Abstract
Reelin is an extracellular matrix protein that is mainly produced in Cajal-Retzius cells and controls neuronal migration, which is important for the proper formation of cortical layers in the developmental stage of the brain. In the adult brain, Reelin plays a crucial role in the regulation of N-methyl-D-aspartate receptor-dependent synaptic function, and its expression decreases postnatally. Clinical studies showed reductions in Reelin protein and mRNA expression levels in patients with psychiatric disorders; however, the causal relationship remains unclear. Reelin-deficient mice exhibit an abnormal neuronal morphology and behavior, while Reelin supplementation ameliorates learning deficits, synaptic dysfunctions, and spine loss in animal models with Reelin deficiency. These findings suggest that the neuronal deficits and brain dysfunctions associated with the down-regulated expression of Reelin are attenuated by enhancements in its expression and functions in the brain. In this review, we summarize findings on the role of Reelin in neuropsychiatric disorders and discuss potential therapeutic approaches for neuropsychiatric disorders associated with Reelin dysfunctions.
Highlights
Reelin is an extracellularly secreted glycoprotein that is necessary for brain development and neuronal function
We summarize research on the involvement of Reelin in neuropsychiatric disorders and discuss potential therapeutic approaches for neuropsychiatric disorders associated with Reelin dysfunctions
The phosphorylation of Cytoplasmic linkerassociated protein 2 (CLASP2) may be necessary for Dab1 interactions and neurite outgrowth [28]. These findings suggest that Reelin promotes neurite development and that the disruption of Reelin signaling may result in an abnormal neurite morphology
Summary
Reelin is an extracellularly secreted glycoprotein that is necessary for brain development and neuronal function. Reelin is produced by CajalRetzius cells, which are mainly present on the surface of the neocortex [1,2]. Cajal-Retzius cell numbers markedly decrease, and Reelin is mainly synthesized in γaminobutyric acid (GABA)-ergic neurons in the hippocampus and cortex [3,4]. Secreted Reelin binds to apolipoprotein E receptor 2 (ApoER2) and very low-density lipoprotein receptors (VLDLR) expressed on neuronal membranes via the fifth and sixth Reelin repeats [6,7], stimulates Src family tyrosine kinases (SFKs), such as Fyn and Src, and promotes the tyrosine phosphorylation of intracellular Dab1 [8,9]. We summarize research on the involvement of Reelin in neuropsychiatric disorders and discuss potential therapeutic approaches for neuropsychiatric disorders associated with Reelin dysfunctions
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