Reactive direction control for a mobile robot: A locust-like control of escape direction emerges when a bilateral pair of model locust visual neurons are integrated

Locusts possess a bilateral pair of uniquely identifiable visual neurons that respond vigorously to the image of an approaching object. These neurons are called the lobula giant movement detectors (LGMDs). The locust LGMDs have been extensively studied and this has lead to the development of an LGMD model for use as an artificial collision detector in robotic applications. To date, robots have been equipped with only a single, central artificial LGMD sensor, and this triggers a non-directional stop or rotation when a potentially colliding object is detected. Clearly, for a robot to behave autonomously, it must react differently to stimuli approaching from different directions. In this study, we implement a bilateral pair of LGMD models in Khepera robots equipped with normal and panoramic cameras. We integrate the responses of these LGMD models using methodologies inspired by research on escape direction control in cockroaches. Using ‘randomised winner-take-all’ or ‘steering wheel’ algorithms for LGMD model integration, the khepera robots could escape an approaching threat in real time and with a similar distribution of escape directions as real locusts. We also found that by optimising these algorithms, we could use them to integrate the left and right DCMD responses of real jumping locusts offline and reproduce the actual escape directions that the locusts took in a particular trial. Our results significantly advance the development of an artificial collision detection and evasion system based on the locust LGMD by allowing it reactive control over robot behaviour. The success of this approach may also indicate some important areas to be pursued in future biological research

Abnormal cortical responses to somatosensory stimulation in medication-overuse headache

BACKGROUND: Medication-overuse headache (MOH) is a frequent, disabling disorder. Despite a controversial pathophysiology convincing evidence attributes a pivotal role to central sensitization. Most patients with MOH initially have episodic migraine without aura (MOA) characterized interictally by an absent amplitude decrease in cortical evoked potentials to repetitive stimuli (habituation deficit), despite a normal initial amplitude (lack of sensitization). Whether central sensitization alters this electrophysiological profile is unknown. We therefore sought differences in somatosensory evoked potential (SEP) sensitization and habituation in patients with MOH and episodic MOA. METHODS: We recorded median-nerve SEPs (3 blocks of 100 sweeps) in 29 patients with MOH, 64 with MOA and 42 controls. Episodic migraineurs were studied during and between attacks. We measured N20-P25 amplitudes from 3 blocks of 100 sweeps, and assessed sensitization from block 1 amplitude, and habituation from amplitude changes between the 3 sequential blocks. RESULTS: In episodic migraineurs, interictal SEP amplitudes were normal in block 1, but thereafter failed to habituate. Ictal SEP amplitudes increased in block 1, then habituated normally. Patients with MOH had larger-amplitude block 1 SEPs than controls, and also lacked SEP habituation. SEP amplitudes were smaller in triptan overusers than in patients overusing nonsteroidal anti-inflammatory drugs (NSAIDs) or both medications combined, lowest in patients with the longest migraine history, and highest in those with the longest-lasting headache chronification. CONCLUSIONS: In patients with MOH, especially those overusing NSAIDs, the somatosensory cortex becomes increasingly sensitized. Sensory sensitization might add to the behavioral sensitization that favors compulsive drug intake, and may reflect drug-induced changes in central serotoninergic transmission

Olfactory Interference during Inhibitory Backward Pairing in Honey Bees

Background: Restrained worker honey bees are a valuable model for studying the behavioral and neural bases of olfactory plasticity. The proboscis extension response (PER; the proboscis is the mouthpart of honey bees) is released in response to sucrose stimulation. If sucrose stimulation is preceded one or a few times by an odor (forward pairing), the bee will form a memory for this association, and subsequent presentations of the odor alone are sufficient to elicit the PER. However, backward pairing between the two stimuli (sucrose, then odor) has not been studied to any great extent in bees, although the vertebrate literature indicates that it elicits a form of inhibitory plasticity. Methodology/Principal Findings: If hungry bees are fed with sucrose, they will release a long lasting PER; however, this PER can be interrupted if an odor is presented 15 seconds (but not 7 or 30 seconds) after the sucrose (backward pairing). We refer to this previously unreported process as olfactory interference. Bees receiving this 15 second backward pairing show reduced performance after a subsequent single forward pairing (excitatory conditioning) trial. Analysis of the results supported a relationship between olfactory interference and a form of backward pairing-induced inhibitory learning/ memory. Injecting the drug cimetidine into the deutocerebrum impaired olfactory interference. Conclusions/Significance: Olfactory interference depends on the associative link between odor and PER, rather than between odor and sucrose. Furthermore, pairing an odor with sucrose can lead either to association of this odor to PER or t

Ubiquitous molecular substrates for associative learning and activity-dependent neuronal facilitation.

Recent evidence suggests that many of the molecular cascades and substrates that contribute to learning-related forms of neuronal plasticity may be conserved across ostensibly disparate model systems. Notably, the facilitation of neuronal excitability and synaptic transmission that contribute to associative learning in Aplysia and Hermissenda, as well as associative LTP in hippocampal CA1 cells, all require (or are enhanced by) the convergence of a transient elevation in intracellular Ca2+ with transmitter binding to metabotropic cell-surface receptors. This temporal convergence of Ca2+ and G-protein-stimulated second-messenger cascades synergistically stimulates several classes of serine/threonine protein kinases, which in turn modulate receptor function or cell excitability through the phosphorylation of ion channels. We present a summary of the biophysical and molecular constituents of neuronal and synaptic facilitation in each of these three model systems. Although specific components of the underlying molecular cascades differ across these three systems, fundamental aspects of these cascades are widely conserved, leading to the conclusion that the conceptual semblance of these superficially disparate systems is far greater than is generally acknowledged. We suggest that the elucidation of mechanistic similarities between different systems will ultimately fulfill the goal of the model systems approach, that is, the description of critical and ubiquitous features of neuronal and synaptic events that contribute to memory induction

Supplementary Materials for Design of a neurally plausible fear learning model

This document contains supporting material for "Design of a neurally plausible fear learning model" by FB Krasne, MS Fanselow, and M Zelikowsky. The model is referred to as FRAT (for Fraidy Rat). The first main section of this paper provides a full mathematical presentation of the model. The second section presents a number of simulations that were not included in the main paper