Maternal adrenalectomy at the early onset of gestation impairs the postnatal development of the rat hippocampal formation: Effects on cell numbers and differentiation, connectivity and calbindin-D28k immunoreactivity

Abstract

The possible role of the maternal glucocorticoids on the postnatal development of the hippocampus was tested with bilateral adrenalectomy of pregnant rats. Surgery was performed 24 hr after sperm‐positiveness was determined. The offspring from adrenalectomized mothers, compared with animals from control sham‐operated mothers, showed decreased body weight and increased brain weight. The CA1 field of the hippocampus of these animals showed lower number of both Nissl‐stained and Calbindin‐immunoreactive cells, whereas the granule cell layer of the dentate gyrus showed higher number of both populations. Both types of cell numbers were statistically similar from postnatal Day 21, however, suggesting some compensatory mechanism. The neuronal populations of adrenalectomized animals appeared with a delay in the development of their dendritic trees, cytoplasmic differentiation, and synaptic connections. In the same way, both septohippocampal and hippocamposeptal projections appeared delayed in the adrenalectomized animals with respect to control ones by several days, mainly with regard to regressive events typical of the first 8 days of age. The ultrastructural study showed that every ADX postnatal group appeared more immature than the corresponding control group. These results suggest that gestational levels of maternal glucocorticoids (that were removed by adrenalectomy) influence the normal postnatal development of the hippocampus as reflected in neuron numbers and cell maturation, as well as in the developmental timing of the pattern of connectivity, and that this effect must be accomplished both in neuroepithelium and post‐mitotic cells before the endogenous fetal hormones are secreted and reach concentrations capable to produce a response. J. Neurosci. Res. 62:644–667, 2000. © 2000 Wiley‐Liss, Inc.

Prenatal Risk for Autism Spectrum Disorder (ASD): Fetal Cortisol Exposure Predicts Child ASD Symptoms

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The hippocampus of the eastern rock sengi: cytoarchitecture, markers of neuronal function, principal cell numbers, and adult neurogenesis

“…In contrast, the absence of calbindin from superficial pyramidal cells in spite of a pronounced condensation of the cell layer suggests an independent development of these characteristics in the sengi, guinea pig and rabbit CA1. Mechanisms related to age- (Poitier et al, 1994; Villa et al, 1994; de Jong et al, 1996), activity- (Lowenstein et al, 1991; Maglóczky et al, 1997), or hormone-dependent (Krugers et al, 1995; Trejo et al, 2000) changes of calbindin content in hippocampal principal cells may mediate species-specific expression patterns. Deep calbindin+ pyramidal cells are present in CA1 of fox and primates and in the distal and temporal CA1 of mouse and rat.…”

Prenatal stress and depression associated neuronal development in neonates

“…During pregnancy, maternal glucocorticoids have direct effects on the fetal hippocampal neurons under normal physiological and stress conditions. Trejo et al (2000) showed that bilateral adrenalectomy in pregnant rats delayed in hippocampal development, reduced dendritic branching and synaptic connections, and conditions were reversed after glucocorticoid administration to adrenalectomized mothers. These revealed that maternal glucocorticoids are essential for hippocampal neuronal development.…”