A Multimodal Emotional Human-Robot Interaction Architecture for Social Robots Engaged in Bidirectional Communication.

For social robots to effectively engage in human-robot interaction (HRI), they need to be able to interpret human affective cues and to respond appropriately via display of their own emotional behavior. In this article, we present a novel multimodal emotional HRI architecture to promote natural and engaging bidirectional emotional communications between a social robot and a human user. User affect is detected using a unique combination of body language and vocal intonation, and multimodal classification is performed using a Bayesian Network. The Emotionally Expressive Robot utilizes the user's affect to determine its own emotional behavior via an innovative two-layer emotional model consisting of deliberative (hidden Markov model) and reactive (rule-based) layers. The proposed architecture has been implemented via a small humanoid robot to perform diet and fitness counseling during HRI. In order to evaluate the Emotionally Expressive Robot's effectiveness, a Neutral Robot that can detect user affects but lacks an emotional display, was also developed. A between-subjects HRI experiment was conducted with both types of robots. Extensive results have shown that both robots can effectively detect user affect during the real-time HRI. However, the Emotionally Expressive Robot can appropriately determine its own emotional response based on the situation at hand and, therefore, induce more user positive valence and less negative arousal than the Neutral Robot.

Dendritic Spine Density is Increased in Arcadlin-deleted Mouse Hippocampus.

The neural network undergoes remodeling in response to neural activity and interventions, such as antidepressants. Cell adhesion molecules that link pre- and post-synaptic membranes are responsible not only for the establishment of the neural circuitry, but also for the modulation of the strength of each synaptic connection. Among the various classes of synaptic cell adhesion molecules, a non-clustered protocadherin, Arcadlin/Paraxial protocadherin/Protocadherin-8 (Acad), is unique in that it is induced quickly in response to neural activity. Although the primary structure of Arcadlin implies its cell adhesion activity, it weakens the adhesion of N-cadherin. Furthermore, Arcadlin reduces the dendritic spine density in cultured hippocampal neurons. In order to gain an insight into the function of Arcadlin in the brain, we examined the dendritic morphologies of the hippocampal neurons in Acad-/- mice. Acad-/- mice showed a higher spine density than wild-type mice. Following an electroconvulsive seizure (ECS), which strongly induces Arcadlin in the hippocampus, the spine density gradually decreased for 8 h. ECS did not reduce the spine density of CA1 apical dendrites in Acad-/- mice. Daily intraperitoneal injection of the antidepressant fluoxetine (25 mg/kg/day) for 18 days resulted in the induction of Arcadlin in the hippocampus. This treatment reduced spine density in the dentate gyrus and CA1. Chronic fluoxetine treatment did not suppress spine density in Acad-/- mice, suggesting that fluoxetine-induced decrease in spine density is largely due to Arcadlin. The present findings confirm the spine-repulsing activity of Arcadlin and its involvement in the remodeling of hippocampal neurons in response to antidepressants.