Reelin downregulation as a prospective treatment target for GABAergic dysfunction in schizophrenia

Erminio Costa, Ying Chen, Erbo Dong, Dennis R. Grayson, Alessandro Guidotti, Marin Veldic

Research output: Chapter in Book/Report/Conference proceedingChapter

1 Scopus citations


The proper functioning of the mammalian cortex depends on the formation of neuronal networks, including principal projection neurons and interneurons that use glutamate and GABA as transmitters, respectively. In the adult brain, cortical interneurons have been implicated in the regulation of the synaptogenesis and neuronal wiring operative in cortical network formation. These neurons are aspiny, express local projecting axons, and their staining with the Golgi method reveals a soma volume smaller than most cortical neurons. They store and synthesize the neurotransmitter GABA and also frequently synthesize and secrete reelin. In embryonic cortex, reelin is synthesized and secreted by the Cajal-Retzius cells, guides neuronal migration and positioning of pyramidal neurons (D'Arcangelo et al., 1995). However, postnatally during CNS development and maturation, this protein is synthesized and secreted from GABAergic interneurons and harmonizes the functional plastic interaction of neuronal axons, dendrites, and their spines (Costa et al., 2001; Niu et al., 2004). Reelin secreted in the extracellular matrix contributes to the modulation of neuronal excitability, firing frequencies, and the morphological properties of the telencephalic neuronal networks regulating their coordinated activity (Liu et al., 2001; Costa et al., 2001; Weeber et al., 2002; Qiu et al., 2007).

Original languageEnglish (US)
Title of host publicationReelin Glycoprotein
Subtitle of host publicationStructure, Biology and Roles in Health and Disease
PublisherSpringer New York
Number of pages23
ISBN (Electronic)9780387767611
ISBN (Print)9780387767604
StatePublished - 2008

ASJC Scopus subject areas

  • General Medicine
  • General Neuroscience


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