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


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2007-01

AUTHORS

HOMA ADLE-BIASSETTE, PAUL OLIVIER, CATHERINE VERNEY, ROMAIN H. FONTAINE, PHILLIPPE EVRARD, DOMINIQUE HÉNIN, LAURENT MASSIAS, PIERRE GRESSENS, OLIVIER BAUD

ABSTRACT

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 alpha-cyano-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 < 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 ethanol-induced hypoglycemia in cortical brain damage induced by CIN. More... »

PAGES

54-60

Identifiers

URI

http://scigraph.springernature.com/pub.10.1203/01.pdr.0000250040.61888.61

DOI

http://dx.doi.org/10.1203/01.pdr.0000250040.61888.61

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1008370149

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/17211141


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18 schema:description 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 alpha-cyano-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 < 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 ethanol-induced hypoglycemia in cortical brain damage induced by CIN.
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28 DMSO
29 GFAP-positive astroglia
30 Injection of CIN
31 P1
32 P10
33 P3
34 addition
35 alpha-cyano-4-hydroxycinnamate
36 astroglia
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38 brain
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40 brain development
41 cell death
42 cerebral cortex
43 combination
44 consequences
45 cortex
46 cortical brain damage
47 cortical consequences
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51 damage
52 data
53 days P1
54 death
55 deleterious effects
56 development
57 disorganization
58 disturbances
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60 energy
61 energy supply
62 ethanol
63 ethanol-induced hypoglycemia
64 evidence
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66 glucose
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68 hypoglycemia
69 immature cerebral cortex
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