Selective losses of brainstem catecholamine neurons after hypoxia-ischemia in the immature rat pup

被引：32

作者：

Buller, Kathryn M. ^{[1
]}

Wixey, Julie A. ^{[1
]}

Pathipati, Praneeti ^{[2
,3
]}

Carty, Michelle ^{[1
]}

Colditz, Paul B. ^{[1
]}

Williams, Christopher E. ^{[2
,3
]}

Scheepens, Arjan ^{[4
]}

机构：

[1] Univ Queensland, Perinatal Res Ctr, Brisbane, Qld 4029, Australia

[2] Univ Auckland, Liggins Inst, Auckland 1, New Zealand

[3] Univ Auckland, Natl Res Ctr Growth & Dev, Auckland 1, New Zealand

[4] Hortres, Auckland, New Zealand

来源：

PEDIATRIC RESEARCH | 2008年 / 63卷 / 04期

关键词：

D O I：

10.1203/PDR.0b013e3181659774

中图分类号：

R72 [儿科学];

学科分类号：

100202 ;

摘要：

Hypoxic-ischemic (HI) injury in the preterm neonate incurs numerous functional deficits, however little is known about the neurochemically-defined brain nuclei that may underpin them. Key candidates are the brainstem catecholamine neurons. Using an immature animal model, the postnatal day (P)-3 (P3) rat pup, we investigated the effects of HI on brainstem catecholamine neurons in the locus coeruleus, nucleus tractus solitarius (NTS), and ventrolateral medulla (VLM). On P21, we found that prior P3 HI significantly reduced numbers of catecholaminergic neurons in the locus coeruleus, NTS, and VLM. Only locus coeruleus A6, NTS A2, and VLM A1 noradrenergic neurons, but not NTS C2 and VLM C1 adrenergic neurons, were lost. There was also an associated reduction in dopamine-beta-hydroxylase-positive immunolabeling in the forebrain. These findings suggest neonatal HI can affect specific neurochemically-defined neuronal populations in the brainstem and that noradrenergic neurons are particularly vulnerable to HI injury.

引用

页码：364 / 369

页数：6

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