[Abstract Title]. - Society for Neuroscience

cortices), only neonatal PCP treatment caused lasting behavioral alterations. (Supported by IAG
#224-07-007 between NCTR/FDA and NIEHS/NTP).
Disclosures: S.Y. Boctor, None; C. Wang, None; S.A. Ferguson, None.
Poster
232. Developmental Cell Death: Biological Effects
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 232.20/B60
Topic: A.06.a. Developmental cell death: Biological effects
Support: NIH Grant R01 548528
California Institute for Regenerative Medicine
Title: Cell-intrinsic mechanisms regulate cell death of cortical interneurons
Authors: *D. SOUTHWELL, A. ALVAREZ-BUYLLA;
Univ. California, San Francisco, CA
Abstract: Cortical interneurons are produced in the ganglionic eminences of the embryonic
ventral forebrain, from which they undergo a dramatic tangential migration into the developing
cortex. While recent studies have uncovered some of the genetic mechanisms that produce
interneuron diversity, less is known about the processes that regulate the maturation and
integration of these cells in the cortex. Developmental cell death is known to eliminate a large
fraction of nascent neural cell types in many regions of the nervous system. In the rodent
olfactory bulb, nearly forty to fifty percent of nascent interneurons die once they have migrated
and reached morphological maturity in the granule cell layer.
To examine the basic mechanisms guiding cortical interneuron cell death, we have performed
heterochronic transplantations of interneuron precursors. After introducing embryonic cells into
the neonatal cortex, we observe that around forty percent of grafted interneuron precursors are
eliminated. Furthermore, over a range of transplant sizes, the same fraction of transplanted cells
dies. Transplanted interneurons can increase the total cortical interneuron population by at least
fifty percent, without affecting the size of the endogenous interneuron cohort. These results
suggest that interneuron cell death does not necessarily follow from a simple intercellular
competition for limited signals. Rather, the cortex can support large numbers of supernumerary
interneurons, implying that programmed cell death does not fine-tune population size to match
an environmentally defined capacity. This further points to the precise control of progenitor
activity as a key determinant of the population size. Should a large fraction of developing