RT Journal Article
SR Electronic
T1 Glucose-Dependent Insulinotropic Polypeptide Is Expressed in Adult Hippocampus and Induces Progenitor Cell Proliferation
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 1816
OP 1825
DO 10.1523/JNEUROSCI.4920-04.2005
VO 25
IS 7
A1 Jenny Nyberg
A1 Michelle F. Anderson
A1 Björn Meister
A1 Ann-Marie Alborn
A1 Anna-Karin Ström
A1 Anke Brederlau
A1 Ann-Christin Illerskog
A1 Ola Nilsson
A1 Timothy J. Kieffer
A1 Max Albert Hietala
A1 Anne Ricksten
A1 Peter S. Eriksson
YR 2005
UL http://www.jneurosci.org/content/25/7/1816.abstract
AB The hippocampal dentate gyrus (DG) is an area of active proliferation and neurogenesis within the adult brain. The molecular events controlling adult cell genesis in the hippocampus essentially remain unknown. It has been reported previously that adult male and female rats from the strains Sprague Dawley (SD) and spontaneously hypertensive (SHR) have a marked difference in proliferation rates of cells in the hippocampal DG. To exploit this natural variability and identify potential regulators of cell genesis in the hippocampus, hippocampal gene expression from male SHR as well as male and female SD rats was analyzed using a cDNA array strategy. Hippocampal expression of the gene-encoding glucose-dependent insulinotropic polypeptide (GIP) varied strongly in parallel with cell-proliferation rates in the adult rat DG. Moreover, robust GIP immunoreactivity could be detected in the DG. The GIP receptor is expressed by cultured adult hippocampal progenitors and throughout the granule cell layer of the DG, including progenitor cells. Thus, these cells have the ability to respond to GIP. Indeed, exogenously delivered GIP induced proliferation of adult-derived hippocampal progenitors in vivo as well as in vitro, and adult GIP receptor knock-out mice exhibit a significantly lower number of newborn cells in the hippocampal DG compared with wild-type mice. This investigation demonstrates the presence of GIP in the brain for the first time and provides evidence for a regulatory function for GIP in progenitor cell proliferation.