Cerebral Cortex Advance Access originally published online on June 15, 2005
Cerebral Cortex 2006 16(3):301-312; doi:10.1093/cercor/bhi120
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Feature Article |
Cell Proliferation in the Adult Hippocampal Formation of Rodents and its Modulation by Entorhinal and Fimbria–Fornix Afferents
1 Development and Regeneration of the CNS, Department of Cell Biology, Barcelona Science Park-IRB, University of Barcelona, E-08028 Barcelona, Spain and 2 Cellular Neurobiology, Cell Biology Department, University of Valencia, Dr. Moliner, 50, Burjassot, E-46100, Spain
Address correspondence to J.A. del Río, Development and Regeneration of the CNS, Department of Cell Biology, Barcelona Science Park, University of Barcelona, Josep Samitier 1–5, E-08028 Barcelona, Spain. Email: jario{at}pcb.ub.es
New granule neurons are produced in the dentate gyrus (DG) of rodents throughout adult life. Recent studies have also reported adult neurogenesis in the cerebral cortex in normal animals or after brain injury. However, few of these studies focused on the hippocampal formation (HF), a cortical area involved in learning and memory in which extensive cell death occurs in neurodegenerative diseases. Thus, we studied cell proliferation in the HF of rodents and the intrinsic putative neurogenic potential of entorhinal cortex (EC) progenitors. We show that only the DG generates new neurons in the HF. In addition, neurospheres from the EC differentiate into neurons and glia in vitro and after transplantation in the adult DG. We also analyzed whether the absence of the synaptic input from the main hippocampal afferents induces neuronal generation in the HF outside the DG and/or regulates the proliferation of DG neuroprogenitors. We show that the denervation of the hippocampus does not induce neurogenesis in HF regions other than the DG. However, neuroprogenitor proliferation in the DG is reduced after fimbria–fornix lesions but not after entorhinal deafferentation, which supports the view that neuroprogenitor proliferation and/or differentiation in the DG are controlled from basal forebrain/septal neurons.
Key Words: fimbria–fornix lesion • hippocampal formation • NG2-positive cells • neural progenitor cells • perforant pathway lesion
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