Penetration of glutamate into brain of 7-day-old rats

Viña,; Mr, DeJoseph; Pa, Hawkins; Hawkins, R. A.

doi:10.1007/bf02674614

Cited by 15 publications

(8 citation statements)

References 12 publications

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“…For example it was reported many years ago that glutamate is toxic to the brain if administered in the neonatal period [89]. Some attributed this to “immaturity” of the blood-brain barrier [90]. However, it can now be seen that the barrier contribution to toxicity is much more likely to be due to greater transport by e.g.…”

Section: Resultsmentioning

confidence: 99%

Molecular Characterisation of Transport Mechanisms at the Developing Mouse Blood–CSF Interface: A Transcriptome Approach

et al. 2012

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Exchange mechanisms across the blood–cerebrospinal fluid (CSF) barrier in the choroid plexuses within the cerebral ventricles control access of molecules to the central nervous system, especially in early development when the brain is poorly vascularised. However, little is known about their molecular or developmental characteristics. We examined the transcriptome of lateral ventricular choroid plexus in embryonic day 15 (E15) and adult mice. Numerous genes identified in the adult were expressed at similar levels at E15, indicating substantial plexus maturity early in development. Some genes coding for key functions (intercellular/tight junctions, influx/efflux transporters) changed expression during development and their expression patterns are discussed in the context of available physiological/permeability results in the developing brain. Three genes: Secreted protein acidic and rich in cysteine (Sparc), Glycophorin A (Gypa) and C (Gypc), were identified as those whose gene products are candidates to target plasma proteins to choroid plexus cells. These were investigated using quantitative- and single-cell-PCR on plexus epithelial cells that were albumin- or total plasma protein-immunopositive. Results showed a significant degree of concordance between plasma protein/albumin immunoreactivity and expression of the putative transporters. Immunohistochemistry identified SPARC and GYPA in choroid plexus epithelial cells in the embryo with a subcellular distribution that was consistent with transport of albumin from blood to cerebrospinal fluid. In adult plexus this pattern of immunostaining was absent. We propose a model of the cellular mechanism in which SPARC and GYPA, together with identified vesicle-associated membrane proteins (VAMPs) may act as receptors/transporters in developmentally regulated transfer of plasma proteins at the blood–CSF interface.

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Section: Resultsmentioning

confidence: 99%

Molecular Characterisation of Transport Mechanisms at the Developing Mouse Blood–CSF Interface: A Transcriptome Approach

et al. 2012

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“…The one reason n-3 PUFAdeficiency in this study is mild is that the decrease in brain DHA is only one-third of the control level. In addition, infant-stage mammals have an immature brain-blood barrier [17]. Therefore, our experimental design might make it conducive to recovering from the n-3 PUFA deficient condition.…”

Section: Discussionmentioning

confidence: 99%

Supplementation of DHA‐Rich Microalgal Oil or Fish Oil During the Suckling Period in Mildly n‐3 Fatty Acid‐Deficient Rat Pups

Kimura

Ito

Endo

et al. 2011

Lipids

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Long-chain polyunsaturated fatty acids (LC-PUFA), particularly arachidonic acid (ARA) and docosahexaenoic acid (DHA), are considered critical for the development of infants and are commonly supplemented in infant formulae. In this study, two common sources of n-3 LC-PUFA, fish oil (FO) and DHA-rich microalgal oil (DMO), were fed to rat pups of mildly n-3 PUFA-deficient dams to compare changes in LC-PUFA of tissue phospholipids. The milk from dams fed a n-3 PUFA-deficient diet contained less n-3 LC-PUFA than that of dams fed a control diet (AIN-93G). The pups' were given orally 1 mg/g weight of either FO or DMO for 17 days between the ages of 5 and 21 days, the pups were weaned, and sacrificed 1 week later for analysis of fatty acid compositions of brain, heart, kidney, spleen, and thymus phospholipids. Although both FO and DMO brought about a recovery in the tissue DHA levels compared to those of the control group (pups from AIN-93G-fed dams), DMO was more effective at restoring tissue LC-PUFA status because it was richer in DHA than FO. FO had a slightly lower PUFA level than that required to bring the LC-PUFA status completely to normal levels in this experiment, and EPA did not accumulate in tissues under the conditions tested here. These results demonstrate the effectiveness of ingesting either FO or DMO in the pre-weaning period for improving mild n-3 PUFA deficiency.

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“…The findings also help to explain a number of important previous observations on developmentally different effects of amino acids on brain function. For example it was reported many years ago that glutamate is toxic to the brain if administered in the neonatal period (Olney and Ho, 1970) which some attributed to “immaturity” of the blood–brain barrier (Viña et al, 1997). However, it can now be seen that the barrier contribution to toxicity is much more likely to be due to greater transport by, e.g., Slc1a4, see Table 4, which summarizes data on expression of influx transporters and published reports on transport function in the developing brain.…”

Section: Influx Mechanisms Across Brain Barriers In the Developing Brainmentioning

confidence: 99%

Barrier Mechanisms in the Developing Brain

Saunders¹,

Liddelow²,

2012

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The adult brain functions within a well-controlled stable environment, the properties of which are determined by cellular exchange mechanisms superimposed on the diffusion restraint provided by tight junctions at interfaces between blood, brain and cerebrospinal fluid (CSF). These interfaces are referred to as “the” blood–brain barrier. It is widely believed that in embryos and newborns, this barrier is immature or “leaky,” rendering the developing brain more vulnerable to drugs or toxins entering the fetal circulation from the mother. New evidence shows that many adult mechanisms, including functionally effective tight junctions are present in embryonic brain and some transporters are more active during development than in the adult. Additionally, some mechanisms present in embryos are not present in adults, e.g., specific transport of plasma proteins across the blood–CSF barrier and embryo-specific intercellular junctions between neuroependymal cells lining the ventricles. However developing cerebral vessels appear to be more fragile than in the adult. Together these properties may render developing brains more vulnerable to drugs, toxins, and pathological conditions, contributing to cerebral damage and later neurological disorders. In addition, after birth loss of protection by efflux transporters in placenta may also render the neonatal brain more vulnerable than in the fetus.

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Penetration of glutamate into brain of 7-day-old rats

Cited by 15 publications

References 12 publications

Molecular Characterisation of Transport Mechanisms at the Developing Mouse Blood–CSF Interface: A Transcriptome Approach

Molecular Characterisation of Transport Mechanisms at the Developing Mouse Blood–CSF Interface: A Transcriptome Approach

Supplementation of DHA‐Rich Microalgal Oil or Fish Oil During the Suckling Period in Mildly n‐3 Fatty Acid‐Deficient Rat Pups

Barrier Mechanisms in the Developing Brain

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