Thursday, May 17, 2012
Sheraton Hall (Sheraton Centre Toronto)
9:00 AM
E. Ejaz, J. Camacho and V. Martinez Cerdeno, Pathology and Laboratory Medicine, University of California, Davis, Sacramento, CA
Background: Autism is characterized by abnormalities in social interaction, communication, and repetitive interest and behavior. This project investigates whether changes in Cajal-Retzius (CR) cell number is associated with autism. CR cells are located in the marginal zone of the cerebral cortex during development and in layer I of the mature adult cortex. CR cells secrete the protein Reelin (RELN) into the extracellular matrix. A large population of CR cells are thought to die after cortical development but a portion of the CR cells persist into adulthood, where they continue to express RELN. The absence of RELN has been shown to alter cellular migration and results in an inversion of the cortical layers in the developing cerebral cortex. In addition, RELN plays an important role in the regulation of neurotransmission and synaptic plasticity in adults. The
RELN gene and RELN protein have been implicated in autism. Previous work has reported that the levels of RELN protein and mRNA are significantly reduced in the cerebellum and frontal cortex of autistic brains. In addition, it has been suggested that the
RELN gene may be one of the loci contributing to the positive linkage between chromosome 7q and autism.
Objectives: Since RELN is produced by CR cells in the adult cerebral cortex, and a decrease in RELN protein has been associated with autism, we hypothesized that the decrease in RELN may be caused by a decrease in the number of CR cells in layer I of the cerebral cortex.
Methods: To test this hypothesis we used unbiased stereological methods to determine the number of CR cells in layer I of the human superior temporal lobe of six autistic and six age-matched control subjects.
Results: We found that the total number and the density of CR cells in layer I of the superior temporal lobe is similar in autistic and control cases.
Conclusions: We conclude that the decreased level of RELN in the human autistic cerebral cortex is not caused by a decrease in the number of Cajal-Retzius cells in layer I of the cerebral cortex.
