[Abstract Title]. - Society for Neuroscience

acute administration of corticosterone significantly reduced proliferation in males but not in
females. There were no significant effects on proliferation in males or females by acute exposure
to sex steroids or to inhibitors of sex-steroid synthesis. Co-incubation of female slices with
ovarian tissue significantly increased the number of BrdU-labeled cells suggesting a role for a
non-steroidal ovarian factor on adult VZ proliferation. Sex differences in VZ proliferation may
be one mechanism maintaining the sexually dimorphic song system of these birds. Stress may
impact adult male neural plasticity by suppressing mitosis along the VZ. Supported by
MH061994 and LNE Training Grant HD07228-26.
Disclosures: A. Mirzatoni , LNE training grant, Schlinger, B. Research Grant (principal
investigator, collaborator or consultant and pending grants as well as grants already received); A.
Katz, None; S. Dong, None; S. Zhen, None; B.A. Schlinger, None.
Poster
229. Neuronal and Glial Proliferation III
Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm
Program#/Poster#: 229.16/A16
Topic: A.02.a. Proliferation
Support: NIH grant NS 32401
Title: Postnatal hippocampal neurogenesis is deficient in PAC1 receptor mutant mice
Authors: *L. TASCAU 1 , A. FALLUEL-MOREL 1 , X. ZHOU 1 , P. BRABET 2 , E. DICICCO-
BLOOM 1,3,4 ;
1 Neurosci. and Cell Biol., UMDNJ, Piscataway, NJ; 2 INSERM U583, Montpellier, France;
3 Dept. of Pediatrics, UMDNJ-RWJMS, New Brunswick, NJ; 4 Cancer Inst. of New Jersey, New
Brunswick, NJ
Abstract: Pituitary adenylate cyclase-activating polypeptide (PACAP) and its main receptor
PAC1 are expressed as early as the development of the neural tube. The PACAP signaling
system is known to regulate multiple processes including proliferation, survival and
differentiation: in embryonic cortex, PACAP plays an antimitogenic role. Postnatally, mice with
PACAP-PAC1 system disruption exhibit poor social interactions, hyperactivity, and deficits in
learning, memory and mossy fiber LTP function, suggesting hippocampal abnormalities. In turn,
we now define developmental functions in the postnatal hippocampus in PAC1 deficient mice,
characterizing effects on cell proliferation and neuron production and survival.
At postnatal day 7 (P7) hippocampal formation DNA content (marker of total cells) was
decreased in PAC1 deficient mice (90.6±4.21% of control, p