Connexin30 in rodent, cat and human brain: selective expression in gray matter astrocytes, co-localization with connexin43 at gap junctions and late developmental appearance

Nagy, J.I.; Patel, Daywin; Ochalski, P.A.Y; Stelmack, Gerald L.

doi:10.1016/s0306-4522(98)00191-2

Cited by 317 publications

(313 citation statements)

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“…9A-C; 12-nm gold beads). In other oligodendrocyte gap junctions, Cx47 was detected without Cx32 (not shown), suggesting that Cx47 becomes abundant prior to Cx32, coincident with the increase in Cx43 at oligodendrocyte-to-astrocyte gap junctions (Nagy et al, 1999). As previously documented in other CNS regions (Rash et al, 2001a;Rash et al, 2001b), Cx32 was present only oligodendrocytes, in the oligodendrocyte-side of astrocyte-to-oligodendrocyte gap junctions, and never in the plasma membranes of astrocytic, neuronal or ependymocyte gap junctions.…”

Section: Cx32: In Gap Junctions or As Dispersed Connexons?supporting

confidence: 71%

“…5G,H; 6-nm and 18-nm gold beads). Cx32 (labeled with 12-nm gold beads; none present) was not detected in neuronal gap junctions and was only very weakly detected in oligodendrocyte gap junctions (see below), which begin to appear at about this time in many other brain regions (Yamamoto et al, 1992;Nagy et al, 1999;Nagy et al, 2003b). Similarly, in P21 mouse LC labeled for Cx32+Cx36, one neuronal gap junction labeled for Cx36 was found on a small diameter dendrite (Fig.…”

mentioning

confidence: 87%

“…Early on, it was proposed that neurons share gap junctions only with neurons, and that glia share intercellular gap junctions only with glia (Brightman and Reese, 1969;Mugnaini, 1986). This "restricted coupling partner" hypothesis gained support based on TEM and FRIL immunocytochemical data showing that neuronal, astrocytic and oligodendrocytic gap junctions each express different complements of connexins Nagy and Dermietzel, 2000;Rash et al, 2000Rash et al, , 2001bKamasawa et al, 2005;Fukuda et al, 2006), with Cx43, Cx30 and (in limited areas) Cx26 in astrocytes and leptomeninges (Li et al, 1997;Nagy et al, 1999Nagy et al, ,2001Rash et al, 2001b); Cx29, Cx32 and Cx47 in oligodendrocytes (Rash et al, 2001a(Rash et al, ,2001bNagy et al, 2004;Kamasawa et al, 2005); and Cx36 exclusively in neurons (Rash et al, 2001b;Fukuda et al, 2006), extending data from immunofluorescence analysis and thin-section immunocytochemistry (Yamamoto et al, 1990a(Yamamoto et al, ,1990bScherer et al, 1995;Mercier and Hatton, 2001;Altevogt et al, 2002;Kleopas et al, 2004;Rash et al, 2005).…”

Section: Connexin Composition Of Neuronal Vs Glial Gap Junctions In Lcmentioning

confidence: 99%

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Identification of connexin36 in gap junctions between neurons in rodent locus coeruleus

et al. 2007

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Locus coeruleus neurons are strongly coupled during early postnatal development, and it has been proposed that these neurons are linked by extraordinarily abundant gap junctions consisting of connexin32 and connexin26, and that those same connexins abundantly link neurons to astrocytes. Based on the controversial nature of those claims, immunofluorescence imaging and freeze-fracture replica immunogold labeling were used to re-investigate the abundance and connexin composition of neuronal and glial gap junctions in developing and adult rat and mouse locus coeruleus. In early postnatal development, connexin36 and Cx43 immunofluorescent puncta were densely distributed in the locus coeruleus, whereas connexin32 and connexin26 were not detected. By freeze-fracture replica immunogold labeling, connexin36 was found in ultrastructurally-defined neuronal gap junctions, whereas connexin32 and connexin26 were not detected in neurons and only rarely detected in glia. In 28-day postnatal (adult) rat locus coeruleus, immunofluorescence labeling for connexin26 was always co-localized with the glial gap junction marker connexin43; connexin32 was associated with the oligodendrocyte marker CNPase; and connexin36 was never co-localized with connexin26, Cx32 or connexin43. Ultrastructurally, connexin36 was localized to gap junctions between neurons, whereas connexin32 was detected only in oligodendrocyte gap junctions; and Cx26 was found only rarely in astrocyte junctions but abundantly in pia mater. Thus, in developing and adult locus coeruleus, neuronal gap junctions contain connexin36 but do not contain detectable connexin32 or connexin26, suggesting that the locus coeruleus has the same cell-type specificity of connexin expression as observed ultrastructurally in other regions of the central nervous system. Moreover, in both developing and adult locus coeruleus, no evidence was found for gap junctions or connexins linking neurons with astrocytes or oligodendrocytes, indicating that neurons in this nucleus are not linked to the pan-glial syncytium by connexin32-or connexin26-containing gap junctions or by abundant free connexons composed of those connexins. 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 July 29. Published in final edited form as:Neuroscience. In the developing mammalian central nervous system (CNS), electrical coupling between neurons is well documented by electrophysiological and dye-coupling approaches (Peinado et al., 1993;Fulton, 1995;Montoro and Yuste, 2004;Bruzzone and...

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Section: Cx32: In Gap Junctions or As Dispersed Connexons?supporting

confidence: 71%

mentioning

confidence: 87%

Section: Connexin Composition Of Neuronal Vs Glial Gap Junctions In Lcmentioning

confidence: 99%

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Identification of connexin36 in gap junctions between neurons in rodent locus coeruleus

et al. 2007

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“…expression but positive for Cx30 expression (as determined by RT-PCR analysis). The Cx30 isoform is not found in astrocytes freshly isolated from neonates but rather is associated with astrocytes of both adult mice (Dahl et al, 1996;Nagy et al, 1999) and those that have been cultured for extensive periods (Nagy et al, 1999;Dermietzel et al, 2000).…”

Section: Discussionmentioning

confidence: 98%

The Complex of Ciliary Neurotrophic Factor-Ciliary Neurotrophic Factor Receptor α Up-Regulates Connexin43 and Intercellular Coupling in Astrocytes via the Janus Tyrosine Kinase/Signal Transducer and Activator of Transcription Pathway

Ozog

Bernier

Bates

et al. 2004

MBoC

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Cytokines regulate numerous cell processes, including connexin expression and gap junctional coupling. In this study, we examined the effect of ciliary neurotrophic factor (CNTF) on connexin43 (Cx43) expression and intercellular coupling in astrocytes. Murine cortical astrocytes matured in vitro were treated with CNTF (20 ng/ml), soluble ciliary neurotrophic factor receptor ␣ (CNTFR␣) (200 ng/ml), or CNTF-CNTFR␣. Although CNTF and CNTFR␣ alone had no effect on Cx43 expression, the heterodimer CNTF-CNTFR␣ significantly increased both Cx43 mRNA and protein levels. Cx43 immunostaining correlated with increased intercellular coupling as determined by dye transfer analysis. By using the pharmacological inhibitor ␣-cyano-(3,4-dihydroxy)-N-benzylcinnamide (AG490), the increase in Cx43 was found to be dependent on the Janus tyrosine kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Immunocytochemical analysis revealed that CNTF-CNTFR␣ treatment produced nuclear localization of phosphorylated STAT3, whereas CNTF treatment alone did not. Transient transfection of constructs containing various sequences of the Cx43 promoter tagged to a LacZ reporter into ROS 17/2.8 cells confirmed that the promoter region between ؊838 to ؊1693 was deemed necessary for CNTF-CNTFR␣ to induce heightened expression. CNTF-CNTFR␣ did not alter Cx30 mRNA levels, suggesting selectivity of CNTF-CNTFR␣ for connexin signaling. Together in the presence of soluble receptor, CNTF activates the JAK/STAT pathway leading to enhanced Cx43 expression and intercellular coupling. INTRODUCTIONGap junctions are intercellular channels between adjacent cells that permit the passage of various substances Ͻ1.2 kDa in size (Kumar and Gilula, 1996). Such junctions are formed when each cell provides a connexon, which itself is composed of six connexins (Cxs) (Kumar and Gilula, 1996). Cx43, the prominent Cx isoform expressed in the central nervous system (CNS), is highly expressed in astrocytes (Yamamoto et al., 1990;Dermietzel et al., 1991;Giaume et al., 1991), neuronal precursors (Rozental et al., 1998Bittman and LoTurco, 1999), and possibly neurons (Bruzzone and Ressot, 1997;Vaney, 1999;SiuYi et al., 2001;Rouach et al., 2002). Several studies using in vitro and in vivo models have demonstrated that impediment of gap junctional coupling and/or connexin43 expression amplifies cell death and tissue damage in the wake of injuries and diseases (Blanc et al., 1998;Naus et al., 2001;Siushansian et al., 2001;Ozog et al., 2002b;Lin et al., 2003;Nakase et al., 2003). Thus, design of an intervention to up-regulate Cx43 expression and intercellular communication may lead to novel therapies against pathological disturbances.Gap junction expression and activity can be altered on a short-term or long-term basis (reviewed by Giaume and McCarthy, 1996;Rouach and Giaume, 2001). Short-term regulation is the result of posttranslational processing such as phosphorylation or channel blocking. Long-term regulation, however, entails modification of gene transcripti...

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“…Anatomical and functional studies of the rodent CNS have demonstrated that astrocytes and oligodendrocytes are coupled by gap junctions (Massa and Mugnaini 1982;Ransom and Kettenmann 1990;Robinson et al 1993;Rash et al 1997), and that each cell type expresses different connexins (Dermietzel et al 1989;Yamamoto et al 1990;Scherer et al 1995;Dermietzel et al 1997;Ochalski et al 1997;Nagy et al 1999;Altevogt et al 2002;Menichella et al 2003;Odermatt et al 2003;Kleopa et al 2004). Astrocyte/astrocyte (A/ A) coupling is likely mediated by Cx43/Cx43 and Cx30/Cx30 homotypic channels, and astrocyte/oligodendrocyte (A/O) coupling is most likely mediated by Cx43/Cx47 and Cx30/ Cx32 heterotypic channels, with an uncertain contribution of Cx26/Cx32 channels (Rash et al 2001;Nagy et al 2003;Altevogt and Paul 2004;Li et al 2004).…”

mentioning

confidence: 99%

Loss-of-function GJA12/Connexin47 mutations cause Pelizaeus–Merzbacher-like disease

Orthmann-Murphy

Enriquez

Abrams

et al. 2007

Molecular and Cellular Neuroscience

120

112

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Connexin30 in rodent, cat and human brain: selective expression in gray matter astrocytes, co-localization with connexin43 at gap junctions and late developmental appearance

Cited by 317 publications

References 48 publications

Identification of connexin36 in gap junctions between neurons in rodent locus coeruleus

Identification of connexin36 in gap junctions between neurons in rodent locus coeruleus

The Complex of Ciliary Neurotrophic Factor-Ciliary Neurotrophic Factor Receptor α Up-Regulates Connexin43 and Intercellular Coupling in Astrocytes via the Janus Tyrosine Kinase/Signal Transducer and Activator of Transcription Pathway

Loss-of-function GJA12/Connexin47 mutations cause Pelizaeus–Merzbacher-like disease

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