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PACAP maintains cell cycling and inhibits apoptosis in chick neuroblasts

Nola M Erhardt1, Nancy M Sherwood

  • 1Department of Biology, University of Victoria, P.O. Box 1700, 3800 Finnerty Road, Victoria, BC, Canada V8W 2Y2.

Molecular and Cellular Endocrinology
|June 30, 2004
PubMed

Insights

Pituitary adenylate cyclase-activating polypeptide (PACAP) is essential for chick neuroblast survival. Blocking PACAP increases cell death, highlighting its role in maintaining brain development and cell proliferation.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cell Biology

Background:

  • Pituitary adenylate cyclase-activating polypeptide (PACAP) increases cAMP in embryonic chick neuroblasts.
  • Neuroblasts express PACAP mRNA, peptide, and receptor.

Purpose of the Study:

  • Investigate downstream effects of PACAP-induced cAMP.
  • Examine PACAP's role in regulating neuroblast cell numbers during brain development.

Main Methods:

  • Utilized flow cytometry to quantify proliferating cell nuclear antigen and DNA.
  • Assessed apoptotic cells and cell cycle compartments under varying conditions.
  • Employed a PACAP receptor antagonist to block endogenous PACAP signaling.

Main Results:

  • Untreated cultures exhibited high proliferation and low apoptosis.
  • Exogenous PACAP addition did not alter proliferation or apoptosis.
  • Blocking endogenous PACAP led to increased cell cycle exit and apoptosis.

Conclusions:

  • Endogenous PACAP is crucial for inhibiting apoptosis in chick neuroblasts.
  • PACAP signaling is required to maintain proliferative activity during early brain development.

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