Direct immunogold labeling of aquaporin-4 in square arrays of astrocyte and ependymocyte plasma membranes in rat brain and spinal cord

Rash, John E.; Yasumura, Thomas; Hudson, C. S.; Agre, Peter; Nielsen, Søren

doi:10.1073/pnas.95.20.11981

Cited by 559 publications

(460 citation statements)

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“…In the brain, AQP4 is strongly expressed in astrocytes and ependymal cells (Yang et al 1995). Expression is strongest at sites of fluid transport including the pial and ependymal surfaces in contact with the cerebrospinal fluid (CSF), in the subarachnoid space, and the ventricular system (Rash et al 1998) suggesting a role for AQP4 in movement of water between brain and CSF compartments (Verkman et al 2006). Additionally, a role for AQP4 in the movement of water between blood and brain is suggested by polarized AQP4 expression found in astrocytic foot processes in direct contact with blood vessels (Verkman et al 2006).…”

Section: Discussionmentioning

confidence: 99%

Viral regulation of aquaporin 4, connexin 43, microcephalin and nucleolin

Fatemi¹,

Folsom²,

Reutiman³

et al. 2008

Schizophrenia Research

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The current study investigated whether human influenza viral infection in midpregnancy leads to alterations in proteins involved in brain development. Human influenza viral infection was administered to E9 pregnant Balb/c mice. Brains of control and virally exposed littermates were subjected to microarray analysis, SDS-PAGE and western blotting at three postnatal stages. Microarray analysis of virally-exposed mouse brains showed significant, two-fold change in expression of multiple genes in both neocortex and cerebellum when compared to sham-infected controls. Levels of mRNA and protein levels of four selected genes were examined in brains of exposed mice. Nucleolin mRNA was significantly decreased in day 0 and day 35 neocortex and significantly increased in day 35 cerebellum. Protein levels were significantly upregulated at days 35 and 56 in neocortex and at day 56 in cerebellum. Connexin 43 protein levels were significantly decreased at day 56 in neocortex. Aquaporin 4 mRNA was significantly decreased in day 0 neocortex. Aquaporin 4 protein levels decreased in neocortex significantly at day 35. Finally, microcephalin mRNA was significantly decreased in day 56 neocortex and protein levels were significantly decreased at 56 cerebellum. These data suggest that influenza viral infection in midpregnancy in mice leads to long term changes in brain markers for enhanced ribosome genesis (nucleolin), increased production of immature neurons (microcephalin), and abnormal glial-neuronal communication (connexin 43 and aquaporin 4).

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Section: Discussionmentioning

confidence: 99%

Viral regulation of aquaporin 4, connexin 43, microcephalin and nucleolin

Fatemi¹,

Folsom²,

Reutiman³

et al. 2008

Schizophrenia Research

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“…Goat anti-rabbit IgG conjugated to 10-nm and 20-nm gold beads was from Chemicon (Temecula, CA; no longer available), goat anti-rabbit IgG and goat anti-mouse IgG conjugated to the 6-nm, 12-nm, and 18-nm gold beads were from Jackson ImmunoResearch, and goat antirabbit IgG conjugated to 20-nm and 30-nm gold was from BBInternational, Ltd. (Ted Pella, Inc.). Controls included omission of primary antibodies to a target connexin, as well as doublelabeling some replicas for one connexin plus one non-connexin membrane protein [e.g., NMDA receptors (Rash and Yasumura, 1999;Rash et al, 2001bRash et al, , 2005 or aquaporin4 (AQP4) (Rash et al, 1998b;Furman et al, 2003)]. Labeled replicas were rinsed in distilled water, air dried at 60°C, and a stabilizing 20-nm coat of carbon was applied to the labeled side of the replica.…”

mentioning

confidence: 99%

Connexin36 vs. connexin32, “miniature” neuronal gap junctions, and limited electrotonic coupling in rodent suprachiasmatic nucleus

et al. 2007

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Suprachiasmatic nucleus (SCN) neurons generate circadian rhythms, and these neurons normally exhibit loosely-synchronized action potentials. Although electrotonic coupling has long been proposed to mediate this neuronal synchrony, ultrastructural studies have failed to detect gap junctions between SCN neurons. Nevertheless, it has been proposed that neuronal gap junctions exist in the SCN; that they consist of connexin32 or, alternatively, connexin36; and that connexin36 knockout eliminates neuronal coupling between SCN neurons and disrupts circadian rhythms. We used confocal immunofluorescence microscopy and freeze-fracture replica immunogold labeling to examine the distributions of connexin30, connexin32, connexin36, and connexin43 in rat and mouse SCN and used whole-cell recordings to re-assess electrotonic and tracer coupling. Connexin32-immunofluorescent puncta were essentially absent in SCN but connexin36 was relatively abundant. Fifteen neuronal gap junctions were identified ultrastructurally, all of which contained connexin36 but not connexin32, whereas nearby oligodendrocyte gap junctions contained connexin32. In adult SCN, one neuronal gap junction was >600 connexons, whereas 75% were smaller than 50 connexons, which may be below the limit of detectability by fluorescence microscopy and thin-section electron microscopy. Whole-cell recordings in hypothalamic slices revealed tracer coupling with Neurobiotin in <5% of SCN neurons, and paired recordings (>40 pairs) did not reveal obvious electrotonic coupling or synchronized action potentials, consistent with few neurons possessing large gap junctions. However, most neurons had partial spikes or spikelets (often <1 mV), which remained after QX-314 had blocked sodium-mediated action potentials within the recorded neuron, consistent with spikelet transmission via small gap junctions. Thus, a few "miniature" gap junctions on most SCN neurons appear to mediate weak electrotonic coupling between limited numbers of neuron pairs, Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2008 February 15. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript thus accounting for frequent detection of partial spikes and hypothetically providing the basis for "loose" electrical or metabolic synchronization of electrical activity commonly observed in SCN neuronal populations during circadian rhythms. Keywordsimmunocytochemistry; electrical synapse; freeze-fracture replica immunogold labeling; spikelet; metabolic coupling; syn...

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“…Water channel AQP4 is the predominant aquaporin in the CNS, and is abundantly expressed in the brain and spinal cord in perimicrovessel astrocyte foot processes, the glia limitans, and ependyma (Rash et al, 1998;Oshio et al, 2004;Vajda et al, 2004). AQP4 plays an important role in brain edema, astrocyte migration, and neuronal excitability (Tait et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

The Relationship Between Aquaporin‐4 Expression and Blood‐Brain and Spinal Cord Barrier Permeability Following Experimental Autoimmune Encephalomyelitis in the Rat

Huang

Wang

et al. 2010

The Anatomical Record

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Aquaporin 4(AQP4) is a water channel protein strongly expressed in the central nervous system in perimicrovessel astrocyte foot processes, the glia limitans, and ependyma. Expression of AQP4 is highest at the bloodbrain barrier and blood-spinal cord barrier, supporting its critical function in material transport across these structures. Recently, presence of the anti-aquaporin-4 antibody in sera has been used as an important diagnostic tool for neuromyelitis optica, suggesting a potential role in central nervous system inflammation. The aim of the present study was to examine AQP4 protein expression in the cerebellum and spinal cord from rats with experimental autoimmune encephalomyelitis. By western blot analysis, AQP4 expression increased during experimental autoimmune encephalomyelitis development, and peaked at onset (lumbar enlargement) or climax (cerebellum) of neurological signs of experimental autoimmune encephalomyelitis. There was also a faster and more pronounced increase in permeability in the cerebellar blood-brain barrier and the lumbar enlargement blood-spinal cord barrier consistent with AQP4 expression, which was manifested by increased Evans Blue leakage and reduced tight junction protein expression. In conclusion, aquaporin upregulation may be involved in the development of inflammation in the acute phase of experimental autoimmune encephalomyelitis, and may correlate with damage to central nervous system barrier function. Anat Rec, 294:46-54, 2011. V V C 2010 Wiley-Liss, Inc.

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Direct immunogold labeling of aquaporin-4 in square arrays of astrocyte and ependymocyte plasma membranes in rat brain and spinal cord

Cited by 559 publications

References 43 publications

Viral regulation of aquaporin 4, connexin 43, microcephalin and nucleolin

Viral regulation of aquaporin 4, connexin 43, microcephalin and nucleolin

Connexin36 vs. connexin32, “miniature” neuronal gap junctions, and limited electrotonic coupling in rodent suprachiasmatic nucleus

The Relationship Between Aquaporin‐4 Expression and Blood‐Brain and Spinal Cord Barrier Permeability Following Experimental Autoimmune Encephalomyelitis in the Rat

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