Abstract
During postnatal development, closure of critical periods coincides with the appearance of extracellular matrix structures, called perineuronal nets (PNN), around various neuronal populations throughout the brain. The absence or presence of PNN strongly correlates with neuronal plasticity. It is not clear how PNN regulate plasticity. The repulsive axon guidance proteins Semaphorin (Sema) 3A and Sema3B are also prominently expressed in the postnatal and adult brain. In the neocortex, Sema3A accumulates in the PNN that form around parvalbumin positive inhibitory interneurons during the closure of critical periods. Sema3A interacts with high-affinity with chondroitin sulfate E, a component of PNN. The localization of Sema3A in PNN and its inhibitory effects on developing neurites are intriguing features and may clarify how PNN mediate structural neural plasticity. In the cerebellum, enhanced neuronal plasticity as a result of an enriched environment correlates with reduced Sema3A expression in PNN. Here, we first review the distribution of Sema3A and Sema3B expression in the rat brain and the biochemical interaction of Sema3A with PNN. Subsequently, we review what is known so far about functional correlates of changes in Sema3A expression in PNN. Finally, we propose a model of how Semaphorins in the PNN may influence local connectivity.
Highlights
Since the early 1990s, chemorepulsion has been recognized as an effective way to guide growing neurites towards their targets in the developing nervous system [1]
The secreted and transmembrane Semaphorins were initially identified as repulsive axon guidance cues [4], in the past decade they have been linked to many other cellular processes, including cell migration, proliferation, and polarization
Semaphorin stimulation leads to an activation of the Plexin interacting protein MICAL and to the phosphorylation of intracellular proteins of the CRMP family, which in turn affects F-actin and microtubule disassembly and thereby growth cone motility [25,26,27,28,29,30,31]
Summary
Since the early 1990s, chemorepulsion has been recognized as an effective way to guide growing neurites towards their targets in the developing nervous system [1]. Semaphorin stimulation leads to an activation of the Plexin interacting protein MICAL (molecule interacting with casL) and to the phosphorylation of intracellular proteins of the CRMP (collapsing responsive mediator protein) family, which in turn affects F-actin and microtubule disassembly and thereby growth cone motility [25,26,27,28,29,30,31] To their role in long distance axon guidance during development of the nervous system, Semaphorins play a role in local target selection (reviewed in [10]). Besides their guidance role in neuronal circuit formation during development, Semaphorins can modulate the functional properties of established synapses in the adult brain. We summarize the localization of Semaphorin 3A protein in the adult rodent brain [51], review the biochemical data on the interaction of this protein with the extracellular matrix [52], and discuss the possible role of Semaphorin 3A and Semaphorin 3B in PNNcontrolled structural plasticity
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