Journal of computational neuroscience
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The temperature-frequency relationship in nerve conduction block induced by high-frequency, biphasic electrical current was investigated by computer simulation using an amphibian myelinated axon model based on Frankenhaeuser-Huxley (FH) equations. For an axon of diameter 10 microm, the minimal blocking frequency was changed from 6 to 3 kHz as the temperature was decreased from 37 degrees C to 15 degrees C. ⋯ Simulation analysis also revealed that activation of potassium channels might determine the temperature-frequency relationship. This study indicates that temperature might be one of the factors that cause the frequency discrepancy as reported in previous animal studies.
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Recently Haas et al. (J Neurophysiol 96: 3305-3313, 2006), observed a novel form of spike timing dependent plasticity (iSTDP) in GABAergic synaptic couplings in layer II of the entorhinal cortex. Depending on the relative timings of the presynaptic input at time t (pre) and the postsynaptic excitation at time t (post), the synapse is strengthened (Deltat = t(post) - t(pre) > 0) or weakened (Deltat < 0). The temporal dynamic range of the observed STDP rule was found to lie in the higher gamma frequency band (> or =40 Hz), a frequency range important for several vital neuronal tasks. ⋯ We then demonstrate a similar enhancement of synchrony in the MCI with dynamic synaptic modulation. For the MCI we also consider heterogeneity introduced in the network through the synaptic parameters: the synaptic decay time of mutual inhibition and the self inhibition synaptic strength. We show that the MCI exhibits enhanced synchrony in the presence of all the above mentioned sources of heterogeneity and the mechanism for this enhanced synchrony is similar to the case of the UCI.
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The influences of stimulation frequency and temperature on mechanisms of nerve conduction block induced by high-frequency biphasic electrical current were investigated using a lumped circuit model of the myelinated axon based on Schwarz and Eikhof (SE) equations. The simulation analysis showed that a temperature-frequency relationship was determined by the axonal membrane dynamics (i.e. how fast the ion channels can open or close.). ⋯ The simulation results also indicated that as the stimulation frequency increased the mechanism of conduction block changed from a cathodal/anodal block to a block dependent upon continuous activation of potassium channels. Understanding the interaction between the minimal blocking frequency and temperature could promote a better understanding of the mechanisms of high frequency induced axonal conduction block and the clinical application of this method for blocking nerve conduction.
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High frequency alternating current (HFAC) sinusoidal waveforms can block conduction in mammalian peripheral nerves. A mammalian axon model was used to simulate the response of nerves to HFAC conduction block. Sinusoidal waveforms from 1 to 40 kHz were delivered to eight simulated axon diameters ranging from 7.3 to 16 microm. ⋯ Upon initiation, the HFAC waveform produced one or more action potentials. These simulation results closely parallel previous experimental results of high frequency motor block of the rat sciatic and cat pudendal nerve. During HFAC block, the axons showed a dynamic steady state depolarization of multiple nodes, strongly suggesting a depolarization mechanism for HFAC conduction block.
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Spike-timing-dependent plasticity (STDP) with asymmetric learning windows is commonly found in the brain and useful for a variety of spike-based computations such as input filtering and associative memory. A natural consequence of STDP is establishment of causality in the sense that a neuron learns to fire with a lag after specific presynaptic neurons have fired. The effect of STDP on synchrony is elusive because spike synchrony implies unitary spike events of different neurons rather than a causal delayed relationship between neurons. ⋯ Even though differences in spike times are lessened as a result of synaptic plasticity, the finite time lag remains so that perfect spike synchrony is not realized. In contrast to traditional mechanisms of large-scale synchrony based on mutual interaction of coupled neurons, the route to synchrony discovered here is enslavement of downstream neurons by upstream ones. Facilitation of such feedforward synchrony does not occur for STDP with symmetric learning windows.