A GABA, reelin, and the neurodevelopmental hypothesis of schizophrenia

Crit Rev Neurobiol. 2004;16(1-2):25-32. doi: 10.1615/critrevneurobiol.v16.i12.20.

Abstract

The GABA-reelin cortical connection (i.e., the expression and secretion of reelin by GABAergic cortical neurons) has been shown to function not only in the adult cortex but also during tangential migration of GABAergic neuroblasts. Therefore, it is of interest to focus on the possibility that a synergic action of these compounds (understood as a topobiological effect, implying place- and time-dependent interactions) may have important implications in regulating developmental processes such as neuronal migration, dendritic sprouting, synaptogenesis, and axon pruning, as well as being involved in regulation of synaptic plasticity trough life. The present review summarizes the actual knowledge in this field and discusses the possible importance that a dysregulation of GABAergic and reelin systems may have as vulnerability factors for the etiology and pathophysiology of schizophrenia.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Brain Chemistry / genetics
  • Brain Chemistry / physiology
  • Cell Adhesion Molecules, Neuronal / physiology*
  • Extracellular Matrix Proteins / physiology*
  • Humans
  • Nerve Tissue Proteins
  • Nervous System / growth & development*
  • Nervous System / physiopathology
  • Reelin Protein
  • Schizophrenia / metabolism
  • Schizophrenia / physiopathology*
  • Serine Endopeptidases
  • gamma-Aminobutyric Acid / physiology*

Substances

  • Cell Adhesion Molecules, Neuronal
  • Extracellular Matrix Proteins
  • Nerve Tissue Proteins
  • Reelin Protein
  • gamma-Aminobutyric Acid
  • RELN protein, human
  • Serine Endopeptidases