussion of the tendency to ignore non neuronal (or even nonsynaptic) changes. THIS HAS BEEN DONE
THESE CONCEPTS SEEMS TO GO WITH THIS SECTION:
Synaptic specificity supported by “synaptic tag” that is localized and protein-synthesis independent (Frey and Morris, 1997). Fits concept of metaplasticity in that history of synapse (even sub optimal stimulation patterns) pre-disposes synapse to subsequent modification.
Could consider integrating notion of differential parameters necessary/sufficient to induce LTP (emphasize model of learning, not that it is equivalent or necessary for) in multiple areas of the brain. That one type of stimulus does not result in the same effect in numerous areas of the brain suggests (obviously) differential make-up of that area and surely different mechanisms. This notion would simply parallel our argument of different “types of plasticity” (as defined anatomically), with physiological correlates (Yun, et al., 2002); (Trepel and Racine, 1998). I AM NOT SURE MORE IS NEEDED
IS THIS THE VENUE TO EVEN BRING UP FRAGILE X/FMRP????
I AGREE WITH YOU THAT THE ANSWER IS NO
On the Horizon: A Role for Protein Synthesis at the synapse
Since the first report of morphological evidence for protein synthesis at the synapse (Steward & Levy, 1992) there has been a growing body of literature investigating this phenomenon. Some forms of synaptic and dendritic protein synthesis have been shown to be activated by metabotropic glutamate receptors (mGluR) in some cases (e.g., Weiler & Greenough, 1993; Weiler et al., 1994, 1997; Eberwine PNAS-still in press?) and by NMDA receptors as well (Sheetz et al., 2000). Proteins synthesized at synapses include the fragile X protein FMRP and calcium/calmodulin-dependent protein kinase II (CAMKII). FMRP has also been shown to be necessary for the mGluR-dependent synthesis, which is not observed in FMR1 knockout mice (cite Spangler abstract). Plasticity-inducing forms of electrical stimulation have been shown to trigger the transcription and transport of mRNA for the protein ARC to dendritic sites of stimulation, where it is translated (Steward and Worley references). mGluR1 activation, ARC synthesis and CAMKII activity have been proposed to be involved in various forms of plasticity (Huber/Bear work; Steward; Mary Kennedy), although details of the specific functions of synaptic or dendritic protein synthesis are still under investigation. Do you think we need to say anything more here? The chapter is really not "about" this, and I am not sure (but open to suggestions) what additional data makes sense to include.
In summary, brain plasticity appears to be a phenomenon that is not restricted to elements that are neuron-specific. In fact, it could be argued that neuronal plasticity is but a small fraction of the overall changes that occur in response to experience and that we are just beginning to understand the importance of these other forms of brain plasticity. A big waving of our hands to and draw grand conclusions, followed by speculations on direction…..
Tissue cultures lacking astrocytes—how good a model? Lack of synapse formation in cultures without astrocytes (Ullian, et al., 2001). Moreover, even when synapses do form, they are functionally immature. Obvious implications on studies of “synaptic plasticity” in vitro. NOT SURE WE HAVE TIME FOR THIS NOR IS THIS NECESSARILY CONSISTENT WITH UNDERLYING THEME OF THE PAPER.
Lack of astro part of ECM. Lack of basis for TPA, other actions probably involved in synaptogenesis. MMP3, MMP6, MMP9 (Metalomatrix proteins), stromolysin, gelatinase. Roles of Astros, ECM, TPA, etc. in synaptogenesis; adhesions; rec aggregation DEFINITELY NOT ENOUGH TIME FOR THIS.
Incorporate Harris, Matus, Segal. Motility and shape issues. Put together a model, slow accumulation of synapses via overproduction-selection as a basis for the stable long-term substrate of memory; plus fast shape changes, PSD size, perfs, interpret multiple synapses from local and wiring diagram view. DONE TO AN EXTENT, NIX THIS SECTION?
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