Dendritic arbors and dendritic excrescences of abnormally positioned neurons in area CA3c of mice carrying the mutation “Hippocampal lamination defect”

Abstract

BALB/cJ and BALB/cByJ mice are homozygous for the autosomal gene “hippocampal lamination defect” (provisional gene symbol: Hld) which produces an abnormality in the lamination of the pyramidal cell layer of area CA3c of the hippocampus such that early‐generated neurons are superficial and late‐generated neurons are deep. Other inbred strains of mice are wild‐type (+/+) at the Hld locus and do not have this inversion in cell position in area CA3c. The Golgi method was used to analyze the dendritic arbors of the abnormally positioned pyramidal cells and to compare the distribution of dendritic excrescences (i.e., the termination sites of the mossy fibers) in +/+ and Hld/Hld mice. It was found that in +/+ mice the late‐generated pyramidal cells (whose cell bodies are positioned just below the suprapyramidal mossy fiber layer) have one set of dendritic excrescences on their apical dendrites as they extend through the suprapyramidal mossy fiber layer and a second set on their basal dendrites as they pass through the infrapyramidal mossy fiber layer. In contrast, in Hld/Hld mice the late‐generated pyramidal cells (whose cell bodies are abnormally positioned just below the intrapyramidal mossy fiber layer) have two sets of dendritic excrescences on their apical dendrites, as they pass through the intrapyramidal and suprapyramidal mossy fiber layers, and none on their basal dendrites. In addition, in the vicinity of the apparent point of contact of the intrapyramidal mossy fibers, the apical dendrites of some of the abnormally positioned pyramidal cells have several fine‐caliber branches. These data indicate that (1) the apical dendrites of hippocampal pyramidal cells can form normally even though the cells never reach their normal position and (2) the dendritic excrescences are induced by contact from the mossy fibers. The anatomical differences produced by the Hld/Hld genotype provide some interesting clues as to the relationship between defects in neuronal migration and the subsequent establishment of axonal connections and could be the basis for some of the behavioral differences reported to exist between BALB/cJ and other inbred strains of mice.