Neuronal Control of Rhythmic Swimming in the Leech

The broad aim of the research presented in this thesis is to understand neuronal control of animal behavior. To this end, I conducted experiments on preparations of the medicinal leech, with a focus on rhythmic swimming, using physiological and anatomical techniques. Hypotheses about the neural underpinnings of the swim system were also tested via computer simulations. Three topics are prevalent throughout this work: 1) The function of a novel command-like neuron, cell E21. 2) The influence of the brain and descending inputs on motor function. 3) The neural mechanisms which control swim episode duration. The thesis introduction is a comparison between the neural mechanisms underlying leech and lamprey swim systems. These species share many commonalities including the properties of swim-circuit neurons, intersegmental coupling mechanisms, malleability of phase lags, and mechanisms of sensory feedback. These examples of convergent evolution demonstrate that results obtained in leeches are broadly relevant to animal behavior. I introduce my experimental work with a characterization of the novel cell E21. Activation of this neuron strongly initiates and modulates swimming. It also directly links mechanosensory and swim-gating neurons (cells 204). Because of its role rapidly transmitting information, cell E21 likely contributes to escape locomotion. Interestingly, cell E21, along with cells 204, are strictly swim-enhancing in preparations lacking the head brain, but can also suppress swimming in preparations with the head brain attached. The interactions between these neurons also differ depending upon the presence or III absence of the brain. These results demonstrate that circuit properties may be fundamentally altered in reduced preparations. The head brain was often removed from leech nerve cords for experiments studying swimming because it inhibits initiation and maintenance of this behavior. Here, I show that the brain has regional influences on swimming; the supraesophageal ganglion is the primary structure that constrains locomotion, whereas the subesophageal ganglion enhances swim-maintenance parameters. Finally, I explore mechanisms underlying swim-maintenance and swim-termination using physiological and modeling experiments. Results from these endeavors indicate that reciprocal excitatory connections among interneurons maintain swimming, and that impulse adaptation among these neurons combined with the slow repolarization of swim-suppressing cells leads to swimtermination.

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