One of the important goals of peripheral nerve electrode development is to design an electrode for selective recruitment of the different functions of a common nerve trunk. A challenging task is gaining selective access to central axon populations. In this paper, a simple electrode that takes advantage of the neural plasticity to reshape the nerve is presented. The flat interface nerve electrode (FINE) reshapes the nerve into a flat geometry to increase the surface area and move central axon populations close to the surface. The electrode was implanted acutely on the sciatic nerve of eight cats. The FINE can significantly reshape the nerve and fascicles (p < 0.0001) while maintaining the same total nerve cross-sectional area. The stimulation thresholds were 2.89 nC for pulse amplitude modulation and 10.2 nC for pulse-width modulation. Monopolar, square-pulse stimulation with single contacts on the FINE selectively recruited each of the four main branches of the sciatic nerve. Simultaneous stimulation with two contacts produced moments about the ankle joint that were a combination of the moments produced by the individual contacts when stimulated separately.
We have developed a method to predict excitation of axons based on the response of passive models. An expression describing the transmembrane potential induced in passive models to an applied electric field is presented. Two terms were found to drive the polarization of each node. The first was a source term described by the activating function at the node, and the other was an ohmic term resulting from redistribution of current from sources at other nodes. A total equivalent driving function including both terms was then defined. We found that the total equivalent driving function can be used to provide accurate predictions of excitation thresholds for any applied field. The method requires only knowledge of the intracellular strength-duration relationship of the axon, the passive step response of the axon to an intracellular current, and the values of the extracellular potentials. Excitation thresholds for any given applied field can then be calculated using a simple algebraic expression. This method eliminates the errors associated with use of the activating function alone, and greatly reduces the computation required to determine fiber response to applied extracellular fields.
Preparation of hippocampal slices and perfusionAll experiments were performed in the CA1 or CA3 regions of hippocampal brain slices prepared from Sprague-Dawley rats (175-250 g). Rats were anaesthetized with ethyl ether and decapitated. The experimental protocol was reviewed and approved by the Institution Animal Care and Use Committee. The brain was rapidly removed and one hemisphere glued to the stage of a Vibroslicer (Vibroslice, Campden Instruments Ltd, London, UK) Slicing was carried out in cold (3-4°C), oxygenated sucrose-based artificial cerebrospinal fluid (ACSF) consisting of (mM): sucrose 220, KCl 3, NaH 2 PO 4 1.25, MgSO 4 2, NaHCO 3 26, CaCl 2 2, dextrose 10. The resulting 350 mm thick slices were immediately transferred to a holding chamber with 'normal' ACSF consisting of (mM): NaCl 124, KCl 3.75, KH 2 PO 4 1.25, CaCl 2 2, MgSO 4 2, NaHCO 3 26, dextrose 10, held at room temperature and bubbled with 95 % O 2 -5 % CO 2 .
Sinusoidal high frequency (20‐50 Hz) electric fields induced across rat hippocampal slices were found to suppress zero‐Ca2+, low‐Ca2+, picrotoxin, and high‐K+ epileptiform activity for the duration of the stimulus and for up to several minutes following the stimulus. Suppression of spontaneous activity by high frequency stimulation was found to be frequency (< 500 Hz) but not orientation or waveform dependent. Potassium‐sensitive microelectrodes showed that block of epileptiform activity was always coincident with a stimulus‐induced rise in extracellular potassium concentration during stimulation. Post‐stimulus inhibition was always associated with a decrease in extracellular potassium activity below baseline levels. Intracellular recordings and optical imaging with voltage‐sensitive dyes showed that during suppression neurons were depolarized yet did not fire action potentials. Direct injection of sinusoidal current into individual pyramidal cells did not result in a tonic depolarization. Injection of large direct current (DC) depolarized neurons and suppressed action potential generation. These findings suggest that high frequency stimulation suppresses epileptiform activity by inducing potassium efflux and depolarization block.
In this paper we present an analysis of magnetic stimulation of finite length neuronal structures using computer simulations. Models of finite neuronal structures in the presence of extrinsically applied electric fields indicate that excitation can be characterized by two driving functions: one due to field gradients and the other due to fields at the boundaries of neuronal structures. It is found that boundary field driving functions play an important role in governing excitation characteristics during magnetic stimulation. Simulations indicate that axons whose lengths are short compared to the spatial extent of the induced field are easier to excite than longer axons of the same diameter. Simulations also indicate that independent cellular dendritic processes are probably not excited during magnetic stimulation. Analysis of the temporal distribution of induced fields indicates that the temporal shape of the stimulus waveform modulates excitation thresholds and propagation of action potentials.
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