Perinatal and early postnatal changes in the expression of monocarboxylate transporters MCT1 and MCT2 in the rat forebrain

被引:36
作者
Baud, O
Fayol, L
Gressens, P
Pellerin, L
Magistretti, P
Evrard, P
Verney, C
机构
[1] Hop Robert Debre, INSERM, E9935, Lab Neurol Dev, F-75019 Paris, France
[2] Univ Lausanne, Inst Physiol, CH-1005 Lausanne, Switzerland
关键词
development; lactate; blood-brain barrier; astrocyte; neuron; radial glia; energy metabolism;
D O I
10.1002/cne.10853
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
In addition to glucose, monocarboxylates including lactate represent a major source of energy for the brain, especially during development. We studied the immunocytochemical expression of the monocarboxylate transporters MCT1 and MCT2 in the rat brain between embryonic day (E) 16 and postnatal day (P) 14. At E16-18, MCT1-like immunoreactivity was found throughout the cortical anlage, being particularly marked medially in the hippocampal anlage next to the ventricle. In a complementary pattern, MCT2-like immunoreactivity was expressed along the medial and ventral border of the ventricle in the medial septum and habenula before birth. The hypothalamic area exhibited MCT2 and MCT1 positive areas from E18 on. These transient labelings revealed four main sites of monocarboxylate and/or glucose exchange: the brain parenchyma, the epithelial cells, the ependymocytes, and the glia limitans. During the first postnatal week, MCT1 immunoreactivity extended massively to the vessel walls and moderately to the developing astrocytes in the cortex. In contrast, MCT2 immunoreactivity was faint in blood vessels but massive in developing astrocytes from P3 to P7. Neither MCT2 nor MCT1 colocalized with neuronal, microglial, or oligodendrocytic markers during the first postnatal week. At P14, a part of the scattered punctate MCT2 staining could be associated with astrocytes and postsynaptic dendritic labeling. The transient pattern of expression of MCTs throughout the perinatal period suggests a potential relationship with the maturation of the blood-brain barrier. (C) 2003 Wiley-Liss, Inc.
引用
收藏
页码:445 / 454
页数:10
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