Glucocorticoids applied prenatally alter birth weight and the maturation of the lungs. Moreover, glucocorticoids impair neuronal proliferation and differentiation in the hippocampal dentate gyrus. In the present study proliferation and neuronal differentiation in the dentate gyrus were studied in newborn common marmoset monkeys which were intrauterinely exposed to the synthetic glucocorticoid dexamethasone (DEX). Pregnant marmoset monkeys received DEX (5 mg/kg body weight) daily either during early (days 42-48) or late (days 90-96) pregnancy. In the hippocampi of newborn monkeys immunohistochemistry was performed with markers of proliferation (Ki-67), apoptosis (in situ tailing) as well as early and late neuronal differentiation (calretinin and calbindin). Both after early and late intrauterine exposure to DEX, proliferation of dentate gyrus cells was significantly decreased (P < 0.05). The density of apoptotic neurons was not altered by DEX treatment. Quantification of calretinin- and calbindin-immunoreactive neurons showed no significant differences between DEX-exposed and control animals. In conclusion, the proliferation of putative precursor cells but not the differentiation into mature cells was impaired in the dentate gyrus of newborn marmosets exposed intrauterinely to DEX.
In selected cases acquired peroneal palsy is caused by intraneural ganglia. In contrast to the much more frequent "loco typico" lesion which is caused by external pressure, intraneural ganglia can be treated by microscopic nerve surgery as part of primary treatment strategy. A careful clinical history as well as a profound clinical and electrophysiological examination is required to disclose unusual findings. These are common in non-typical peroneal palsy. In this situation high resolution nerve sonography is a fast and sensitive method to detect intraneural ganglia. We report a case series of three patients with peroneal palsy caused by intraneural ganglia and give a review of the literature.
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