Dendrite matrix9/11/2023 (A) Schematic of a dendritic spine apposed to a presynaptic terminal. Dendritic spines are highly structured and plastic synaptic specializations. These and other dendritic spine proteins regulate actin filament formation, turnover, and stability, thereby controlling dendritic spine structure.įigure 1. Adhesion molecules also connect to both the presynaptic partner and the extracellular matrix (ECM) in and around the synaptic cleft (Figure 1A). Scaffolding proteins and cell adhesion molecules (CAMs) connect the PSD to the spine actin cytoskeleton. The spine head also contains the membrane-associated postsynaptic density (PSD), a highly organized network of neurotransmitter receptors, adhesion receptors, scaffolding proteins, and downstream signaling molecules ( Harris and Stevens, 1989 Kennedy, 1994, 1997 Hunt et al., 1996 Walikonis et al., 2000 Sheng and Kim, 2011 Harris and Weinberg, 2012). ![]() Ultrastructurally, dendritic spines are composed of a thin neck supported by unbranched filamentous actin (F-actin) and a bulbous head containing a network of branched F-actin ( Korobova and Svitkina, 2010 Tønnesen et al., 2014). Here, we review the evidence for a role of several brain ECM ligands and remodeling proteases in the regulation of dendritic spine and synapse formation, plasticity, and stability in adults.ĭendritic Spines are Highly Structured Postsynaptic Signaling Compartmentsĭendritic spines are protrusions from the dendrite shaft of neurons that comprise the receptive contact at most excitatory synapses in the brain ( Gray, 1959a, b Harris and Kater, 1994 Hering and Sheng, 2001). While the role of ECM receptors in spine regulation has been extensively studied, considerably less research has focused directly on the role of specific ECM ligands. The extracellular matrix (ECM), composed of a meshwork of proteins and proteoglycans, is a critical regulator of spine and synapse stability and plasticity. As such, the regulation of spine stability and remodeling in the adult animal is critical for normal function, and disruption of these processes is associated with a variety of late onset diseases including schizophrenia and Alzheimer’s disease. At the same time, adult spines must retain some plasticity so their structure can be modified by activity and experience. Spines become much more stable in adulthood, and spine structure must be actively maintained to support established circuit function. Spines are dynamic in the developing brain, changing shape as they mature as well as appearing and disappearing as they make and break connections.
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