Activity-dependent presynaptic and postsynaptic structural plasticity in the mature cerebellum.
Two models of spine formation have been proposed. Spines can derive from emerging dendritic filopodia that have encountered presynaptic partners, or presynaptic molecules may induce the spine maturation event directly from the dendritic shaft. The first model applies better to the Purkinje cell (PC), because numerous free spines have been described in several conditions, particularly when granule cells degenerate before parallel fiber (PF) synapses are formed. A large number of new spines, many of them being free, appear in the proximal dendritic domain after blockage of electrical activity by tetrodotoxin (TTX). A complete blockage of the AMPA receptors by NBQX (2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzoquinoxaline-7-sulfonamide), leading to a complete absence of PF- and climbing fiber (CF)-evoked EPSCs and of spontaneous glutamatergic quantal events, mimics the TTX effect. In contrast, metabotropic glutamate receptor blockage by MCPG [(S)-alpha-methyl-4-carboxyphenylglycine] is ineffective. In normal conditions, in the proximal dendritic domain of the PC, clusters of a few spines are present only under each CF varicosity. It has been proposed that the active CF is responsible for spine pruning in the territory surrounding the CF synapses. Here, we show that such a pruning is mediated by AMPA but not by metabotropic receptors. Finally, after AMPA receptor blockage, there is a reduced number of spines in each spine cluster underlying CF varicosity. In conclusion, PCs tend to express spines over the entire dendritic territory. CF activity reinforces the CF synaptic contacts and actively suppresses spines in the surrounding territory, which is an effect mediated by AMPA receptors.
Cesa
Roberta
R
Department of Neuroscience, University of Turin, 10125 Torino, Italy. roberta.cesa@unito.it
Scelfo
Bibiana
B
Strata
Piergiorgio
P
D000818:Animals; D002531:Cerebellum / Q000166:cytology / Q000502:physiology*; D049229:Dendritic Spines / Q000502:physiology* / Q000648:ultrastructure; D004594:Electrophysiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects / Q000502:physiology; D008854:Microscopy, Electron; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D017729:Presynaptic Terminals / Q000502:physiology*; D011689:Purkinje Cells / Q000502:physiology* / Q000648:ultrastructure; D011810:Quinoxalines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D017470:Receptors, Glutamate / Q000502:physiology
D018691:Excitatory Amino Acid Antagonists; D011810:Quinoxalines; D017470:Receptors, Glutamate; C062865:2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline