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

Baud, Olivier; Fayol, L; Gressèns, Pierre; Pellerin, Luc; Magistretti, Pierre J.; Evrard, Philippe; Verney, Catherine

doi:10.1002/cne.10853

Cited by 36 publications

(43 citation statements)

References 39 publications

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“…Currently available endothelial cell models for glutamatergic excitotoxicity studies consist of immortalized BMECs (Scott et al, 2007) and primary cultures of adult BMECs (Andras et al, 2007;Kuhlmann et al, 2008;Sharp et al, 2003Sharp et al, , 2005. We found that cultured neonatal and adult BMECs differed regarding both phenotype and function compared with adult BMECs, neonatal BMECs showed evidence of metabolic immaturity, with higher MCT1 and lower GLUT1 expression, in agreement with earlier published data (Baud et al, 2003;Vannucci and Simpson, 2003); higher NMDA subunit expression, with no difference, however, in the receptor-evoked [Ca 2 + ] i increase; and greater RT-PCR quantification of MCT1 and GLUT1 mRNA in neonatal (n = 7 and n = 4, respectively) and adult (n = 8 and n = 3, respectively) BMECs. Results are reported as relative units±s.e.m.…”

Section: Discussionsupporting

confidence: 91%

Newborn- and Adult-Derived Brain Microvascular Endothelial Cells Show Age-Related Differences in Phenotype and Glutamate-Evoked Protease Release

Legros¹,

Launay²,

Roussel³

et al. 2009

J Cereb Blood Flow Metab

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Few data are available on the involvement of brain microvascular endothelial cells (BMECs) in excitotoxic neonatal brain lesions. Therefore, we developed an original approach for investigating mouse-derived BMECs in vitro. We hypothesized that newborn and adult BMEC cultures would show age-related differences in phenotype and sensitivity to glutamate. Expression of the monocarboxylate transporter, MCT1, was higher in neonatal than in adult BMECs, whereas expression of the glucose transporter, GLUT1, was higher in adult than in neonatal BMECs that overexpressed the N-methyl-D-aspartate receptor NR1 subunit (NMDAR1) compared with adult BMECs. The ability of neonatal and adult BMECs to be activated by glutamate was confirmed through intracellular calcium ([Ca 2 + ] i ) recording. The glutamate-induced [Ca 2 + ] i increase was blocked by the selective NMDAR antagonist, MK-801. Significant glutamate-evoked concentrationdependent release of tissue-type plasminogen activator (t-PA) and matrix metalloproteinases (MMPs) activities was found in supernatants of neonatal, but not in adult BMECs. The glutamatemediated release of t-PA, MMP-2, and MMP-9 proteolytic activities in neonatal BMECs was blocked by MK-801. Conceivably, this protease release from neonatal BMECs may participate in neonatal brain lesions.

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Section: Discussionsupporting

confidence: 91%

Newborn- and Adult-Derived Brain Microvascular Endothelial Cells Show Age-Related Differences in Phenotype and Glutamate-Evoked Protease Release

Legros¹,

Launay²,

Roussel³

et al. 2009

J Cereb Blood Flow Metab

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“…The cerebral cortex in animals who received CIN just after birth displayed slight abnormalities in cortical architecture but significant disturbed neurons migration processes. Neuronal migration is an active process requiring high levels of energy demand along radial glial cells containing large amounts of glycogen (25) and maybe the presence of MCT1 (8). Most of neuronal migration is prenatal and CIN administration to pregnant mice just before birth, induced dramatic death for the embryos associated with critical cerebral dystrophy as neuronal ectopies (unpublished data).…”

Section: Metabolic Changes Following Cin Administrationmentioning

confidence: 94%

“…In parallel, the pattern of expression MCTs in the cerebral cortex varied at different stages of development (8,23). In particular, during early postnatal life, vessel walls expressed preferentially MCT1 whereas mature astrocytes expressed preferentially MCT2 (8,24).…”

Section: Metabolic Changes Following Cin Administrationmentioning

confidence: 99%

“…We previously emphasized the presence of monocarboxylate transporters (MCTs) in the different cell populations of the developing rat cerebral cortex and in the human visual cortex at midgestation including radial glia, mature astrocytes and ependimocytes (8,9). These studies demonstrate that lactate could be used as energy substrate in perinatal period, but physiologic relevance of its trafficking in developing brain have never been studied in vivo.…”

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confidence: 99%

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Cortical Consequences of In Vivo Blockade of Monocarboxylate Transport During Brain Development in Mice

et al. 2007

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In addition to glucose, monocarboxylates including lactate represent a major source of energy for the developing brain and appears to be crucial in the pathogenesis and recovery after brain damage. We hypothesized a role of monocarboxylates transport in the energy supply of neurons of the immature cerebral cortex. The effects of the blockade of monocarboxylates transport in vivo on the cortical development was investigated in neonatal mice using alphacyano-4-hydroxycinnamate (CIN) diluted either in DMSO (CD) or in ethanol (CE) administered intraperitoneally over postnatal day (P) P1 to P3. Injection of CIN induced a cytoarchitectonic disorganization in the parietal cortex likely due to a combination of slight disturbance of cortical neuronal migration and an increased neuronal cell death observed in CE (p Ͻ 0.05) but not in CD group. An increased number of activated GFAP-positive astroglia was observed in the neocortex in groups treated with CIN (CD and CE) on P10. These data: 1) Provide first evidence of deleterious effects observed in vivo after blockade of monocarboxylates transport in the developing brain; 2) emphasize the role of lactate during neuronal migration as a major source of energy; and 3) suggest the synergistic effect of ethanolinduced hypoglycemia in cortical brain damage induced by CIN. C erebral activity requires delivery of an adequate amount of energy substrates to neurons. In addition to glucose, the main source of energy for the brain, monocarboxylates including lactate play a significant role as alternative energy suppliers (1). Delivery of energy substrates from the blood to the brain requires specific transporters across the endothelial cells involved in blood-brain barrier and cellular membranes of the neurons and glia (2). Therefore, monocarboxylate transporters (MCTs) were supposed to play a key role in astrocyte/ neuronal shuttle as lactate release by astrocytes is likely to be a major energy substrate coupled with neuronal activity as suggested in adults (3). Moreover, monocarboxylate including lactate play a significant role as alternative energy suppliers in developing brain (4) and under challenged conditions including excitotoxic insult or inadequate glucose supply (5-7).Little is known about the energy trafficking during CNS development (4). We previously emphasized the presence of monocarboxylate transporters (MCTs) in the different cell populations of the developing rat cerebral cortex and in the human visual cortex at midgestation including radial glia, mature astrocytes and ependimocytes (8,9). These studies demonstrate that lactate could be used as energy substrate in perinatal period, but physiologic relevance of its trafficking in developing brain have never been studied in vivo.Alpha-cyano-4-hydroxycinnamate (CIN) is a competitive inhibitor of monocarboxylate transporters which is blood brain barrier permeable and appears to block lactate utilization by cells that import monocarboxylates (10). In vitro, using this transporter blocker, lactate has been reporte...

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“…astrocytes evolve in parallel with the maturation of the vascular endothelial cells involved in blood-brain barrier (BBB) formation [68,117]. During development, monocarboxylates including lactate represent a major source of energy for the developing neurons [118].…”

Section: Serotonin -A Chemical Messenger Between All Types Of Living mentioning

confidence: 99%

Sculpting Cerebral Cortex with Serotonin in Rodent and Primate

Vitalis¹,

Verney²

2017

Serotonin - A Chemical Messenger Between All Types of Living Cells

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The mammalian cerebral cortex is critical for sensory and motor integrations and, for higher-order cognitive functions. The construction of mammalian cortical circuits involves the coordinated interplay between cellular processes such as proliferation, migration and differentiation of neural and glial cell subtypes followed by accurate connectivity evolving in complexity in primates. Alteration in cortical development may induce the emergence of various pathological traits and behaviours. Among the large array of factors that regulate the assembly of cortical circuits, serotonin (5-HT) plays important role as a developmental signal that impacts on a broad diversity of cellular processes. 5-HT plays distinct roles during specific sensitive periods and is produced from various sources depending on the perinatal stage. Its roles are mediated by more than fourteen 5-HT receptors that are all G-protein coupled receptors except the ionotropic 5-HT type 3A receptor (5-HT 3A ) mediating rapid neuronal activation. Importantly, 5-HT metabolism and signalling are influenced by numerous epigenetic and genetic factors, including nutrition and gut microbiota, perinatal stress, infection and inflammation. In this review, we will recapitulate some evidences showing that dysregulation of 5-HT homeostasis and 5-HT 3A signalling impairs distinct steps of cortical circuit formation leading to the predisposition of the onset of various psychiatric diseases.

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

Cited by 36 publications

References 39 publications

Newborn- and Adult-Derived Brain Microvascular Endothelial Cells Show Age-Related Differences in Phenotype and Glutamate-Evoked Protease Release

Newborn- and Adult-Derived Brain Microvascular Endothelial Cells Show Age-Related Differences in Phenotype and Glutamate-Evoked Protease Release

Cortical Consequences of In Vivo Blockade of Monocarboxylate Transport During Brain Development in Mice

Sculpting Cerebral Cortex with Serotonin in Rodent and Primate

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