Expression and high glucose-mediated regulation of K+ channel interacting protein 3 (KChIP3) and KV4 channels in retinal Müller glial cells

Chavira-Suárez, Erika; Sandoval, Alejandro; Felix, Ricardo; Lamas, Marta

doi:10.1016/j.bbrc.2010.12.041

Cited by 11 publications

(8 citation statements)

References 41 publications

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“…Significantly, expression of the Kv4.2 subunit was observed in glia, suggesting that modulation of Kv4.2 channel activity would have a more complex effect on cell function in the BNST than that of Kv4.3. Consistent with this observation, both Kv4 a subunits and KChIPs are reportedly expressed by cultured hippocampal astrocytes (Bekar et al, 2005) and Muller glial cells of the retina (Chavira-Suarez et al, 2011). Moreover, whereas the signal for Kv4.3 was observed primarily in dendrites, the Kv4.2 signal was observed in both the dendrites and spines of BNST ALG neurons.…”

Section: Kv4 Modulates Synaptic Plasticity In the Bnstsupporting

confidence: 72%

Distribution and functional expression of Kv4 family α subunits and associated KChIP β subunits in the bed nucleus of the stria terminalis

Rainnie

Hazra

Dabrowska

et al. 2013

J of Comparative Neurology

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Regulation of BNSTALG neuronal firing activity is tightly regulated by the opposing actions of the fast outward potassium current, IA, mediated by α subunits of the Kv4 family of ion channels, and the transient inward calcium current, IT. Together, these channels play a critical role in regulating the latency to action potential onset, duration, and frequency, as well as dendritic back-propagation and synaptic plasticity. Previously we have shown that Type I–III BNSTALG neurons express mRNA transcripts for each of the Kv4 α subunits. However, the biophysical properties of native IA channels are critically dependent on the formation of macromolecular complexes of Kv4 channels with a family of chaperone proteins, the potassium channel-interacting proteins (KChIP1–4). Here we used a multidisciplinary approach to investigate the expression and function of Kv4 channels and KChIPs in neurons of the rat BNSTALG. Using immunofluorescence we demonstrated the pattern of localization of Kv4.2, Kv4.3, and KChIP1–4 proteins in the BNSTALG. Moreover, our single-cell reverse-transcription polymerase chain reaction (scRT-PCR) studies revealed that mRNA transcripts for Kv4.2, Kv4.3, and all four KChIPs were differentially expressed in Type I–III BNSTALG neurons. Furthermore, immunoelectron microscopy revealed that Kv4.2 and Kv4.3 channels were primarily localized to the dendrites and spines of BNSTALG neurons, and are thus ideally situated to modulate synaptic transmission. Consistent with this observation, in vitro patch clamp recordings showed that reducing postsynaptic IA in these neurons lowered the threshold for long-term potentiation (LTP) induction. These results are discussed in relation to potential modulation of IA channels by chronic stress.

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Section: Kv4 Modulates Synaptic Plasticity In the Bnstsupporting

confidence: 72%

Distribution and functional expression of Kv4 family α subunits and associated KChIP β subunits in the bed nucleus of the stria terminalis

Rainnie

Hazra

Dabrowska

et al. 2013

J of Comparative Neurology

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“…Other experiments are required to explain whether KCNQ5 somehow participates in the activity of glial cells during retina remodeling in response to retinitis pigmentosa. A possible relationship between KCNQ5 and GFAP in the rat retina has been sustained by the presence of potassium channels, potassium currents and GFAP expression in astrocytes or Müller cells in the retina (Bay and Butt, 2012;Chavira-Su arez et al, 2011;Connors and Kofuji, 2006;Zhao et al, 2012). KCNQ5 currents have been reported in monkey retina (Pattnaik and Hughes, 2012) and KCNQ5 expression has been described in brain astrocytes (Yus-N ajera et al, 2003).…”

Section: Kcnq5/gfapmentioning

confidence: 97%

Relationship between rat retinal degeneration and potassium channel KCNQ5 expression

Caminos

Vaquero

Martinez-Galán

2015

Experimental Eye Research

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KCNQ5/Kv7.5 is a low-threshold non-inactivating voltage-gated potassium channel preferentially targeted to excitatory endings in brain neurons. The M-type current is mediated by KCNQ5 channel subunits in monkey retinal pigment epithelium cells and in brain neurons. This study was undertaken to analyze KCNQ5 expression and the interaction signals of KCNQ5 with other proteins in normal rat retina and during photoreceptor degeneration. The KCNQ5 expression pattern was studied by immunocytochemistry and Western blot in normal rat retinas (Sprague-Dawley, SD) and P23H-1 rats as a retinitis pigmentosa model. The physical interactions of KCNQ5 with calmodulin (CaM), vesicular glutamate transporter 1 (VGluT1) and glial fibrillary acidic protein (GFAP) were analyzed by in situ proximity ligation assays and were supported by calcium recording. KCNQ5 expression was found in the plexiform layers, ganglion cell layer and basal membrane of the retinal pigment epithelium. The physical interactions among KCNQ5 and CaM, VGluT1 and GFAP changed with age and during retinal degeneration. The maximal level of KCNQ5/CaM interaction was found when photoreceptors had almost completely disappeared; the KCNQ5/VGluT1 interaction signal decreased and the KCNQ5/GFAP interaction increased in the inner retina, while degeneration progressed. The basal calcium levels in the astrocytes and neurons of P23H-1 were higher than in the control SD retinas. This study demonstrates that KCNQ5 is present in the rat retina where its activity may be moderated by CaM. Retinal degeneration progression in P23H-1 rats can be followed by an interaction between KCNQ5 with CaM in an in situ system. The relationship between KCNQ5 and VGluT1 or GFAP needs to be more cautiously interpreted.

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“…Data from rat primary Müller cell cultures are controversial. In some studies, no cell death was observed after 72 h [ 30 ] or after 5 days in HG [ 90 ], while others detected Müller cell apoptosis after 72 h in the same conditions, possibly related to AKT inhibition [ 33 ]. In favor of an apoptotic mechanism is the observation that in rMC-1 and in cultured human primary Müller cells incubated in HG conditions, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) translocates to the nucleus [ 91 ].…”

Section: Müller Glia Involvement In Drmentioning

confidence: 99%

Primary Retinal Cultures as a Tool for Modeling Diabetic Retinopathy: An Overview

Matteucci

Varano

Mallozzi

et al. 2015

BioMed Research International

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Experimental models of diabetic retinopathy (DR) have had a crucial role in the comprehension of the pathophysiology of the disease and the identification of new therapeutic strategies. Most of these studies have been conducted in vivo, in animal models. However, a significant contribution has also been provided by studies on retinal cultures, especially regarding the effects of the potentially toxic components of the diabetic milieu on retinal cell homeostasis, the characterization of the mechanisms on the basis of retinal damage, and the identification of potentially protective molecules. In this review, we highlight the contribution given by primary retinal cultures to the study of DR, focusing on early neuroglial impairment. We also speculate on possible themes into which studies based on retinal cell cultures could provide deeper insight.

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Expression and high glucose-mediated regulation of K+ channel interacting protein 3 (KChIP3) and KV4 channels in retinal Müller glial cells

Cited by 11 publications

References 41 publications

Distribution and functional expression of Kv4 family α subunits and associated KChIP β subunits in the bed nucleus of the stria terminalis

Distribution and functional expression of Kv4 family α subunits and associated KChIP β subunits in the bed nucleus of the stria terminalis

Relationship between rat retinal degeneration and potassium channel KCNQ5 expression

Primary Retinal Cultures as a Tool for Modeling Diabetic Retinopathy: An Overview

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