From neuro-glue (‘nervenkitt’) to glia: A prologue

Dermietzel, Rolf; Spray, David C.

doi:10.1002/(sici)1098-1136(199809)24:1<1::aid-glia1>3.0.co;2-a

Cited by 74 publications

(34 citation statements)

References 78 publications

(52 reference statements)

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“…Previous studies have demonstrated that astrocytes, the predominant cell type in the brain, receive signals from neurons and also release neuroactive substances (27), provide energy substrates to neurons (28) and are important in neuronal support in normal and pathological conditions. In the central nervous system, astrocytes established a glial syncytium through intercellular connections via gap junctions (29). CX43 is the primary component protein in astrocytic gap junctions (30).…”

Section: Discussionmentioning

confidence: 99%

Astrocytic p-connexin 43 regulates neuronal autophagy in the hippocampus following traumatic brain injury in rats

Gao

Cui

et al. 2013

Molecular Medicine Reports

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Abstract. Gap junctions are conductive channels formed by membrane proteins termed connexins, which permit the intercellular exchange of metabolites, ions and small molecules. Previous data demonstrated that traumatic brain injury (TBI) activates autophagy and increases microtubule-associated protein 1 light chain 3 (LC3) immunostaining predominantly in neurons. Although previous studies have identified several extracellular factors that modulate LC3 expression, knowledge of the regulatory network controlling LC3 in health and disease remains incomplete. The aim of the present study was to assess whether gap junctions control the in vivo expression of LC3 in TBI. Using a modified weight-drop device, adult male Sprague-Dawley rats (weight, 350-375 g) were subjected to TBI. Phosphorylated gap junction protein levels and LC3-Ⅱ levels were quantified using western blot analysis. The spatial distribution of immunoreactivity for phosphorylated connexin 43 (p-CX43) and LC3-Ⅱ was analyzed by immunofluorescence. The results showed that p-CX43 expression in the hippocampus reached a maximum level 6 h following injury. In addition, the immunoreactivity of p-CX43 was localized in the astrocytes surrounding pyramidal neurons. The LC3-Ⅱ protein content remained at high levels 24 h following injury. Double immunolabeling demonstrated that LC3-II dots colocalized with the hippocampus pyramidal neurons. Furthermore, inhibition of p-CX43 reduced TBI-induced autophagy, according to western blot analysis. As astrocytic gap junction coupling is affected in various forms of brain injury, the results suggest that point gap junctions/connexins are important regulators of autophagy in the hippocampal neurons following TBI.

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Section: Discussionmentioning

confidence: 99%

Astrocytic p-connexin 43 regulates neuronal autophagy in the hippocampus following traumatic brain injury in rats

Gao

Cui

et al. 2013

Molecular Medicine Reports

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“…C6-Cx43-labeled cells (positive controls) received calcium signals at a frequency of 93 Ϯ 3%, indicating that the existence of gap junctions between donor and recipient cells did increase the cell-cell transfer of Ca 2ϩ signals. Both oligodendrocytes and neurons express Cx32 (Dermietzel and Spray, 1998). Interestingly, although C6-Cx32 cells among themselves propagated robust calcium waves, no further increase in receiving calcium signaling was observed when labeled Cx-deficient cells were exchanged with C6-Cx32 cells.…”

Section: Cx-deficient Cells Can Receive But Not Propagate Calcium Sigmentioning

confidence: 96%

“…This issue is of particular interest because the brain is composed of multiple cell types with highly variable expression levels of Cxs. In the adult brain, Cx expression in neurons and oligodendrocytes is low compared with astrocytes, which may be the only cell type that express Cxs at a level high enough to support propagation of calcium waves (Dermietzel and Spray, 1998). To define the role of Cx in receiving calcium signals, we next constructed a culture system composed of cells with both high and low Cx expression.…”

Section: Cx-deficient Cells Can Receive But Not Propagate Calcium Sigmentioning

confidence: 99%

ATP-Mediated Glia Signaling

Cotrina¹,

et al. 2000

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Glia calcium signaling has recently been identified as a potent modulator of synaptic transmission. We show here that the spatial expansion of calcium waves is mediated by ATP and subsequent activation of purinergic receptors. Ectopic expression of gap junction proteins, connexins (Cxs), leads to an increase in both ATP release and the radius of calcium wave propagation. Cx expression was also associated with a phenotypic transformation, and cortical neurons extended longer neurites when co-cultured with Cx-expressing than with Cxdeficient cells. Purinergic receptor activation mediated both these effects, because treatment with receptor antagonists restored the glia phenotype and slowed neurite outgrowth. These results identify a key role of ATP in both short-term calcium signaling events and in long-term differentiation regulated by glia. (Cornell-Bell et al., 1990;Charles et al., 1991). Astrocytic calcium signaling is transmitted to neurons (Nedergaard, 1994;Parpura et al., 1994;Hassinger et al., 1995), and recent reports have confirmed a direct role of astrocytes in modulating synaptic transmission. Astrocytic calcium signaling reduced the magnitude of action potential-evoked EPSCs and IPSCs in cultures (Araque et al., 1998a,b), modulated light-evoked spike activity of ganglion cells in intact retina (Newman and Zahs, 1998), and potentiated inhibitory synaptic transmission between synaptically coupled pairs of interneurons and CA1 pyramidal cells (Kang et al., 1998).Originally, it was debated to which extent astrocyte-to-neuron signaling was mediated by gap junctions (Nedergaard, 1994), by release of extracellular glutamate (Parpura et al., 1994), or by a combination of both mechanisms (Charles, 1994;Smith, 1994). Gap junctions connecting astrocytes and neurons have been identified by electron microscopy in brain (Morales and Duncan, 1974;Nadarajah et al., 1996), and functional gap junctions have been visualized by diffusion of permeable tracers from neurons to astrocytes in cultures (Fróes et al., 1999). On the other hand, glutamate is released from astrocytes in a Ca 2ϩ -dependent manner, and astrocyte-to-neuron signaling is sensitive to glutamate receptor antagonists (Araque et al., 1998a,b;Bezzi et al., 1998). Thus, both connexin-and glutamate-mediated pathways may contribute to astrocyte-to-neuron signaling. These discussions were, however, based on the assumption that astrocytic calcium waves are propagated by diffusion of intracellular messengers, such as Ca 2ϩ and IP 3 , across gap junctions. Very recently it has been demonstrated that astrocytic calcium waves are mediated by extracellular ATP and subsequent activation of purinergic receptors (Cotrina et al., 1998b;Guthrie et al., 1999). Accordingly, intercellular calcium signaling does not appear to require physical contact or formation of functional gap junctions (Hassinger et al., 1996). It is at present not established whether ATP participates in glial-neuronal communication or what role connexin (Cx) expression plays in propagating versus receiv...

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“…In the CNS, a number of different connexins are expressed, which could be localized to astrocytes and oligodendrocytes (Dermietzel and Spray, 1998), as well as pigment epithelial cells in the vertebrate retina (Janssen-Bienhold et al, 1998). Recently, a novel connexin (Cx35) has been cloned, which is expressed at high levels in the skate retina (O'Brien et al, 1996) and the homologous Cx34.7 expressed in both retina and brain of the perch (O'Brien et al, 1998).…”

Section: Abstract: Gap Junction; Connexin36; Retina; Aii Amacrine Cementioning

confidence: 99%

Expression of Neuronal Connexin36 in AII Amacrine Cells of the Mammalian Retina

et al. 2001

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We have studied the expression pattern of neuronal connexin36 (Cx36) in the mouse and rat retina. In vertical sections of both retinas, a polyclonal antibody directed against Cx36 produced punctate labeling in the inner plexiform layer (IPL). Intense immunoreactivity was localized to the entire OFF sublamina of the IPL, and much weaker staining could be observed in the ON sublamina. Double-labeling experiments in the rat retina with antibodies directed against parvalbumin indicate that Cx36 is expressed on dendrites of AII amacrine cells. Cx36-like immunoreactivity in sublamina a of the IPL did not overlap with lobular appendages or cell bodies of AII amacrine cells. In a mouse retinal slice preparation, AII amacrine and ON cone bipolar cells were intracellularly injected with Neurobiotin and counterstained with antibody against Cx36. Punctate labeling appeared to be in register with dendritic arborization of AII amacrines and cone bipolar cells in the ON sublamina of the IPL. Whereas AII amacrine cells isolated from the rat retina clearly displayed Cx36-like immunoreactivity, isolated ON cone bipolar cells were negative for Cx36. Axon terminals of rod bipolar cells were decorated with Cx36-positive contacts but did not express Cx36 themselves.These results indicate that Cx36 is expressed by AII amacrine cells in homologous and heterologous gap junctions made with AII amacrines and cone bipolar cells, respectively. The heterologous gap junctions appear to be heterotypic, because ON cone bipolar cells do not express Cx36.

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From neuro-glue (‘nervenkitt’) to glia: A prologue

Cited by 74 publications

References 78 publications

Astrocytic p-connexin 43 regulates neuronal autophagy in the hippocampus following traumatic brain injury in rats

Astrocytic p-connexin 43 regulates neuronal autophagy in the hippocampus following traumatic brain injury in rats

ATP-Mediated Glia Signaling

Expression of Neuronal Connexin36 in AII Amacrine Cells of the Mammalian Retina

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