Invest Ophthalmol Vis Sci

PURPOSE. The roles of dystrophins in retinal physiology remain elusive. The lack of proper clustering of the potassium channel Kir4.1 and of the aquaporin AQP4 was proposed to be the basis of the ERG abnormality observed in many Duchenne muscular dystrophy (DMD) patients. However, the electroretinogram of Dp71-null mice, in which this clustering is disrupted, shows only a moderate reduction of the b-wave with no change in the implicit times. Additionally, the deficit in color discrimination found in DMD patients is hard to explain through the known expression of DMD gene products. The authors thus decided to reexamine their distribution in the mouse retina. METHODS. Messenger RNA distribution was assessed by PCR coupled to laser microdissection of the outer and inner nuclear layers and by in situ hybridization for Dp427. Mouse retinas were double labeled for dystrophins versus presynaptic and postsynaptic proteins or antibodies specific for Dp427 or Dp427+Dp260. RESULTS. Messengers for Dp427, Dp260, and Dp140 were present in the inner nuclear layer. Dp427 mRNA was further detected in bipolar cells and in some amacrine cells by in situ hybridization. Comparative labeling in wild-type and mdx(5Cv) retinas (lacking Dp427) indicated a differential distribution of Dp427 and Dp260 between rod and cone terminals. CONCLUSIONS. In addition to their localization in photoreceptor terminals, Dp427, Dp260, and Dp140 are expressed in inner nuclear layer neurons, notably in bipolar cells for Dp427. Dp427 was proportionally more expressed in cone- than in rod-associated synapses compared with Dp260

Functional Implication of Dp71 in Osmoregulation and Vascular Permeability of the Retina

Functional alterations of Müller cells, the principal glia of the retina, are an early hallmark of most retina diseases and contribute to their further progression. The molecular mechanisms of these reactive Müller cell alterations, resulting in disturbed retinal homeostasis, remain largely unknown. Here we show that experimental detachment of mouse retina induces mislocation of the inwardly rectifying potassium channels (Kir4.1) and a downregulation of the water channel protein (AQP4) in Müller cells. These alterations are associated with a strong decrease of Dp71, a cytoskeleton protein responsible for the localization and the clustering of Kir4.1 and AQP4. Partial (in detached retinas) or total depletion of Dp71 in Müller cells (in Dp71-null mice) impairs the capability of volume regulation of Müller cells under osmotic stress. The abnormal swelling of Müller cells In Dp71-null mice involves the action of inflammatory mediators. Moreover, we investigated whether the alterations in Müller cells of Dp71-null mice may interfere with their regulatory effect on the blood-retina barrier. In the absence of Dp71, the retinal vascular permeability was increased as compared to the controls. Our results reveal that Dp71 is crucially implicated in the maintenance of potassium homeostasis, in transmembraneous water transport, and in the Müller cell-mediated regulation of retinal vascular permeability. Furthermore, our data provide novel insights into the mechanisms of retinal homeostasis provided by Müller cells under normal and pathological conditions

Long-haul transmission of PM-16QAM, PM-32QAM and PM-64QAM based terabit superchannels over a field deployed legacy fiber

Increase in transmission symbol-rate as well as order of quadrature amplitude modulation (QAM) is identified as the most economical way to reduce cost per transmitted bit. In particular, next generation transponders aim at supporting datarates up to 1 Tb/s employing superchannels due to electrical components’ bandwidth limitations. Furthermore, the introduction of a flexible-grid architecture can maximize throughput by minimizing spectral gaps in available optical spectrum. Keeping in view these design options, we conducted several high capacity experiments with tier1 operator Orange using their field deployed standard single mode fiber (SSMF, G.652), having a total length of 762 km, connecting the cities Lyon and Marseille in France. In particular we employed four subcarriers per Tb/s superchannel, each modulated by PM-16QAM, PM-32QAM and PM-64QAM with per carrier symbol-rates of 41.2 GBd, 33 GBd and 34 GBd, respectively. The subcarrier spacing was 50 GHz for the PM- 16QAM case and 37.5 GHz for both the PM-32QAM and PM-64QAM cases allowing in total 241.0 Tb/s, 321.0 Tb/s and 321.2 Tb/s superchannels over C-band and resulting in potential C-band capacities of 24.0 Tb/s, 32.0 Tb/s and 38.4 Tb/s, respectively. After field transmission the maximum available OSNR0:1nm margin compared to the required OSNR0:1nm at forward error correction (FEC) threshold was 8.2 dB, 5.4 dB and 4.2 dB for PM-16QAM, PM-32QAM and PM-64QAM, respectively. The transmission reach for PM-16QAM and PM- 32QAM modulated superchannels was extended to 1571 km and 1065 km using erbium doped fiber amplified SSMF spans of 101 km length

Record field demonstration of C-band multi-terabit 16QAM, 32QAM and 64QAM over 762km of SSMF

We demonstrate a record 38.4Tb/s 64QAM C-band transmission over 762km of field deployed SSMF fiber, connecting Lyon and Marseille, France, employing hybrid EDFA-Raman amplification and achieve a spectral efficiency of 8b/s/Hz. Furthermore, we demonstrate, for the first time to our knowledge, flexi-rate transmission over the same commercial link, using quad-carrier 1Tb/s 16QAM (24.0 Tb/s), 1Tb/s 32QAM (32.0 Tb/s) and 1.2Tb/s 64QAM (38.4 Tb/s)

Multi-flex field trial over 762km of G. 652 SSMF using programmable modulation formats up to 64QAM

We demonstrate next-generation network upgrade scenarios using flexi-format (PM-QPSK→PM-64QAM) and flexi-rate (100G→300G) transmission over field-deployed fiber (762km). The back-to-back penalties are limited to ~2.6dB, whereas after transmission, available margin in excess of ~7.6dB is reported