Numerous neurological dysfunctions are characterized by undesirable nerve activity. By providing reversible nerve blockage, electric stimulation with an implanted electrode holds promise in the treatment of these conditions. However, there are several limitations to its application, including poor bio-compatibility and decreased efficacy during chronic implantation. A magnetic coil of miniature size can mitigate some of these problems, by coating it with biocompatible material for chronic implantation. However, it is unknown if miniature coils could be effective in axonal blockage and, if so, what the underlying mechanisms are. Here we demonstrate that a submillimeter magnetic coil can reversibly block action potentials in the unmyelinated axons from the marine mollusk Aplysia californica. Using a multi-compartment model of the Aplysia axon, we demonstrate that the miniature coil causes a significant local depolarization in the axon, alters activation dynamics of the sodium channels, and prevents the traveling of the invading action potentials. With improved biocompatibility and capability of emitting high-frequency stimuli, micro coils provide an interesting alternative for electric blockage of axonal conductance in clinical settings.

Inhibitory neurons embedded within mammalian neural circuits shape breathing, walking, chewing, and other rhythmic motor behaviors. At the core of the neural circuit controlling breathing is the preBötzinger Complex (preBötC), a nucleus in the ventrolateral medulla necessary for generation of inspiratory rhythm. In the preBötC, a recurrently connected network of glutamatergic Dbx1-derived (Dbx1+) neurons generates rhythmic inspiratory drive to inspiratory premotoneurons and motoneurons. Functionally and anatomically intercalated among Dbx1+preBötC neurons are GABAergic (GAD1/2+) and glycinergic (GlyT2+) neurons, whose functions have not been clearly determined. We first characterized the spatial distribution of molecularly-defined inhibitory preBötC subpopulations in double reporter mice expressing either the red fluorescent protein tdTomato or EGFP in GlyT2+, GAD1+, or GAD2+neurons. We found that, in postnatal mice, the majority of inhibitory preBötC neurons expressed a combination of GlyT2 and GAD2 while a much smaller subpopulation also expressed GAD1. To determine the functional role of these subpopulations, we used holographic photostimulation, a patterned illumination technique with high spatiotemporal resolution, to specifically excite small groups of GlyT2+or GAD1+preBötC subpopulations in rhythmically active medullary slices from Dbx1tdTomato;GlyT2EGFPand Dbx1tdTomato;GAD1EGFPdouble reporter mice. Stimulation of 4 or 8 GlyT2+preBötC neurons during endogenous rhythmic activity prolonged the interburst interval in a phase-dependent manner and increased the latency to burst initiation when bursts were evoked by stimulation of Dbx1+neurons. In contrast, stimulation of 4 or 8 GAD1+preBötC neurons did not affect interburst interval or latency to burst initiation, but did prolong both endogenous and evoked burst duration when stimulation occurred during the burst. We conclude that the majority of inhibitory preBötC neurons express both GlyT2 and GAD2 and affect breathing rhythm by delaying burst initiation while a smaller GAD1+subpopulation affects inspiratory patterning by prolonging burst duration.