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Locomotor behaviors are critical for survival and enable animals to navigate their environment, find food and evade predators. The circuits in the brain and spinal cord that initiate and maintain such different modes of locomotion in vertebrates have been studied in numerous species for over a century. In recent decades, the zebrafish has emerged as one of the main model systems for the study of locomotion, owing to its experimental amenability, and work in zebrafish has revealed numerous new insights into locomotor circuit function. Here, we review the literature that has led to our current understanding of the neural circuits controlling swimming and escape in zebrafish. We highlight recent studies that have enriched our comprehension of key topics, such as the interactions between premotor excitatory interneurons (INs) and motoneurons (MNs), supraspinal and spinal circuits that coordinate escape maneuvers, and developmental changes in overall circuit composition. We also discuss roles for neuromodulators and sensory inputs in modifying the relative strengths of constituent circuit components to provide flexibility in zebrafish behavior, allowing the animal to accommodate changes in the environment. We aim to provide a coherent framework for understanding the circuitry in the brain and spinal cord of zebrafish that allows the animal to flexibly transition between different speeds, and modes, of locomotion.

THE NEUROETHOLOGY OF PREDATION AND ESCAPE To eat and not get eaten is key to animal survival, and the arms race between predators and prey has driven the evolution of many rapid and spectacular behaviours. This book explores the neural mechanisms controlling predation and escape, where specialisations in afferent pathways, central circuits, motor control and biomechanics can be traced through to natural animal behaviour. Each chapter provides an integrated and comparative review of case studies in neuroethology. Ranging from the classic studies on bat biosonar and insect counter-measures, through to fish-eating snails armed with powerful neurotoxins, the book covers a diverse and fascinating range of adaptations. Common principles of biological design and organization are highlighted throughout the text. The book is aimed at several audiences: * for lecturers and students. This synthesis will help to underpin the curriculum in neuroscience and behavioural biology, especially for courses focusing on neuroethology * for postgraduate students. The sections devoted to your area of specialism will give a flying start to your research reading, while the other chapters offer breadth and insights from comparative studies * for academic researchers. The book will provide a valuable resource and an enjoyable read Above all, we hope this book will inspire the next generation of neuroethologists.

Dopamine plays important roles in the development and modulation of motor control circuits. Here we show that dopamine exerts potent effects on the central pattern generator circuit controlling locomotory swimming in post-embryonic Xenopus tadpoles. Dopamine (0.5–100 μM) reduced fictive swim bout occurrence and caused both spontaneous and evoked episodes to become shorter, slower and weaker. The D2-like receptor agonist quinpirole mimicked this repertoire of inhibitory effects on swimming, whilst the D4 receptor antagonist, L745,870, had the opposite effects. The dopamine reuptake inhibitor bupropion potently inhibited fictive swimming, demonstrating that dopamine constitutes an endogenous modulatory system. Both dopamine and quinpirole also inhibited swimming in spinalised preparations, suggesting spinally located dopamine receptors. Dopamine and quinpirole hyperpolarised identified rhythmically active spinal neurons, increased rheobase and reduced spike probability both during swimming and in response to current injection. The hyperpolarisation was TTX-resistant and was accompanied by decreased input resistance, suggesting that dopamine opens a K + channel. The K + channel blocker barium chloride (but not TEA, glybenclamide or tertiapin-Q) significantly occluded the hyperpolarisation. Overall, we show that endogenously released dopamine acts upon spinally located D2-like receptors, leading to a rapid inhibitory modulation of swimming via the opening of a K + channel.

Activity-dependent modification of neural network output usually results from changes in neurotransmitter release and/or membrane conductance. In Xenopus frog tadpoles, spinal locomotor network output is adapted by an ultraslow afterhyperpolarization (usAHP) mediated by an increase in Na + pump current. Here we systematically explore how the interval between two swimming episodes affects the second episode, which is shorter and slower than the first episode. We find the firing reliability of spinal rhythmic neurons to be lower in the second episode, except for excitatory descending interneurons (dINs). The sodium/proton antiporter, monensin, which potentiates Na + pump function, induced similar effects to short inter-swim intervals. A usAHP induced by supra-threshold pulses reduced neuronal firing reliability during swimming. It also increased the threshold current for spiking and introduced a delay to the first spike in a train, without reducing subsequent firing frequency. This delay was abolished by ouabain or zero K + saline, which eliminate the usAHP. We present evidence for an A-type K + current in spinal CPG neurons which is inactivated by depolarization and de-inactivated by hyperpolarization and accounts for the prolonged delay. We conclude that the usAHP attenuates neuronal responses to excitatory network inputs by both membrane hyperpolarization and enhanced de-inactivation of an A-current.

Scientific Reports 5: Article number: 16188; published online: 06 November 2015; updated: 22 December 2017. In this Article, ‘Centre for Neuroregeneration, University of Edinburgh, Chancellor’s Building, 49 Little France Crescent, Edinburgh, EH16 4SB’ is incorrectly listed as a present address for Hong-Yan Zhang and should be listed as a second affiliation.

This corrects the article DOI: 10.1038/srep16188.

Rhythmically active, locomotor networks of the spinal cord are subject to both neuromodulation and activity-dependent homeostatic regulation. I first show that the neuromodulator dopamine exerts potent inhibitory effects on the central pattern generator (CPG) circuit controlling locomotory swimming in post-embryonic Xenopus tadpoles. Dopamine, acting endogenously on spinal D2-like receptors, reduces spontaneous fictive swimming occurrence and shortens, slows and weakens swimming. The mechanism involves a TTX-resistant hyperpolarisation of rhythmically active CPG neurons, mediated by the direct opening of a K+ channel with GIRK-like pharmacology. This increases rheobase and reduces spike probability. I next explore how sodium pumps contribute to the activity-dependent regulation of the Xenopus swim circuit, and possible interactions of the pumps with modulators, temperature and ionic conductances. I characterise the pump-mediated ultra-slow afterhyperpolarisation (usAHP), and show that monensin, a sodium ionophore, enhances pump activity, converting the usAHP into a tonic hyperpolarisation; this decreases swim episode duration and cycle frequency. I also characterise a ZD7288-sensitive Ih current, which is active in excitatory dIN interneurons and contributes to spiking. Blocking Ih with ZD7288 decreases swim episode duration and destabilises swim bursts. Both Ih and the usAHP increase with temperature, which depolarises CPG neurons, decreases input resistance, and increases spike probability; this increases cycle frequency, but the enhanced usAHP shortens swimming. I also show that the usAHP is diminished by nitric oxide, but enhanced by dopaminergic signalling. Finally, I explore sodium pumps in the neonatal mouse. The sodium pump blocker ouabain increases the duration and frequency of drug- and sensory-induced locomotion, whilst monensin has opposite effects. Decreasing inter-episode interval also shortens and slows activity, a relationship abolished by ouabain, implicating sodium pumps in a feedforward motor memory mechanism. Finally, I show that the effects of ouabain on locomotion are dependent on dopamine, which enhances a TTX- and ouabain-sensitive usAHP in spinal neurons.

While the inflammatory processes in rheumatoid arthritis have been described, mechanisms driving pain are poorly defined. Here, we used a multitude of approaches to uncover the neural basis, mediators, intracellular signaling pathway and the mechanism of inflammatory pain. In cartilage autoantibody-induced arthritis mice, an early immune-activation and a cytokine storm were mainly driven by vascular cells and monocyte/macrophages in the dorsal root ganglion. However, persistently elevated interferons and receptor-activation of the MNK1/2-eIF4E signaling pathway at all disease phases caused sensory-motor dysfunction and pain by inducing hyperexcitability and sensitization of Gfra3+ sensory neurons. Like mice, human sensory neurons expressed interferon receptors and interferons were elevated only in individuals with painful rheumatoid arthritis. Signaling pathway inhibition in vivo reversed pain and restored limb function. The finding that joint pain before and during arthritis is caused by a defined cytokine and signaling pathway holds promise for targeted therapies for pain relief in arthritis.Competing Interest StatementThe authors have declared no competing interest.

This chapter provides an overview of the three aspects: passive electrolocation; the generation of electric fields; and active electrolocation. There are two basic types of fish electroreceptors, tuberous and ampullary. The tuberous receptors are concerned with active electrolocation, while the ampullary receptors are the ones that detect the 'unintentional' electrical emissions of other animals. Although the weak electric organ discharge (EOD) almost certainly evolved before the strong, the chapter deals with the latter first. The electric eel, Electrophoros electricus, is a big freshwater fish. It is an apex predator that stuns its prey by electric shock using the large and complex electric organ. The organ has three compartments; a main organ, which is responsible for generating most of the high voltage EOD, a more caudal organ of Sachs and a ventrally located Hunter's organ. The latter two compartments generate weaker electric fields that are used in active electrolocation.

The mammalian startle response is extremely widespread within the class, occurring in most mammals, including humans. The response is highly labile, showing rapid short‐term habituation, mediated by anti‐facilitation at afferent synapses onto the PnC neurons, as well as longer‐term learning processes. Startle threshold and amplitude are very dependent on the emotional state of the subject, and this can in part be traced directly to regulation of the giant PnC neurons. Serotonin (5‐HT) is a neuromodulator that may play an important role in dynamically regulating the startle circuit via the giant PnC neurons, since elevated 5‐HT appears to enhance the reflex. The importance of 5‐HT in regulating startle threshold in humans has been emphasised by the demonstration that people carrying the 'short' allele of the transcriptional control region of the 5‐HT transporter gene (5‐HTTLPR) have stronger startle responses than those who are homozygous for the 'long' allele.