Abstracts

Rationale: We recently have shown that multiple early-life seizures attenuate glutamate stimulated calcium permeability which may increase adaptive responses later in life that lead to neuroprotection. An important function of dendritic spines may be to protect neurons from highly elevated concentrations of calcium that follow sustained early-life seizures.Methods: Our previously established model was used to determine whether typical changes in morphology of CA1 pyramidal and granule cell neurons induced by a single episode of status epilepticus in prepubescent animals are attenuated by early-life seizures. The Golgi method was used for morphological analysis of the hippocampus of postnatal (P) day 20 rats 72 hrs after a single kainate (KA) seizure (1x KA) or following three seizures (3x KA), induced on P6, P9 and P20. Results: After 1x KA in the CA1, a large decrease in the number of apical, but not basal branches, was observed. Long thin and short stubby dendritic spine density was significantly reduced. Spine loss was accompanied by swellings and shortening of dendritic segments. In the dentate gyrus, a five fold increase in basal dendrites of granule neurons was measured relative to naive P20 controls. After 3x KA, relatively similar decreases or increases were observed among respective pyramidal and granule cell populations. Conclusions: The lack of further CA1 dendritic pruning after 3x KA may be due to adaptive responses whereby significant loss in excitatory morphology may be complete after the initial insult. Similarly, non-progressive changes in granule cell basal dendrite number or outgrowth present evidence for their role in adaptation following early-life seizures possibly by reducing calcium permeability.