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Evidence that spinal interneurons undergo programmed cell death postnatally in the rat
S J Lawson1, H J Davies, J P Bennett
1Department of Anatomy and Cell Biology, Imperial College, School of Medicine at St. Mary's, London, UK.
The European Journal of Neuroscience
|April 1, 1997
Summary
This study reveals that spinal interneurons undergo programmed cell death after birth, a process previously undocumented in these neurons. This apoptosis may be a response to the shrinking of their synaptic targets during development.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- Programmed cell death (apoptosis) is a known mechanism for regulating neuronal population size after differentiation.
- However, its occurrence in all neuronal types, particularly spinal interneurons, remains unclear.
- Previous evidence for apoptosis in spinal interneurons has been lacking.
Purpose of the Study:
- To investigate the incidence and characteristics of programmed cell death in the rat spinal cord shortly after birth.
- To determine if spinal interneurons undergo apoptosis.
- To explore the potential triggers for this process.
Main Methods:
- Utilized three distinct methods to study apoptosis in the rat spinal cord.
- Confirmed apoptotic morphology using ultrastructural analysis.
- Employed immunocytochemical labeling for neuronal markers to identify dying cells as neurons.
Main Results:
- Identified a previously undocumented wave of apoptosis in the spinal grey matter occurring shortly after birth.
- Confirmed dying cells exhibited apoptotic morphology ultrastructurally.
- Immunocytochemical analysis indicated that the majority of apoptotic cells were interneurons, not motoneurons.
- This apoptotic wave occurred later than that in ventral horn motoneurons or dorsal root ganglion cells.
Conclusions:
- Spinal interneurons do undergo programmed cell death (apoptosis).
- This developmental process appears to be a discrete event occurring postnatally.
- The findings suggest that interneuron apoptosis may be triggered by the reduction in size of their primary synaptic targets.