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PERSPECTIVES |
The Weizmann Institute, Rehovot, Israel
Email: menahem.segal{at}weizmann.ac.il
Dendritic spines, the locus of excitatory synaptic communication, were always considered to be the stationary storage site of long-term memories. The presence of actin filaments in the spine led, over 20 years ago, to the prediction that the spines may twitch (Crick, 1982), and indeed, 6 years ago it was first found that mature spines actually twitch (Fischer et al. 1998). Spines appeared to undergo local changes in shape, in a way that did not expand them into new territories or lead to production of a new synapse, as is the case of young filopodia. This local ‘morphing’ was initially observed in cultured neurones which were transfected with green fluorescent protein (GFP), but later found also in different spiny neurones, in brain slices and even in cortical neurones in the intact brain (Matus, 2000). Thus, it appears that this fascinating behaviour is not a developmental prelude to the final stabilization of the spine, but an ongoing local change in morphology of the spine. The question, then, is why does the neurone spend so much energy to cause its thousands of spines to move constantly?
On the way to understanding the functions of spine motility, attempts have been made to control this behaviour. Two complementary observations were made: exposure to the glutamate agonist AMPA caused cessation of spine motility (Matus, 2000), down to a total shrinkage of the spines and their disappearance following exposure to glutamate; and on the other hand, spine motility was enhanced by blocking network activity with TTX (Korkotian & Segal, 2001). Thus, it appears that synaptic activity, via release of glutamate, regulates spine motility, with higher activity blocking it, and reduced activity enhancing motility.
But what is the function of spine motility? The paper by Richards et al. (2004) in this isssue of The Journal of Physiology provides the first clue to this question: Using recovery from photobleaching of membrane-bound GFP, they suggest that diffusion of membrane particles (e.g. GFP) is slower in motile than in stationary spines. Furthermore, latrunculin, a drug that blocks actin polymerization and reduces spine motility, also speeds up membrane particle diffusion, indicating that actin cytoskeleton affects membrane diffusion. These observations imply that the diffusion of particles along the membrane can be used to detect the status of actin polymerization inside the cell, but even more, that actin cytoskeleton controls these two somehow related events, spine morphing and membrane diffusion. This is relevant only in spines, as the dendritic membrane diffusion is too fast to be modulated by actin cytoskeleton. Intuitively, this observation makes sense, since a spine that is reactive to afferent stimulation may need to replenish/add receptors or synaptic proteins, some of which may diffuse along the membrane to reach their target.
What then is the role of the spine motility? Can we assume that motility is there to slow down diffusion of membrane particles? After all, motility is associated with younger spines than with older ones, so intuitively one may want to load these new spines faster than the more established ones, and not the other way around. Notwithstanding, these observations linking membrane diffusion to cytoskeleton and spine motility provide an important step in understanding the roles and modes of operation of this unique, tiny structure, which is loaded with dozens of molecule species and without which we may not remember.
References
Crick F (1982). Trends Neurosci 5, 44–46.[CrossRef]
Fischer M, Kaech S, Knutti D & Matus A (1998). Neuron 20, 847–854.[CrossRef][Medline]
Korkotian E & Segal M (2001). J Neurosci 21, 6115–6124.
Matus A (2000). Science 290, 754–758.
Richards DA, de Paola V, Caroni P, Gahwiler BH & McKinney RA (2004). J Physiol 558, 503–512.
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