Maternal Perinatal Undernutrition Alters Postnatal Development of Chromaffin Cells in the Male Rat Adrenal Medulla
Maternal Perinatal Undernutrition Alters Postnatal Development of Chromaffin Cells in the Male Rat Adrenal Medulla
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DOI：
10.1159/000209222
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发表时间：
2009-01-01
影响因子：
4.1
通讯作者：
Breton, Christophe
中科院分区：
文献类型：
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作者：
Molendi-Coste, Olivier;Laborie, Christine;Breton, Christophe
大量数据表明，交感肾上腺系统的发展是高度敏感的围产期环境。我们以前曾报道，母亲围产期食物限制50%（FR50）改变了嗜铬细胞（CC）的组织和活动在断奶的后代。本研究探讨了FR 50对出生后CC功能和结构适应的时间过程的影响。FR 50幼崽早在出生后第7天（P7）就表现出较小且更丰富的分散去甲肾上腺素能CC簇，这表明形态变化在发育过程中发生得更早。出生时，肾上腺素的释放是有缺陷的FR 50幼崽，这表明母亲FR 50受损的非神经源性控制的儿茶酚胺释放。在P4时，FR 50幼仔中也不存在对胰岛素诱导的低血糖反应的儿茶酚胺释放。这与肾上腺儿茶酚胺含量减少有关，表明不能合成儿茶酚胺可能导致分泌受损。我们假设母体FR50加速了CC和内脏神经末梢之间的功能连接，导致非神经源性反应的过早丧失。含乙酰胆碱的突触末梢似乎更早熟的功能在FR 50的幼崽，在P14的乙酰胆碱酯酶活性水平的增加所建议的。在P7时，胰岛素诱导的低血糖导致两组中肾上腺素优先释放，并伴有儿茶酚胺含量增加。然而，在FR 50幼仔中反应加重。在P14时，胰岛素激发增加了对照大鼠的血浆肾上腺素水平，而它显着提高了FR 50幼崽中两种儿茶酚胺的循环水平。我们证明，母体FR50导致发育受损的去甲肾上腺素能CC聚集和先进的内脏神经传递成熟与改变髓质活动，以应对代谢应激。这可能导致肾上腺髓质的长期编程不良和慢性成人疾病的发展。版权所有（C）2009 S. Karger AG，巴塞尔
Numerous data suggest that the development of the sympathoadrenal system is highly sensitive to the perinatal environment. We previously reported that maternal perinatal food restriction by 50% (FR50) altered chromaffin cell (CC) organization and activity in offspring at weaning. This study investigated the effects of FR50 on the postnatal time course of CC functional and structural adaptations. FR50 pups exhibited smaller and more abundant scattered clusters of noradrenergic CCs as early as postnatal day 7 (P7), indicating that morphological changes took place earlier during development. At birth, the adrenaline release was defective in FR50 pups, suggesting that maternal FR50 impaired the non-neurogenic control of catecholamine release. At P4, the catecholamine release in response to insulin-induced hypoglycaemia was also absent in FR50 pups. This was associated with the reduction of adrenal catecholamine contents, indicating that the failure to synthesize catecholamine might lead to impaired secretion. We hypothesized that maternal FR50 accelerated the functional connections between CCs and splanchnic nerve endings, leading to the premature loss of the non-neurogenic response. Acetylcholine-containing synaptic endings seemed more precociously functional in FR50 pups, as suggested by increased levels of acetylcholine esterase activity at P14. At P7, insulin-induced hypoglycaemia caused preferential adrenaline release associated with increased catecholamine contents in both groups. However, the response was accentuated in FR50 pups. At P14, the insulin challenge increased plasma levels of adrenaline in control rats, whereas it markedly enhanced the circulating level of both catecholamines in FR50 pups. We demonstrated that maternal FR50 leads to developmentally impaired noradrenergic CC aggregation and advanced splanchnic neurotransmission maturation associated with altered medulla activity in response to metabolic stress. This might contribute to the long-lasting malprogramming of the adrenal medulla and to the development of chronic adult diseases. Copyright (C) 2009 S. Karger AG, Basel