Reduced expression of brain-derived neurotrophic factor in mice deficient for pituitary adenylate cyclase activating polypeptide type-I-receptor

Mathias Zink, Christiane Otto, Björn Zörner, Christiane Zacher, Günther Schütz, Fritz A. Henn, Peter Gass

Research output: Contribution to journalArticlepeer-review

30 Scopus citations

Abstract

In vitro pituitary adenylate cyclase activating polypeptide (PACAP) induces the expression of brain-derived neurotrophic factor (BDNF) via its specific receptor PAC1. Since BDNF has been implicated in learning paradigms and mice lacking functional PAC1 have deficits in hippocampus-dependent associative learning, we investigated whether PAC1 mutants show alterations in hippocampal expression of BDNF and its receptor TrkB. Semi-quantitative in situ-hybridization using exon-specific BDNF-probes revealed significantly reduced expression of the exon-III and exon-V-specific transcripts within the hippocampal CA3 region in PAC1-deficient mice. A similar trend was observed for the exon-I-specific transcript. The expression of the exon-III-specific transcript was also reduced within the dentate gyrus, while Trk B-expression did not differ between genotypes. Our data demonstrate that even in vivo PAC1-mediated signaling seems to play a pivotal role for the transcriptional regulation of BDNF.

Original languageEnglish
Pages (from-to)106-108
Number of pages3
JournalNeuroscience Letters
Volume360
Issue number1-2
DOIs
StatePublished - 22 Apr 2004
Externally publishedYes

Keywords

  • Brain-derived neurotrophic factor
  • In situ-hybridization
  • PACAP-type-I-receptor
  • Pituitary adenylate cyclase activating polypeptide (PACAP)

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