The effects of CRF and the urocortins on [3H]GABA release from the rat amygdala-An in vitro superfusion study

Zsolt Bagosi, Miklós Jászberényi, Gyula Szabó, Gyula Telegdy

Research output: Contribution to journalArticle

14 Citations (Scopus)


Corticotropin-releasing factor (CRF) is the major neuromodulator of the hypothalamic-pituitary-adrenal axis, regulating the behavioural, endocrine, autonomic and immune responses to stress. Together with the recently discovered members of the CRF peptide family, urocortin 1, urocortin 2 and urocortin 3, it also has neurotransmitter actions. Previous publication has demonstrated that stress induces CRF release in the paraventricular nucleus of the hypothalamus and the release of both CRF and GABA in the amygdala. Accordingly, the aim of the present study was to determine the effects of the members of the CRF peptide family on GABA release from the amygdala by using an in vitro superfusion system. In order to study the participation of different CRF receptors (CRF1 and CRF2) in this process, rat amygdalar slices were pretreated with selective CRF1 and CRF2 antagonists. CRF and urocortin 1 significantly increased the release of [3H]GABA from the slices following electrical stimulation, whereas urocortin 2 and urocortin 3 were ineffective. The actions of CRF and urocortin 1 were blocked by the selective CRF1 receptor antagonist antalarmin, but were not inhibited by the selective CRF2 receptor antagonist astressin 2B, both administered in equimolar doses. Our results demonstrate that the release of GABA from the amygdala is mediated by CRF and urocortin 1 through the activation of CRF1 receptors.

Original languageEnglish
Pages (from-to)15-17
Number of pages3
JournalBrain Research Bulletin
Issue number1
Publication statusPublished - Jan 31 2008


  • Amygdala
  • CRF
  • GABA
  • Urocortin

ASJC Scopus subject areas

  • Neuroscience(all)

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