The role of cortical inhibition in the pathophysiology and treatment of schizophrenia

Zafiris J. Daskalakis, Paul B. Fitzgerald, Bruce K. Christensen

Research output: Contribution to journalReview ArticleResearchpeer-review

77 Citations (Scopus)

Abstract

Dysfunctional cortical inhibition (CI) has been suggested as a mechanism through which symptoms of schizophrenia (SCZ) are mediated. Cortical inhibition refers to a neurophysiological process in which γ-aminobutyric acid (GABA) inhibitory interneurons selectively attenuate the activity of other neurons (e.g., pyramidal neurons) in the cortex. Here we review the neuroanatomic and neurophysiological evidence suggesting CI deficits among persons with SCZ. We also review genetic studies that have linked CI deficits to a polymorphism in the α7-nicotinic cholinergic receptor, thereby positing that a specific genetic mechanism underlies SCZ-related GABA interneuron dysfunction. We will conclude by reviewing the role of CI as a mechanism mediating the therapeutic action of antipsychotic medications.

Original languageEnglish
Pages (from-to)427-442
Number of pages16
JournalBrain Research Reviews
Volume56
Issue number2
DOIs
Publication statusPublished - 1 Dec 2007

Keywords

  • Antipsychotic
  • GABA
  • Inhibition cortex
  • Interneuron
  • Schizophrenia
  • Transcranial magnetic stimulation

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