Robots facilitate human language production.

Despite recent developments in integrating autonomous and human-like robots into many aspects of everyday life, social interactions with robots are still a challenge. Here, we focus on a central tool for social interaction: verbal communication. We assess the extent to which humans co-represent (simulate and predict) a robot's verbal actions. During a joint picture naming task, participants took turns in naming objects together with a social robot (Pepper, Softbank Robotics). Previous findings using this task with human partners revealed internal simulations on behalf of the partner down to the level of selecting words from the mental lexicon, reflected in partner-elicited inhibitory effects on subsequent naming. Here, with the robot, the partner-elicited inhibitory effects were not observed. Instead, naming was facilitated, as revealed by faster naming of word categories co-named with the robot. This facilitation suggests that robots, unlike humans, are not simulated down to the level of lexical selection. Instead, a robot's speaking appears to be simulated at the initial level of language production where the meaning of the verbal message is generated, resulting in facilitated language production due to conceptual priming. We conclude that robots facilitate core conceptualization processes when humans transform thoughts to language during speaking.

ATR regulates neuronal activity by modulating presynaptic firing.

Ataxia Telangiectasia and Rad3-related (ATR) protein, as a key DNA damage response (DDR) regulator, plays an essential function in response to replication stress and controls cell viability. Hypomorphic mutations of ATR cause the human ATR-Seckel syndrome, characterized by microcephaly and intellectual disability, which however suggests a yet unknown role for ATR in non-dividing cells. Here we show that ATR deletion in postmitotic neurons does not compromise brain development and formation; rather it enhances intrinsic neuronal activity resulting in aberrant firing and an increased epileptiform activity, which increases the susceptibility of ataxia and epilepsy in mice. ATR deleted neurons exhibit hyper-excitability, associated with changes in action potential conformation and presynaptic vesicle accumulation, independent of DDR signaling. Mechanistically, ATR interacts with synaptotagmin 2 (SYT2) and, without ATR, SYT2 is highly upregulated and aberrantly translocated to excitatory neurons in the hippocampus, thereby conferring a hyper-excitability. This study identifies a physiological function of ATR, beyond its DDR role, in regulating neuronal activity.

Bringing Together Robotics, Neuroscience, and Psychology: Lessons Learned From an Interdisciplinary Project.

The diversified methodology and expertise of interdisciplinary research teams provide the opportunity to overcome the limited perspectives of individual disciplines. This is particularly true at the interface of Robotics, Neuroscience, and Psychology as the three fields have quite different perspectives and approaches to offer. Nonetheless, aligning backgrounds and interdisciplinary expectations can present challenges due to varied research cultures and practices. Overcoming these challenges stands at the beginning of each productive collaboration and thus is a mandatory step in cognitive neurorobotics. In this article, we share eight lessons that we learned from our ongoing interdisciplinary project on human-robot and robot-robot interaction in social settings. These lessons provide practical advice for scientists initiating interdisciplinary research endeavors. Our advice can help to avoid early problems and deal with differences between research fields, prepare for and anticipate challenges, align project expectations, and speed up research progress, thus promoting effective interdisciplinary research across Robotics, Neuroscience, and Psychology.

NBS1 interacts with Notch signaling in neuronal homeostasis.

NBS1 is a critical component of the MRN (MRE11/RAD50/NBS1) complex, which regulates ATM- and ATR-mediated DNA damage response (DDR) pathways. Mutations in NBS1 cause the human genomic instability syndrome Nijmegen Breakage Syndrome (NBS), of which neuronal deficits, including microcephaly and intellectual disability, are classical hallmarks. Given its function in the DDR to ensure proper proliferation and prevent death of replicating cells, NBS1 is essential for life. Here we show that, unexpectedly, Nbs1 deletion is dispensable for postmitotic neurons, but compromises their arborization and migration due to dysregulated Notch signaling. We find that Nbs1 interacts with NICD-RBPJ, the effector of Notch signaling, and inhibits Notch activity. Genetic ablation or pharmaceutical inhibition of Notch signaling rescues the maturation and migration defects of Nbs1-deficient neurons in vitro and in vivo. Upregulation of Notch by Nbs1 deletion is independent of the key DDR downstream effector p53 and inactivation of each MRN component produces a different pattern of Notch activity and distinct neuronal defects. These data indicate that neuronal defects and aberrant Notch activity in Nbs1-deficient cells are unlikely to be a direct consequence of loss of MRN-mediated DDR function. This study discloses a novel function of NBS1 in crosstalk with the Notch pathway in neuron development.

Connecting Artificial Brains to Robots in a Comprehensive Simulation Framework: The Neurorobotics Platform.

Combined efforts in the fields of neuroscience, computer science, and biology allowed to design biologically realistic models of the brain based on spiking neural networks. For a proper validation of these models, an embodiment in a dynamic and rich sensory environment, where the model is exposed to a realistic sensory-motor task, is needed. Due to the complexity of these brain models that, at the current stage, cannot deal with real-time constraints, it is not possible to embed them into a real-world task. Rather, the embodiment has to be simulated as well. While adequate tools exist to simulate either complex neural networks or robots and their environments, there is so far no tool that allows to easily establish a communication between brain and body models. The Neurorobotics Platform is a new web-based environment that aims to fill this gap by offering scientists and technology developers a software infrastructure allowing them to connect brain models to detailed simulations of robot bodies and environments and to use the resulting neurorobotic systems for in silico experimentation. In order to simplify the workflow and reduce the level of the required programming skills, the platform provides editors for the specification of experimental sequences and conditions, environments, robots, and brain-body connectors. In addition to that, a variety of existing robots and environments are provided. This work presents the architecture of the first release of the Neurorobotics Platform developed in subproject 10 "Neurorobotics" of the Human Brain Project (HBP). At the current state, the Neurorobotics Platform allows researchers to design and run basic experiments in neurorobotics using simulated robots and simulated environments linked to simplified versions of brain models. We illustrate the capabilities of the platform with three example experiments: a Braitenberg task implemented on a mobile robot, a sensory-motor learning task based on a robotic controller, and a visual tracking embedding a retina model on the iCub humanoid robot. These use-cases allow to assess the applicability of the Neurorobotics Platform for robotic tasks as well as in neuroscientific experiments.