This article is a US Government work and, as such, is in the public domain in the United States of America.
Endogenous IGF1 enhances cell survival in the postnatal dentate gyrus †
Article first published online: 30 APR 2001
Published 2001 Wiley-Liss, Inc.
Journal of Neuroscience Research
Volume 64, Issue 4, pages 341–347, 15 May 2001
How to Cite
Cheng, C. M., Cohen, M., Tseng, V. and Bondy, C. A. (2001), Endogenous IGF1 enhances cell survival in the postnatal dentate gyrus . J. Neurosci. Res., 64: 341–347. doi: 10.1002/jnr.1084
- Issue published online: 30 APR 2001
- Article first published online: 30 APR 2001
- Manuscript Accepted: 1 FEB 2001
- Manuscript Revised: 30 JAN 2001
- Manuscript Received: 14 DEC 2000
The dentate gyrus is selectively reduced in size in the insulin-like growth factor 1 (IGF1) null mouse brain. The purpose of this study was to determine whether this defect is due to reduced granule cell numbers, and if so, to determine whether altered cell proliferation, survival, or both contribute to attenuation of dentate gyrus size. At postnatal day 10 (P10), granule cell numbers were not significantly different in IGF1 null and littermate wildtype (WT) dentate gyri. The subgranular zone cell population, however, was relatively increased, and the granule cell layer population relatively decreased in the IGF1 null dentate gyrus. By P50, total dentate cell numbers were decreased by 20% (P = 0.01) in the IGF1 null mouse, although IGF1 null subgranular zone progenitor cells remained relatively increased compared with WT (38%, P < 0.05). IGF1 null dentate cell proliferation, assessed by thymidine analogue incorporation, was actually increased at P10 (33%, P < 0.05) and P50 (167%, P = 0.001). Dentate granule cell death, assessed by the appearance of pycnotic cells and DNA fragmentation, was also significantly increased in the IGF1 null dentate (61%, P < 0.05 and 101%, P = 0.03). These data suggest that endogenous IGF1 serves an important role in dentate granule cell survival during the course of postnatal brain development. In addition, this work suggests the potential of a compensatory mechanism promoting increased dentate cell proliferation in the face of impaired cell survival during postnatal neurogenesis. J. Neurosci. Res. 64:341–347, 2001. Published 2001 Wiley-Liss, Inc.