Cellular localization of Na+/MYO-inositol co-transporter mRNA in the rat brain

Inoue, Kiyoshi; Shimada, Shoichi; Minami, Yoichi; Morimura, Hiroyuki; Miyai, Akiko; Yamauchi, Atsushi; Tohyama, Masaya

doi:10.1097/00001756-199604260-00020

Cited by 19 publications

(20 citation statements)

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“…Moreover, no known reported literature has cited exogenous pathways as highly inducible under salinity challenge in the brain of fishes. In contrast, several studies on mammalian systems highlight the exogenous cotransporter pathways as a primary mechanism for intracellular myo-inositol accumulation (Fenili et al, 2011;Ibsen and Strange, 1996;Inoue et al, 1996) in the brain. It is possible that mammalian systems have diverged in their preferred mechanism for myo-inositol accumulation in the cell.…”

Section: Selective Permeability Of Teleost Bbb Favors Mib Pathwaymentioning

confidence: 99%

“…These studies could be performed by systematic inhibition of the various MIB enzymes or cotransporters using pharmacological agents. In mammalian systems, SMIT and other pathways have been localized in the brain of mammalian systems, demonstrating specialization in various areas of the brain (Ibsen and Strange, 1996;Inoue et al, 1996), and may also reflect differences in permeability of the capillaries. This may also be the case for MIB enzyme activity, and future studies should localize the specific region(s) of tilapia brain that contribute to the observed high MIB induction.…”

Section: Selective Permeability Of Teleost Bbb Favors Mib Pathwaymentioning

confidence: 99%

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Tilapia (Oreochromis mossambicus) brain cells respond to hyperosmotic challenge by inducingmyo-inositol biosynthesis

Gardell

Yang

Sacchi

et al. 2013

Journal of Experimental Biology

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SUMMARYThis study aimed to determine the regulation of the de novo myo-inositol biosynthetic (MIB) pathway in Mozambique tilapia (Oreochromis mossambicus) brain following acute (25 ppt) and chronic (30, 60 and 90 ppt) salinity acclimations. The MIB pathway plays an important role in accumulating the compatible osmolyte, myo-inositol, in cells in response to hyperosmotic challenge and consists of two enzymes, myo-inositol phosphate synthase and inositol monophosphatase. In tilapia brain, MIB enzyme transcriptional regulation was found to robustly increase in a time (acute acclimation) or dose (chronic acclimation) dependent manner. Blood plasma osmolality and Na + and Cl -concentrations were also measured and significantly increased in response to both acute and chronic salinity challenges. Interestingly, highly significant positive correlations were found between MIB enzyme mRNA and blood plasma osmolality in both acute and chronic salinity acclimations. Additionally, a mass spectrometry assay was established and used to quantify total myo-inositol concentration in tilapia brain, which closely mirrored the hyperosmotic MIB pathway induction. Thus, myo-inositol is a major compatible osmolyte that is accumulated in brain cells when exposed to acute and chronic hyperosmotic challenge. These data show that the MIB pathway is highly induced in response to environmental salinity challenge in tilapia brain and that this induction is likely prompted by increases in blood plasma osmolality. Because the MIB pathway uses glucose-6-phosphate as a substrate and large amounts of myo-inositol are being synthesized, our data also illustrate that the MIB pathway likely contributes to the high energetic demand posed by salinity challenge.

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Section: Selective Permeability Of Teleost Bbb Favors Mib Pathwaymentioning

confidence: 99%

Section: Selective Permeability Of Teleost Bbb Favors Mib Pathwaymentioning

confidence: 99%

Tilapia (Oreochromis mossambicus) brain cells respond to hyperosmotic challenge by inducingmyo-inositol biosynthesis

Gardell

Yang

Sacchi

et al. 2013

Journal of Experimental Biology

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“…Clarifying the mechanism of inositol transport into the CNS, the sodium-dependent myo-inositol transporter (SMIT l) was cloned, expressed and found to be present in large amounts in CP and in much lesser amounts in some neurons (44). The transporter, as expected, is located on the basal side of the CP and both, in vivo, and in monolayers of porcine CP in vitro is part of the mechanism that pumps inositol from the basal surface into the CP cell (16,17,38,39,44).…”

Section: Inositol Transport Through Choroid Plexusmentioning

confidence: 99%

Micronutrient and Urate Transport in Choroid Plexus and Kidney: Implications for Drug Therapy

2006

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With application of molecular biology techniques, there has been rapid progress in understanding how many drugs and micronutrients (e.g., vitamins) are transferred across the choroid plexus (CP), the main transport locus of the blood-cerebrospinal fluid (CSF) barrier, and the renal tubular epithelial cells. In many cases, these molecules are transported by separate, specific carriers or receptors on the apical and/or basal side of the CP or renal epithelial cells. This commentary focuses on four micronutrient transport systems in CP (ascorbic acid, folate, inositol, and riboflavin), all of which have been recently cloned, expressed and for which knockout mice models were developed and transporter localization studies performed. Also reviewed is the recently cloned uric acid transport system in human kidney in which there exists a human "knockout" model. The implications of these transport systems for drug therapy of central nervous system and renal disorders are discussed, especially with regard to methods to circumvent the blood-brain and blood-CSF barriers to deliver drugs to the brain.

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“…It is present in all regions of the brain, but there are large differences in mRNA distribution and transporter activity. 24,25 A second transporter of unrelated sequence is activated as the pH lowers, and is known as the H þ /myoinositol transporter (HMIT). 26 Following depolarization and protein kinase C (PKC) activation HMIT translocates to the plasma membrane at growth cones, leading to increased myo-inositol uptake.…”

Section: Inositol Uptake and Mood Stabilizersmentioning

confidence: 99%

Lithium and bipolar mood disorder: the inositol-depletion hypothesis revisited

2004

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Inositol, a simple six-carbon sugar, forms the basis of a number of important intracellular signaling molecules. Over the last 35 years, a series of biochemical and cell biological experiments have shown that lithium (Li þ ) reduces the cellular concentration of myo-inositol and as a consequence attenuates signaling within the cell. Based on these observations, inositol-depletion was proposed as a therapeutic mechanism in the treatment of bipolar mood disorder. Recent results have added significant new dimensions to the original hypothesis. However, despite a number of clinical studies, this hypothesis still remains to be either proven or refuted. In this review of our current knowledge, I will consider where the inositol-depletion hypothesis stands today and how it may be further investigated in the future.

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Cellular localization of Na+/MYO-inositol co-transporter mRNA in the rat brain

Cited by 19 publications

References 0 publications

Tilapia (Oreochromis mossambicus) brain cells respond to hyperosmotic challenge by inducingmyo-inositol biosynthesis

Tilapia (Oreochromis mossambicus) brain cells respond to hyperosmotic challenge by inducingmyo-inositol biosynthesis

Micronutrient and Urate Transport in Choroid Plexus and Kidney: Implications for Drug Therapy

Lithium and bipolar mood disorder: the inositol-depletion hypothesis revisited

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