Secretin deficiency causes impairment in survival of neural progenitor cells in mice

Peter I. Jukkola, Justin T. Rogers, Brian K. Kaspar, Edwin J. Weeber, Ichiko Nishijima

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)

Abstract

Hippocampal neurogenesis is the lifelong production of new neurons in the central nervous system (CNS), and affects many physiological and pathophysiological conditions, including neurobehavioral disorders. The early postnatal stage is the most prominent neurogenesis period; however, the functional role of neurogenesis in this developing stage has not been well characterized. To understand the role of hippocampal neurogenesis in the postnatal developing period, we analyzed secretin, a neuropeptide, which is expressed significantly higher in the development stage. Secretin is a pleiotropic neuropeptide hormone that belongs to the secretin/VIP/glucagon peptide family. Although secretin was originally isolated in the gastrointestinal system, it has been found that secretin itself acts as a neuropeptide in the CNS. Here, we report a new function of secretin as a survival factor for neural progenitor cells in the hippocampus. We found that secretin-deficient mice exhibit decreased numbers of BrdU-labeled new neurons and dramatically increased apoptosis of doublecortin-positive neural progenitor cells in the subgranular zone of the dentate gyrus (DG) during the early postnatal period. Furthermore, we found that reduced survival of neural progenitor cells leads to decreased volume of DG, reduced long-term potentiation and impaired spatial learning ability in adults. Our studies demonstrate that secretin has important implications for neurogenesis in postnatal development, and affects neurobehavioral function in the adult mouse.

Original languageEnglish
Article numberddq545
Pages (from-to)1000-1007
Number of pages8
JournalHuman molecular genetics
Volume20
Issue number5
DOIs
Publication statusPublished - 2011 Mar
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics
  • Genetics(clinical)

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