This article explores dynamical properties of the olivo-cerebellar system that arise from the specific wiring of inferior olive (IO), cerebellar cortex, and deep cerebellar nuclei (DCN). We show that the irregularity observed in the firing pattern of the IO neurons is not necessarily produced by noise but can instead be the result of a purely deterministic network effect. We propose that this effect can serve as a dynamical working memory or as a neuronal clock with a characteristic timescale of about 100 ms that is determined by the slow calcium dynamics of IO and DCN neurons. This concept provides a novel explanation of how the cerebellum can solve timing tasks on a timescale that is two orders of magnitude longer than the millisecond timescale usually attributed to neuronal dynamics. One of the key ingredients of our model is the observation that due to postinhibitory rebound, DCN neurons can be driven by GABAergic (“inhibitory”) input from cerebellar Purkinje cells. Topographic projections from the DCN to the IO form a closed reverberating loop with an overall synaptic transmission delay of about 100 ms that is in resonance with the intrinsic oscillatory properties of the inferior olive. We use a simple time-discrete model based on McCulloch-Pitts neurons in order to investigate in a first step some of the fundamental properties of a network with delayed reverberating projections. The macroscopic behavior is analyzed by means of a mean-field approximation. Numerical simulations, however, show that the microscopic dynamics has a surprisingly rich structure that does not show up in a mean-field description. We have thus performed extensive numerical experiments in order to quantify the ability of the network to serve as a dynamical working memory and its vulnerability by noise. In a second step, we develop a more realistic conductance-based network model of the inferior olive consisting of about 20 multicompartment neurons that are coupled by gap junctions and receive excitatory and inhibitory synaptic input via AMPA and GABAergic synapses. The simulations show that results for the time-discrete model hold true in a time-continuous description.

We investigate the propagation of pulses of spike activity in a neuronal network with feedforward couplings. The neurons are of the spike-response type with a firing probability that depends linearly on the membrane potential. After firing, neurons enter a phase of refractoriness. Spike packets are described in terms of the moments of the firing-time distribution so as to allow for an analytical treatment of the evolution of the spike packet as it propagates from one layer to the next. Analytical results and simulations show that depending on the synaptic coupling strength, a stable propagation of the packet with constant waveform is possible. Crucial for this observation is neither the existence of a firing threshold nor a sigmoidal gain function—both are absent in our model—but the refractory behavior of the neurons.

We present a spiking neuron model that allows for an analytic calculation of the correlations between pre- and postsynaptic spikes. The neuron model is a generalization of the integrate-and-fire model and equipped with a probabilistic spike-triggering mechanism. We show that under certain biologically plausible conditions, pre- and postsynaptic spike trains can be described simultaneously as an inhomogeneous Poisson process. Inspired by experimental findings, we develop a model for synaptic long-term plasticity that relies on the relative timing of pre- and post-synaptic action potentials. Being given an input statistics, we compute the stationary synaptic weights that result from the temporal correlations between the pre- and postsynaptic spikes. By means of both analytic calculations and computer simulations, we show that such a mechanism of synaptic plasticity is able to strengthen those input synapses that convey precisely timed spikes at the expense of synapses that deliver spikes with a broad temporal distribution. This may be of vital importance for any kind of information processing based on spiking neurons and temporal coding.

We develop a minimal time-continuous model for use-dependent synaptic short-term plasticity that can account for both short-term depression and short-term facilitation. It is analyzed in the context of the spike response neuron model. Explicit expressions are derived for the synaptic strength as a function of previous spike arrival times. These results are then used to investigate the behavior of large networks of highly interconnected neurons in the presence of short-term synaptic plasticity. We extend previous results so as to elucidate the existence and stability of limit cycles with coherently firing neurons. After the onset of an external stimulus, we have found complex transient network behavior that manifests itself as a sequence of different modes of coherent firing until a stable limit cycle is reached.

It is generally believed that a neuron is a threshold element that fires when some variable u reaches a threshold. Here we pursue the question of whether this picture can be justified and study the four-dimensional neuron model of Hodgkin and Huxley as a concrete example. The model is approximated by a response kernel expansion in terms of a single variable, the membrane voltage. The first-order term is linear in the input and its kernel has the typical form of an elementary postsynaptic potential. Higher-order kernels take care of nonlinear interactions between input spikes. In contrast to the standard Volterra expansion, the kernels depend on the firing time of the most recent output spike. In particular, a zero-order kernel that describes the shape of the spike and the typical after-potential is included. Our model neuron fires if the membrane voltage, given by the truncated response kernel expansion, crosses a threshold. The threshold model is tested on a spike train generated by the Hodgkin-Huxley model with a stochastic input current. We find that the threshold model predicts 90 percent of the spikes correctly. Our results show that, to good approximation, the description of a neuron as a threshold element can indeed be justified.