GABAergic synchronization in the limbic system and its role in the generation of epileptiform activity

Massimo Avoli, Marco de Curtis

Research output: Contribution to journalArticlepeer-review

Abstract

GABA is the main inhibitory neurotransmitter in the adult forebrain, where it activates ionotropic type A and metabotropic type B receptors. Early studies have shown that GABA A receptor-mediated inhibition controls neuronal excitability and thus the occurrence of seizures. However, more complex, and at times unexpected, mechanisms of GABAergic signaling have been identified during epileptiform discharges over the last few years. Here, we will review experimental data that point at the paradoxical role played by GABA A receptor-mediated mechanisms in synchronizing neuronal networks, and in particular those of limbic structures such as the hippocampus, the entorhinal and perirhinal cortices, or the amygdala. After having summarized the fundamental characteristics of GABA A receptor-mediated mechanisms, we will analyze their role in the generation of network oscillations and their contribution to epileptiform synchronization. Whether and how GABA A receptors influence the interaction between limbic networks leading to ictogenesis will be also reviewed. Finally, we will consider the role of altered inhibition in the human epileptic brain along with the ability of GABA A receptor-mediated conductances to generate synchronous depolarizing events that may lead to ictogenesis in human epileptic disorders as well.

Original languageEnglish
Pages (from-to)104-132
Number of pages29
JournalProgress in Neurobiology
Volume95
Issue number2
DOIs
Publication statusPublished - Oct 2011

Keywords

  • Epileptiform synchronization
  • GABA
  • High frequency oscillations
  • Limbic structures

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'GABAergic synchronization in the limbic system and its role in the generation of epileptiform activity'. Together they form a unique fingerprint.

Cite this