International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
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Int. J. Dev. Neurosci. · Jun 2007
Insulin-like growth factor-I (IGF-I) inhibits neuronal apoptosis in the developing cerebral cortex in vivo.
Increased expression of insulin-like growth factor-I (IGF-I) in embryonic neural progenitors in vivo has been shown to accelerate neuron proliferation in the neocortex. In the present study, the in vivo actions of (IGF-I) on naturally occurring neuron death in the cerebral cortex were investigated during embryonic and early postnatal development in a line of transgenic (Tg) mice that overexpress IGF-I in the brain, directed by nestin genomic regulatory elements, beginning at least as early as embryonic day (E) 13. The areal density of apoptotic cells (N(A), cells/mm2) at E16 in the telencephalic wall of Tg and littermate control embryos was determined by immunostaining with an antibody specific for activated caspase-3. ⋯ Transgenic mice at P0 and P5 exhibited significant decreases in the N(V) of apoptotic cells in the cerebral cortex (31% and 39%, respectively). The vast majority of these apoptotic cells (> 90%) were judged to be neurons by their morphological appearance. Increased expression of IGF-I inhibits naturally occurring (i.e. apoptotic) neuron death during early postnatal development of the cerebral cortex to a degree that sustains a persistent increase in total neuron number even in the adult animal.
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Int. J. Dev. Neurosci. · Jun 2007
Sex and region difference of the expression of ERK in prenatal stress offspring hippocampus.
Prenatal stress is known to cause neuronal loss and oxidative damage in the hippocampus of offspring rats. The underlying molecular mechanism has not been fully understood. The extracellularsignal-regulated kinase (ERK1/2) is recruited when the brain undergoes synaptic plasticity and remodeling. ⋯ However, ERK optical density was not significantly different between male control and PNS groups in CA1, CA4 fields and DG in offspring hippocampus. These findings suggest the sex and region-dependent effects of prenatal stress on the expression of ERK in offspring hippocampus. ERK expression changes induced by prenatal stress may contribute to hippocampus synaptic plasticity changes of the offspring.