Role of astroglial connexin30 in hippocampal gap junction coupling

Gosejacob, Dominic; Dublin, Pavel; Bedner, Peter; Hüttmann, Kerstin; Zhang, Jiong; Tress, Oliver; Willecke, Klaus; Pfrieger, Frank W.; Steinhäuser, Christian; Theis, Martin

doi:10.1002/glia.21120

Cited by 76 publications

(67 citation statements)

References 18 publications

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“…Modulating the expression of one Cx could affect expression of other Cxs. For example, astrocytic Cx30 plays an important function in neuronal transmission in the mouse hippocampus (Gosejacob et al, 2011) and deletion of astrocytic Cx43 resulted in increased expression of Cx30 Theis et al, 2003). However, in the current study, the expression of astrocytic Cx30 was unchanged following either PSNL or intrathecal treatment with Cx43-targeting siRNA.…”

Section: Discussioncontrasting

confidence: 73%

Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice

Morioka

Zhang

Nakamura

et al. 2015

Brain, Behavior, and Immunity

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Section: Discussioncontrasting

confidence: 73%

Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice

Morioka

Zhang

Nakamura

et al. 2015

Brain, Behavior, and Immunity

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“…In the mouse hippocampus, astrocytes express both Cx43 and Cx30 (Dermietzel et al, 1989;Nagy et al, 1999) and animals that lack either of those show reduced dye-coupling (Gosejacob et al, 2011;Theis et al, 2003), whereas animals lacking both show complete absence of dye-coupling (Kunze et al, 2009;Rouach et al, 2008;Wallraff et al, 2006). Mice lacking Cx43 in astrocytes showed an increased velocity of spreading depression which indicated impaired potassium ion homeostasis (Theis et al, 2003).…”

Section: Spread Of Sodium Depends On Cx30/43mentioning

confidence: 96%

Gap junctions mediate intercellular spread of sodium between hippocampal astrocytes in situ

Langer

Stephan

Theis

et al. 2011

Glia

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115

138

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Activation of glutamatergic synapses results in long-lasting sodium transients in astrocytes mediated mainly by sodium-dependent glutamate uptake. Sodium elevations activate Na(+) /K(+) -ATPase and glucose uptake by astrocytes, representing key signals for coupling glial metabolism to neuronal activity. Here, we analyzed the spread of sodium signals between astrocytes in hippocampal slice preparations. Stimulation of a single astrocyte resulted in an immediate sodium elevation that spread to neighboring astrocytes within a distance of ∼ 100 μm. Amplitude, slope, and propagation speed of sodium elevations in downstream cells decayed monotonically with increasing distance, indicative of a diffusion process. In contrast to sodium, calcium increases elicited by electrical stimulation were restricted to the stimulated cell and a few neighboring astrocytes. Pharmacological inhibition of mGluR1/5 slightly dampened the spread of sodium, whereas inhibition of glutamate uptake or purinergic receptors had no effect. Spread of sodium to neighboring cells was disturbed on pharmacological inhibition of gap junctions, reduced in animals at P4 and virtually omitted in Cx30/Cx43 double-deficient mice. In contrast to results obtained earlier in cultured astrocytes, our data thus indicate that calcium signaling and metabotropic glutamate receptors are supportive of, but not prerequisites for, the spread of sodium between hippocampal astrocytes in situ, whereas expression of Cx30 and Cx43 is essential. Cx30/Cx43-mediated sodium diffusion between astrocytes could represent a signal indicating increased metabolic needs, independent of concomitant calcium signaling. Spread of sodium might also serve a homeostatic function by supporting the re-establishment of steep sodium gradients and by lowering the metabolic burden imposed on single cells.

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“…Of the 21 different mammalian connexin isoforms (31), astrocytes express primarily Cx30 and Cx43 (and possibly Cx26), whereas Cx36 is the major neuronal connexin (3,(32)(33)(34)(35). Connexins create gap junctional channels at cell to cell interfaces, allowing intercellular communication by transfer of current and small molecules (31).…”

mentioning

confidence: 99%

Activation, Permeability, and Inhibition of Astrocytic and Neuronal Large Pore (Hemi)channels

Hansen

Calloe

et al. 2014

Journal of Biological Chemistry

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Background:The permeability and physiological role of several large pore (hemi)channels are unresolved. Results: Large pore (hemi)channels, when heterologously expressed, display isoform-specific permeability and gating for ions and fluorescent dyes. Conclusion: Large pore channels have isoform-specific transport characteristics that can be used for their identification. Significance: Although large pore channels have characteristic properties in overexpression systems, these properties may be undetectable in native cells.

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Role of astroglial connexin30 in hippocampal gap junction coupling

Cited by 76 publications

References 18 publications

Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice

Tumor necrosis factor-mediated downregulation of spinal astrocytic connexin43 leads to increased glutamatergic neurotransmission and neuropathic pain in mice

Gap junctions mediate intercellular spread of sodium between hippocampal astrocytes in situ

Activation, Permeability, and Inhibition of Astrocytic and Neuronal Large Pore (Hemi)channels

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