Differential localization and colocalization of two neuron-types of sodium-dependent inorganic phosphate cotransporters in rat forebrain

Sakata‐Haga, Hiromi; Kanemoto, Mizuki; Maruyama, Daisuke; Hoshi, Koich; Mogi, Koich; Narita, Minoru; Okado, Nobuo; Ikeda, Yayoi; Nogami, Hisashi; Fukui, Yoshihiro; Kojima, Itaru; Takeda, Jun; Hisano, Setsuji

doi:10.1016/s0006-8993(01)02290-9

Cited by 103 publications

(113 citation statements)

References 25 publications

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“…We also did not detect changes in VGLUT2 protein expression. In the DLPFC, VGLUT2 protein expression is highest in layer IV and is found at lower levels in layers I, II, III and VI [41,47,70,74,75]. Thus, our results suggest that presynaptic innervation arising from intrinsic PFC neurons expressing VGLUT2 is not altered in schizophrenia.…”

Section: Discussionmentioning

confidence: 53%

Altered Vesicular Glutamate Transporter Expression in the Anterior Cingulate Cortex in Schizophrenia

Oni-Orisan

Kristiansen

Haroutunian

et al. 2008

Biological Psychiatry

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Background-Schizophrenia is a chronic, severe mental illness with profound emotional and economic burdens for those afflicted and their families. An increasing number of studies have found that schizophrenia is marked by dysregulation of glutamatergic neurotransmission. While numerous studies have found alterations of postsynaptic molecules in schizophrenia, a growing body of evidence implicates presynaptic factors. Vesicular glutamate transporters (VGLUTs) have been identified and are known to package glutamate into vesicles in the presynaptic terminal for subsequent release into the synaptic cleft. Recent studies have shown that VGLUTs regulate synaptic activity via the amount of glutamate released. Accordingly, we hypothesized that VGLUTs are altered in schizophrenia, contributing to dysfunction of presynaptic activity.

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Section: Discussionmentioning

confidence: 53%

Altered Vesicular Glutamate Transporter Expression in the Anterior Cingulate Cortex in Schizophrenia

Oni-Orisan

Kristiansen

Haroutunian

et al. 2008

Biological Psychiatry

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“…In the last year, two groups have independently reported that BNPI is vesicular glutamate transporter itself and that BNPI is a potential tool for substantial studies on vesicular glutamate transporter. DNPI is a potential candidate for another vesicular glutamate transporter since DNPI is distributed throughout the brain, being especially abundant in the nerve endings of glutamatergic neurons where BNPI is scarce (15,16). Here we showed that DNPI actually functions as a vesicular glutamate transporter when expressed in COS7 cells.…”

Section: Discussionmentioning

confidence: 59%

Differentiation-associated Na+-dependent Inorganic Phosphate Cotransporter (DNPI) Is a Vesicular Glutamate Transporter in Endocrine Glutamatergic Systems

Hayashi

Otsuka

Morimoto

et al. 2001

Journal of Biological Chemistry

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108

111

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“…Hence, astrocytic Ca 2ϩ -dependent glutamate release can be blocked with bafilomycin A 1 (Araque et al, 2000;Bezzi et al, 2001;Pasti et al, 2001), which specifically interferes with V-ATPase, leading to alkalinization of vesicular lumen and collapsing the proton gradient necessary for VGLUTs to transport glutamate into vesicles. Brain tissue expresses VGLUT 1 and 2 isoforms (Ni et al, 1994(Ni et al, , 1995Hisano et al, 2000;Bai et al, 2001) in glutamatergic neurons (Bellocchio et al, 1998;Fremeau et al, 2001;Fujiyama et al, 2001;Herzog et al, 2001;Sakata-Haga et al, 2001;Kaneko et al, 2002;Varoqui et al, 2002). Recently, there have been reports indicating the presence of a VGLUT 3 isoform in subpopulations of GABAergic (Fremeau et al, 2002), cholinergic, and monoaminergic neurons (Fremeau et al, 2002;Gras et al, 2002;Schafer et al, 2002) and some astrocytes (Fremeau et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Vesicular Glutamate Transporter-Dependent Glutamate Release from Astrocytes

Montana¹,

Ni²,

Sunjara³

et al. 2004

J. Neurosci.

337

353

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Astrocytes exhibit excitability based on variations of their intracellular Ca 2ϩ concentrations, which leads to glutamate release, that in turn can signal to adjacent neurons. This glutamate-mediated astrocyte-neuron signaling occurs at physiological intracellular Ca 2ϩ levels in astrocytes and includes modulation of synaptic transmission. The mechanism underlying Ca 2ϩ -dependent glutamate release from astrocytes is most likely exocytosis, because astrocytes express the protein components of the soluble N-ethyl maleimide-sensitive fusion protein attachment protein receptors complex, including synaptobrevin 2, syntaxin, and synaptosome-associated protein of 23 kDa. Although these proteins mediate Ca 2ϩ -dependent glutamate release from astrocytes, it is not well understood whether astrocytes express functional vesicular glutamate transporters (VGLUTs) that are critical for vesicle refilling. Here, we find in cultured and freshly isolated astrocytes the presence of brain-specific Na ϩ -dependent inorganic phosphate cotransporter and differentiation-associated Na ϩ -dependent inorganic phosphate cotransporter that have recently been identified as VGLUTs 1 and 2. Indirect immunocytochemistry showed a punctate pattern of VGLUT immunoreactivity throughout the entire cell body and processes, whereas pharmacological inhibition of VGLUTs abolished mechanically and agonist-evoked Ca 2ϩ -dependent glutamate release from astrocytes. Taken together, these data indicate that VGLUTs play a functional role in exocytotic glutamate release from astrocytes.

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Differential localization and colocalization of two neuron-types of sodium-dependent inorganic phosphate cotransporters in rat forebrain

Cited by 103 publications

References 25 publications

Altered Vesicular Glutamate Transporter Expression in the Anterior Cingulate Cortex in Schizophrenia

Altered Vesicular Glutamate Transporter Expression in the Anterior Cingulate Cortex in Schizophrenia

Differentiation-associated Na+-dependent Inorganic Phosphate Cotransporter (DNPI) Is a Vesicular Glutamate Transporter in Endocrine Glutamatergic Systems

Vesicular Glutamate Transporter-Dependent Glutamate Release from Astrocytes

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