A Place to Rest Your (Burnt) Bones? Mortuary Houses in Early Anglo-Saxon England

This is an Accepted Manuscript of an article published by Taylor & Francis in Archaeological Journal on 5th October 2017, available online: doi: 10.1080/00665983.2017.1366704This article presents a fresh interpretation of square and rectangular mortuary structures found in association with deposits of cremated material and cremation burials in a range of early Anglo-Saxon (fifth-/sixth-century AD) cemeteries across southern and eastern England. Responding to a recent argument that they could be traces of pyre structures, a range of ethnographic analogies are drawn upon, and the full-range of archaeological evidence is synthesized, to re-affirm and extend their interpretation as unburned mortuary structures. Three interleaving significances are proposed: (i) demarcating the burial place of specific individuals or groups from the rest of the cemetery population, (ii) operating as ‘columbaria’ for the above-ground storage of the cremated dead (i.e. not just to demarcate cremation burials), and (iii) providing key nodes of commemoration between funerals as the structures were built, used, repaired and eventually decayed within cemeteries. The article proposes that timber ‘mortuary houses’ reveal that groups in early Anglo-Saxon England perceived their cemeteries in relation to contemporary settlement architectures, with some groups constructing and maintaining miniaturized canopied buildings to store and display the cremated remains of the dead

26th Annual Computational Neuroscience Meeting (CNS*2017): Part 3 - Meeting Abstracts - Antwerp, Belgium. 15–20 July 2017

This work was produced as part of the activities of FAPESP Research,\ud Disseminations and Innovation Center for Neuromathematics (grant\ud 2013/07699-0, S. Paulo Research Foundation). NLK is supported by a\ud FAPESP postdoctoral fellowship (grant 2016/03855-5). ACR is partially\ud supported by a CNPq fellowship (grant 306251/2014-0)

Prevention of age-associated neuronal hyperexcitability with improved learning and attention upon knockout or antagonism of LPAR2

Recent studies suggest that synaptic lysophosphatidic acids (LPAs) augment glutamate-dependent cortical excitability and sensory information processing in mice and humans via presynaptic LPAR2 activation. Here, we studied the consequences of LPAR2 deletion or antagonism on various aspects of cognition using a set of behavioral and electrophysiological analyses. Hippocampal neuronal network activity was decreased in middle-aged LPAR2(-/-)mice, whereas hippocampal long-term potentiation (LTP) was increased suggesting cognitive advantages of LPAR2(-/-)mice. In line with the lower excitability, RNAseq studies revealed reduced transcription of neuronal activity markers in the dentate gyrus of the hippocampus in naive LPAR2(-/-)mice, including ARC, FOS, FOSB, NR4A, NPAS4 and EGR2. LPAR2(-/-)mice behaved similarly to wild-type controls in maze tests of spatial or social learning and memory but showed faster and accurate responses in a 5-choice serial reaction touchscreen task requiring high attention and fast spatial discrimination. In IntelliCage learning experiments, LPAR2(-/-)were less active during daytime but normally active at night, and showed higher accuracy and attention to LED cues during active times. Overall, they maintained equal or superior licking success with fewer trials. Pharmacological block of the LPAR2 receptor recapitulated the LPAR2(-/-)phenotype, which was characterized by economic corner usage, stronger daytime resting behavior and higher proportions of correct trials. We conclude that LPAR2 stabilizes neuronal network excitability upon aging and allows for more efficient use of resting periods, better memory consolidation and better performance in tasks requiring high selective attention. Therapeutic LPAR2 antagonism may alleviate aging-associated cognitive dysfunctions

Precise somatotopic thalamocortical axon guidance depends on LPA-mediated PRG-2/radixin signaling

Precise connection of thalamic barreloids with their corresponding cortical barrels is critical for processing of vibrissal sensory information. Here, we show that PRG-2, a phospholipid-interacting molecule, is important for thalamocortical axon guidance. Developing thalamocortical fibers both in PRG-2 full knockout (KO) and in thalamus-specific KO mice prematurely entered the cortical plate, eventually innervating non-corresponding barrels. This misrouting relied on lost axonal sensitivity toward lysophosphatidic acid (LPA), which failed to repel PRG-2-deficient thalamocortical fibers. PRG-2 electroporation in the PRG-2(-/-) thalamus restored the aberrant cortical innervation. We identified radixin as a PRG-2 interaction partner and showed that radixin accumulation in growth cones and its LPA-dependent phosphorylation depend on its binding to specific regions within the C-terminal region of PRG-2. In vivo recordings and whisker-specific behavioral tests demonstrated sensory discrimination deficits in PRG-2(-/-) animals. Our data show that bioactive phospholipids and PRG-2 are critical for guiding thalamic axons to their proper cortical targets