Status and plans for the Array Control and Data Acquisition System of the Cherenkov Telescope Array

The Cherenkov Telescope Array (CTA) is the next-generation atmospheric Cherenkov gamma-ray observatory. CTA will consist of two installations, one in the northern, and the other in the southern hemisphere, containing tens of telescopes of different sizes. The CTA performance requirements and the inherent complexity associated with the operation, control and monitoring of such a large distributed multi-telescope array leads to new challenges in the field of the gamma-ray astronomy. The ACTL (array control and data acquisition) system will consist of the hardware and software that is necessary to control and monitor the CTA arrays, as well as to time-stamp, read-out, filter and store -at aggregated rates of few GB/s- the scientific data. The ACTL system must be flexible enough to permit the simultaneous automatic operation of multiple sub-arrays of telescopes with a minimum personnel effort on site. One of the challenges of the system is to provide a reliable integration of the control of a large and heterogeneous set of devices. Moreover, the system is required to be ready to adapt the observation schedule, on timescales of a few tens of seconds, to account for changing environmental conditions or to prioritize incoming scientific alerts from time-critical transient phenomena such as gamma ray bursts. This contribution provides a summary of the main design choices and plans for building the ACTL system

Glutamate acts at NMDA receptors on fresh bovine and on cultured human retinal pigment epithelial cells to trigger release of ATP

The photoreceptors lie between the inner retina and the retinal pigment epithelium (RPE). The release of glutamate by the phototoreceptors can signal changes in light levels to inner retinal neurons, but the role of glutamate in communicating with the RPE is unknown. Since RPE cells are known to release ATP, we asked whether glutamate could trigger ATP release from RPE cells and whether this altered cell signalling. Stimulation of the apical face of fresh bovine RPE eyecups with 100 μm NMDA increased ATP levels more than threefold, indicating that both receptors for NMDA and release of ATP occurred across the apical membrane of fresh RPE cells. NMDA increased ATP levels bathing cultured human ARPE-19 cells more than twofold, with NMDA receptor inhibitors MK-801 and d-AP5 preventing this release. Blocking the glycine site of the NMDA receptor with 5,7-dichlorokynurenic acid prevented ATP release from ARPE-19 cells. Release was also blocked by channel blocker NPPB and Ca2+ chelator BAPTA, but not by cystic fibrosis transmembrane conductance regulator (CFTR) blocker glibenclamide or vesicular release inhibitor brefeldin A. Glutamate produced a dose-dependent release of ATP from ARPE-19 cells that was substantially inhibited by MK-801. NMDA triggered a rise in cell Ca2+ that was blocked by MK-801, by the ATPase apyrase, by the P2Y1 receptor antagonist MRS2179 and by depletion of intracellular Ca2+ stores with thapsigargin. These results suggest that glutamate stimulates NMDA receptors on the apical membrane of RPE cells to release ATP. This secondary release can amplify the glutaminergic signal by increasing Ca2+ inside RPE cells, and might activate Ca2+-dependent conductances. The interplay between glutaminergic and purinergic systems may thus be important for light-dependent interactions between photoreceptors and the RPE