Implications of Selfish Neighbor Selection in Overlay Networks

In a typical overlay network for routing or content sharing, each node must select a fixed number of immediate overlay neighbors for routing traffic or content queries. A selfish node entering such a network would select neighbors so as to minimize the weighted sum of expected access costs to all its destinations. Previous work on selfish neighbor selection has built intuition with simple models where edges are undirected, access costs are modeled by hop-counts, and nodes have potentially unbounded degrees. However, in practice, important constraints not captured by these models lead to richer games with substantively and fundamentally different outcomes. Our work models neighbor selection as a game involving directed links, constraints on the number of allowed neighbors, and costs reflecting both network latency and node preference. We express a node's "best response" wiring strategy as a k-median problem on asymmetric distance, and use this formulation to obtain pure Nash equilibria. We experimentally examine the properties of such stable wirings on synthetic topologies, as well as on real topologies and maps constructed from PlanetLab and AS-level Internet measurements. Our results indicate that selfish nodes can reap substantial performance benefits when connecting to overlay networks composed of non-selfish nodes. On the other hand, in overlays that are dominated by selfish nodes, the resulting stable wirings are optimized to such great extent that even non-selfish newcomers can extract near-optimal performance through naive wiring strategies.

The Hippocampus and Cerebellum in Adaptively Timed Learning, Recognition, and Movement

The concepts of declarative memory and procedural memory have been used to distinguish two basic types of learning. A neural network model suggests how such memory processes work together as recognition learning, reinforcement learning, and sensory-motor learning take place during adaptive behaviors. To coordinate these processes, the hippocampal formation and cerebellum each contain circuits that learn to adaptively time their outputs. Within the model, hippocampal timing helps to maintain attention on motivationally salient goal objects during variable task-related delays, and cerebellar timing controls the release of conditioned responses. This property is part of the model's description of how cognitive-emotional interactions focus attention on motivationally valued cues, and how this process breaks down due to hippocampal ablation. The model suggests that the hippocampal mechanisms that help to rapidly draw attention to salient cues could prematurely release motor commands were not the release of these commands adaptively timed by the cerebellum. The model hippocampal system modulates cortical recognition learning without actually encoding the representational information that the cortex encodes. These properties avoid the difficulties faced by several models that propose a direct hippocampal role in recognition learning. Learning within the model hippocampal system controls adaptive timing and spatial orientation. Model properties hereby clarify how hippocampal ablations cause amnesic symptoms and difficulties with tasks which combine task delays, novelty detection, and attention towards goal objects amid distractions. When these model recognition, reinforcement, sensory-motor, and timing processes work together, they suggest how the brain can accomplish conditioning of multiple sensory events to delayed rewards, as during serial compound conditioning.

A Neural Network of Adaptively Timed Reinforcement Learning and Hippocampal Dynamics

A neural model is described of how adaptively timed reinforcement learning occurs. The adaptive timing circuit is suggested to exist in the hippocampus, and to involve convergence of dentate granule cells on CA3 pyramidal cells, and NMDA receptors. This circuit forms part of a model neural system for the coordinated control of recognition learning, reinforcement learning, and motor learning, whose properties clarify how an animal can learn to acquire a delayed reward. Behavioral and neural data are summarized in support of each processing stage of the system. The relevant anatomical sites are in thalamus, neocortex, hippocampus, hypothalamus, amygdala, and cerebellum. Cerebellar influences on motor learning are distinguished from hippocampal influences on adaptive timing of reinforcement learning. The model simulates how damage to the hippocampal formation disrupts adaptive timing, eliminates attentional blocking, and causes symptoms of medial temporal amnesia. It suggests how normal acquisition of subcortical emotional conditioning can occur after cortical ablation, even though extinction of emotional conditioning is retarded by cortical ablation. The model simulates how increasing the duration of an unconditioned stimulus increases the amplitude of emotional conditioning, but does not change adaptive timing; and how an increase in the intensity of a conditioned stimulus "speeds up the clock", but an increase in the intensity of an unconditioned stimulus does not. Computer simulations of the model fit parametric conditioning data, including a Weber law property and an inverted U property. Both primary and secondary adaptively timed conditioning are simulated, as are data concerning conditioning using multiple interstimulus intervals (ISIs), gradually or abruptly changing ISis, partial reinforcement, and multiple stimuli that lead to time-averaging of responses. Neurobiologically testable predictions are made to facilitate further tests of the model.