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Additional file 1: Supplemental figures S1-S9. Figure S1. Nlgn3−/y rats display reduced classic freezing behaviour in a contextual fear conditioning paradigm. Figure S2. Freezing analysed as “paw immobility response” (all four paws unmoving but allowing for movement of head and neck). Figure S3. WT and Nlgn3−/y rats show similar activity in an open field, rotational platform & marble interaction tasks. Figure S4. Effect of repeated footshocks & thermal stimulus on WT and Nlgn3−/y rats. Figure S5. Intrinsic properties of PAG cells recorded from WT and Nlgn3−/y rats. Figure S6. Hyperexcitability of dorsal, but not ventral PAG neurons in 8-10 week old Nlgn3−/y rats. Figure S7. PAG LFPs during fear recall are significantly shorter duration in Nlgn3−/y rats. Figure S8. Defensive reactions were not elicited by electrical stimulation of primary somatosensory cortex in WT or Nlgn3−/y rats. Figure S9. Western blots showing lack expression of NLGN3 in Nlgn3−/y rats both in sensory cortex and periaqueductal grey.

Additional file 2: Supplemental table 1. Summary of statistics for main figures 2–7. Supplemental table 2. Summary of statistics for supplemental figures 1–7.

For the upgrade of the LHC to the High Luminosity LHC the ATLAS detector will install a new all-silicon Inner Tracker (ITk). The innermost part is composed by pixel detectors, the outer part by strip detectors. All together ca. 28000 detector modules will be installed in the ITk volume. Although different technologies were chosen for the inner and outer part, both detectors share a lot of commonalities concerning their requirements. These are operation in the harsh radiation environment, the restricted space for services, and the high power density, which requires a high efficient cooling system. While the sub detectors have chosen different strategies to reduce their powering services, they share the same cooling system, CO₂. The main risks for operation are heat ups and condensation, therefore a common detector control system is under development. It provides a detailed monitoring of the temperature, the radiation and the humidity in the tracker volume. Additionally an interlock system, a hardware based safety system, is designed to protect the sensitive detector elements against upcoming risks. The components of the ITk common monitoring and interlock system are presented., Proceedings of the 17th International Conference on Accelerator and Large Experimental Physics Control Systems, ICALEPCS2019, New York, NY, USA

Summary The GluN2 subtype (2A versus 2B) determines biophysical properties and signaling of forebrain NMDA receptors (NMDARs). During development, GluN2A becomes incorporated into previously GluN2B-dominated NMDARs. This “switch” is proposed to be driven by distinct features of GluN2 cytoplasmic C-terminal domains (CTDs), including a unique CaMKII interaction site in GluN2B that drives removal from the synapse. However, these models remain untested in the context of endogenous NMDARs. We show that, although mutating the endogenous GluN2B CaMKII site has secondary effects on GluN2B CTD phosphorylation, the developmental changes in NMDAR composition occur normally and measures of plasticity and synaptogenesis are unaffected. Moreover, the switch proceeds normally in mice that have the GluN2A CTD replaced by that of GluN2B and commences without an observable decline in GluN2B levels but is impaired by GluN2A haploinsufficiency. Thus, GluN2A expression levels, and not GluN2 subtype-specific CTD-driven events, are the overriding factor in the developmental switch in NMDAR composition., Graphical Abstract, Highlights • Mutating the GluN2B CaMKII site affects phosphorylation of its C-terminal domain • The developmental changes in NMDAR composition and synaptogenesis occur normally • Changes in NMDAR composition do not require distinct GluN2 C-terminal domains • Developmental changes in NMDAR composition are primarily sensitive to GluN2A levels, An important milestone in forebrain neuronal development is the switch in composition of the NMDA receptor: GluN2A becomes incorporated into previously GluN2B-dominated NMDARs. Using knockin mice, McKay et al. find that, contrary to earlier proposed models, the switch does not require GluN2A and GluN2B to possess distinct C-terminal domain sequences.