Photoreceptor Coupling Mediated by Connexin36 in the Primate Retina

OʼBrien, Jennifer; Chen, Xiaoming; MacLeish, Peter R.; O’Brien, John; Massey, Stephen C.

doi:10.1523/jneurosci.4749-11.2012

Cited by 86 publications

(133 citation statements)

References 70 publications

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“…These Cx36 plaques were often located on the side or apical surface of cone telodendria or even more distal axonal areas but typically lacked contacts with other cones. These population 1 and 2 Cx36 plaques resembled to sites previously described as coneto-rod GJs in the primate retina (O'Brien et al 2012). In fact, we found that some rod spherules labeled with an antiserum against rod transducin (rTR) displayed a close vicinity to these Cx36 plaques (Fig.…”

Section: Cx36 Colocalization With Photoreceptor Axon Terminalssupporting

confidence: 78%

“…It has been shown that the human retina, similar to those of other mammalian species, expresses Cx36 both in the IPL and OPL (Söhl et al 2010), and the distribution of immunostained plaques resembled patterns found previously in the mouse, rabbit, rat and the monkey Mills et al 2001;Deans et al 2002;Kihara et al 2006Kihara et al , 2010O'Brien et al 2012;Kovács-Ö ller et al 2014). However, it has been difficult to obtain details on the GJ forming neurons of the human retina due to the postmortem decomposition of available tissue.…”

Section: Introductionsupporting

confidence: 79%

“…This antiserum has been widely used to recognize Cx36 GJs in the nervous tissue of various mammals including macaque (O'Brien et al 2012;Rash et al 2012;Kovács-Ö ller et al 2014;Pereda et al 2003). Similar to other species, the antibody recognized a number of Cx36 GJ plaques in both plexiform layers of the human retina ( Fig.…”

Section: Cx36 Distribution In the Human Retinamentioning

confidence: 99%

“…In the mammalian retina, Cx36 and Cx45 have been found in both plexiform layers (Gülde-nagel et al 2000;Petrasch-Parwez et al 2004), whereas Cx50 and Cx57 (Massey et al 2003;Hombach et al 2004) are restricted to the outer plexiform layer (OPL) and Cx30.2 is found only in the inner plexiform layer (IPL) (Müller et al 2010). Cx36 and Cx45 have been shown to process rod-mediated signals between AII amacrine and ON cone bipolar cells (BC) and between rod and cone photoreceptors (Feigenspan et al , 2004Güldenagel et al 2001;Mills et al 2001;Deans et al 2002;Lee et al 2003;Völgyi et al 2004;Han and Massey 2005;Maxeiner et al 2005;Lin et al 2005;O'Brien et al 2012), and also serve to correlate ganglion cell signals (Hidaka et al 2004;Schubert et al 2005a, b;Völgyi et al 2005Völgyi et al , 2009Völgyi et al , 2013aPan et al 2010).…”

Section: Introductionmentioning

confidence: 99%

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Characterization of connexin36 gap junctions in the human outer retina

et al. 2015

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Retinal connexins (Cx) form gap junctions (GJ) in key circuits that transmit average or synchronize signals. Expression of Cx36, -45, -50 and -57 have been described in many species but there is still a disconcerting paucity of information regarding the Cx makeup of human retinal GJs. We used well-preserved human postmortem samples to characterize Cx36 GJ constituent circuits of the outer plexiform layer (OPL). Based on their location, morphometric characteristics and co-localizations with outer retinal neuronal markers, we distinguished four populations of Cx36 plaques in the human OPL. Three of these were comprised of loosely scattered Cx36 plaques; the distalmost population 1 formed cone-to-rod GJs, population 2 in the mid-OPL formed cone-to-cone GJs, whereas the proximalmost population 4 likely connected bipolar cell dendrites. The fourth population (population 3) of Cx36 plaques conglomerated beneath cone pedicles and connected dendritic tips of bipolar cells that shared a common presynaptic cone. Overall, we show that the human outer retina displays a diverse cohort of Cx36 GJ that follows the general mammalian scheme and display a great functional diversity.

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Section: Cx36 Colocalization With Photoreceptor Axon Terminalssupporting

confidence: 78%

Section: Introductionsupporting

confidence: 79%

Section: Cx36 Distribution In the Human Retinamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Characterization of connexin36 gap junctions in the human outer retina

et al. 2015

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“…There, Cx36 forms direct functional connections between ganglion cells and amacrine cells (44). Cx36 expression is also present at the intersection of retinal rod and bipolar cells (43). The other likely possibility is paracrine control of islet blood flow arising from products secreted from the islet cells.…”

Section: E328 Connexin 36 Mediates Blood Cell Flow In Isletsmentioning

confidence: 99%

Connexin 36 mediates blood cell flow in mouse pancreatic islets

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Piston

2014

American Journal of Physiology-Endocrinology and Metabolism

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The insulin-secreting β-cells are contained within islets of Langerhans, which are highly vascularized. Blood cell flow rates through islets are glucose-dependent, even though there are no changes in blood cell flow within in the surrounding exocrine pancreas. This suggests a specific mechanism of glucose-regulated blood flow in the islet. Pancreatic islets respond to elevated glucose with synchronous pulses of electrical activity and insulin secretion across all β-cells in the islet. Connexin 36 (Cx36) gap junctions between islet β-cells mediate this synchronization, which is lost in Cx36 knockout mice (Cx36−/−). This leads to glucose intolerance in these mice, despite normal plasma insulin levels and insulin sensitivity. Thus, we sought to investigate whether the glucose-dependent changes in intraislet blood cell flow are also dependent on coordinated pulsatile electrical activity. We visualized and quantified blood cell flow using high-speed in vivo fluorescence imaging of labeled red blood cells and plasma. With the use of a live animal glucose clamp, blood cell flow was measured during either hypoglycemia (∼50 mg/dl) or hyperglycemia (∼300 mg/dl). In contrast to the large glucose-dependent islet blood velocity changes observed in wild-type mice, only minimal differences are observed in both Cx36+/− and Cx36−/− mice. This observation supports a novel model where intraislet blood cell flow is regulated by the coordinated electrical activity in the islet β-cells. Because Cx36 expression and function is reduced in type 2 diabetes, the resulting defect in intraislet blood cell flow regulation may also play a significant role in diabetic pathology.

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Dopaminergic Retinal Cell Loss and Visual Dysfunction in Parkinson Disease

Ortuño‐Lizarán

Sánchez‐Sáez

Lax

et al. 2020

Annals of Neurology

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Objective: Considering the demonstrated implication of the retina in Parkinson disease (PD) pathology and the importance of dopaminergic cells in this tissue, we aimed to analyze the state of the dopaminergic amacrine cells and some of their main postsynaptic neurons in the retina of PD. Methods: Using immunohistochemistry and confocal microscopy, we evaluated morphology, number, and synaptic connections of dopaminergic cells and their postsynaptic cells, AII amacrine and melanopsin-containing retinal ganglion cells, in control and PD eyes from human donors. Results: In PD, dopaminergic amacrine cell number was reduced between 58% and 26% in different retinal regions, involving a decline in the number of synaptic contacts with AII amacrine cells (by 60%) and melanopsin cells (by 35%). Despite losing their main synaptic input, AII cells were not reduced in number, but they showed cellular alterations compromising their adequate function: (1) a loss of mitochondria inside their lobular appendages, which may indicate an energetic failure; and (2) a loss of connexin 36, suggesting alterations in the AII coupling and in visual signal transmission from the rod pathway. Interpretation: The dopaminergic system impairment and the affection of the rod pathway through the AII cells may explain and be partially responsible for the reduced contrast sensitivity or electroretinographic response described in PD. Also, dopamine reduction and the loss of synaptic contacts with melanopsin cells may contribute to the melanopsin retinal ganglion cell loss previously described and to the disturbances in circadian rhythm and sleep reported in PD patients. These data support the idea that the retina reproduces brain neurodegeneration and is highly involved in PD pathology.

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Photoreceptor Coupling Mediated by Connexin36 in the Primate Retina

Cited by 86 publications

References 70 publications

Characterization of connexin36 gap junctions in the human outer retina

Characterization of connexin36 gap junctions in the human outer retina

Connexin 36 mediates blood cell flow in mouse pancreatic islets

Dopaminergic Retinal Cell Loss and Visual Dysfunction in Parkinson Disease

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