Origin of excitation underlying locomotion in the spinal circuit of zebrafish.

Neural circuits in the spinal cord transform instructive signals from the brain into well-coordinated locomotor movements by virtue of rhythm-generating components. Although evidence suggests that excitatory interneurons are the essence of locomotor rhythm generation, their molecular identity and the assessment of their necessity have remained unclear. Here we show, using larval zebrafish, that V2a interneurons represent an intrinsic source of excitation necessary for the normal expression of the locomotor rhythm. Acute and selective ablation of these interneurons increases the threshold of induction of swimming activity, decreases the burst frequency, and alters the coordination of the rostro-caudal propagation of activity. Thus, our results argue that V2a interneurons represent a source of excitation that endows the spinal circuit with the capacity to generate locomotion.

Principles governing recruitment of motoneurons during swimming in zebrafish.

Locomotor movements are coordinated by a network of neurons that produces sequential muscle activation. Different motoneurons need to be recruited in an orderly manner to generate movement with appropriate speed and force. However, the mechanisms governing recruitment order have not been fully clarified. Using an in vitro juvenile/adult zebrafish brainstem-spinal cord preparation, we found that motoneurons were organized into four pools with specific topographic locations and were incrementally recruited to produce swimming at different frequencies. The threshold of recruitment was not dictated by the input resistance of motoneurons, but was instead set by a combination of specific biophysical properties and the strength of the synaptic currents. Our results provide insights into the cellular and synaptic computations governing recruitment of motoneurons during locomotion.

Modelling and sensitivity analysis of the reactions involving receptor, G-protein and effector in vertebrate olfactory receptor neurons.

A biochemical model of the receptor, G-protein and effector (RGE) interactions during transduction in the cilia of vertebrate olfactory receptor neurons (ORNs) was developed and calibrated to experimental recordings of cAMP levels and the receptor current (RC). The model describes the steps from odorant binding to activation of the effector enzyme which catalyzes the conversion of ATP to cAMP, and shows how odorant stimulation is amplified and delayed by the RGE transduction cascade. A time-dependent sensitivity analysis was performed on the model. The model output-the cAMP production rate-is particularly sensitive to a few, dominant parameters. During odorant stimulation it depends mainly on the initial density of G-proteins and the catalytic constant for cAMP production.