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Programmed cell death of an identified motoneuron in vitro: temporal requirements for steroid exposure and protein

K L Hoffman1, J C Weeks

  • 11254 Institute of Neuroscience, University of Oregon, Eugene 97403-1254, USA.

Insights

Ecdysteroid hormones induce programmed cell death (PCD) in specific moth neurons. APR(6) neurons commit to PCD late in larval development, independent of further steroid exposure.

Area of Science:

  • Developmental biology
  • Neuroscience
  • Endocrinology

Background:

  • Ecdysteroid hormones regulate insect development and metamorphosis.
  • Specific motoneurons undergo programmed cell death (PCD) during insect development.
  • Accessory planta retractor (APR) motoneurons in Manduca sexta exhibit differential survival during pupation.

Purpose of the Study:

  • To investigate the cellular and molecular mechanisms underlying ecdysteroid-induced PCD in APR motoneurons.
  • To determine the critical timing of developmental commitment to PCD in APR(6) neurons.
  • To elucidate the role of ecdysteroids and protein synthesis in APR(6) neuron death.

Main Methods:

  • Retrograde labeling with DiI to visualize motoneuron morphology in vivo.
  • In vitro culture of APR neurons with and without ecdysteroids and cycloheximide (CHX).
  • Microscopic examination of cell morphology, plasma membrane integrity, DNA condensation, and mitochondrial activity.

Main Results:

  • APR(4) motoneurons survive pupation, while APR(6) motoneurons undergo PCD 24-48 hours after pupal ecdysis.
  • APR(6) neurons exhibit somatic shrinkage, DNA condensation, and loss of mitochondrial activity during PCD.
  • APR(6) neurons cultured at pupal ecdysis die independently of further ecdysteroids and CHX, but those cultured earlier require ecdysteroids and are sensitive to CHX.

Conclusions:

  • The final 24 hours of larval life are crucial for APR(6) neuron commitment to PCD.
  • Steroid-induced PCD involves a critical transition period in late larval development.
  • Further research is needed to uncover the molecular pathways of steroid-induced PCD in these neurons.

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