Related Experiment Video
Updated: Jun 11, 2026

Dissection of Hippocampal Dentate Gyrus from Adult Mouse
Published on: November 17, 2009
Reelin in the Infant Hippocampus, and Relationship to Sudden Infant Death Syndrome (SIDS) and Dentate Gyrus
Vanessa Despotovski1, Arunnjah Vivekanandarajah2, Karen A Waters2,3
1Discipline of Science, Life and Environmental Science, University of Sydney, Sydney, New South Wales, Australia.
Abstract:
Morphological features within the hippocampal dentate gyrus (DG) granule cell layer (GCL) have been identified in some cases of sudden unexpected infant death (SUDI), including sudden infant death syndrome (SIDS). Reelin, an extracellular matrix protein, is critical in neuronal migration and cell positioning. An altered reelin expression is hypothesized as a contributor to altered DG morphology. This study aimed to determine whether the number of reelin-expressing cells within the infant hippocampus is altered in (1) SIDS, and according to the presence of (2) SIDS risk factors (age, cigarette smoke exposure [CSE], sleep position, bed sharing, and upper respiratory tract infection [URTI]), and (3) DG morphology. Immunohistochemical staining of reelin was quantified (measured as the number of positive reelin cells/mm2) within the layers of the DG, CA4/Hilus, CA3-CA1, and subiculum in cases of explained SUDI (eSUDI, n = 12), SIDS I (n = 7), and SIDS II (n = 33). Reelin was highly correlated with age. After adjusting for age, SIDS II infants had a lower number of reelin immunopositive cells in the CA1, a finding that was more pronounced in bed sharers. Analysis of risk factors indicated lower reelin in the DG and CA3 of males, and in the DG of infants with URTI (when excluding bed sharers). The presence of the DG morphological feature of cluster ectopic cells was associated with a lower number of reelin cells across several hippocampal layers, whereas gaps were associated with higher numbers, with layers predominantly affected being the DG molecular layer and CA2 stratum radiatum.

