Model of spatio-temporal propagation of action potentials in the Schaffer collateral pathway of the CA1 area of the rat hippocampus

Abstract

There is a sharp contrast between the profuse in vivo axonal arborization of CA3 pyramidal cells in the CA1 area and the low probability of finding pairs of connected CA3‐CA1 pyramidal cells in vitro. These anatomical differences contribute to a connectivity argument for discrepancies between electrophysiological data recorded in vitro and in vivo. In order to investigate this issue, we have developed a realistic computer model of the Schaffer collateral pathway of the hippocampus and analyzed the spatio‐temporal distribution of action potentials along this pathway following three different types of electrical test stimulus. Direct activation of mossy fibers, CA3 pyramidal cells and focal stimulation of CA1 stratum radiatum were investigated. The parameters of the model were selected from available biological data. Spikes in Schaffer collaterals were followed from their onset in the CA3 pyramidal cell initial segment to the last order branches of their axonal tree in two types of configuration: the whole hippocampus and the slice configuration. The anatomical and electropysiological characteristics of the mossy fibre and Schaffer collateral pathways were found to impose strong constraints on the spatio‐temporal distribution of action potentials in the CA1 area. Specific projection zones are determined by the spatial localization of the emitting CA3 pyramidal cells. Their position also defines precise time windows during which some CA1 projection zones receive a large number of correlated signals. Moreover, the variability of the delay at the mossy fibre/CA3 pyramidal cell synapse seems to provide the CA1 projection zones with a background level of excitation. Finally, we show how the patterns of activation obtained in the whole hippocampus are different from those obtained in the slice. Hippocampus 7:58–72, 1997. © 1997 Wiley‐Liss, Inc.

Topological Determinants of Epileptogenesis in Large-Scale Structural and Functional Models of the Dentate Gyrus Derived From Experimental Data

“…Indeed, prior modeling studies of idealized networks indicated the importance of altered network architecture in epileptogenesis (Buzsáki et al 2004;Netoff et al 2004;Percha et al 2005). However, to test the role of structural changes actually taking place during epileptogenesis, the network models must be strongly data driven, i.e., incorporate key structural and functional properties of the biological network (Ascoli and Atkeson 2005;Bernard et al 1997;Traub et al 2005a,b). Such models should also be based on as realistic cell numbers as possible, to minimize uncertainties resulting from the scaling-up of experimentally measured synaptic inputs to compensate for fewer cells in reduced networks.…”

Ionic Mechanisms Underlying Spontaneous CA1 Neuronal Firing in Ca2+-Free Solution

“…Computer simulations of epileptiform activity have provided powerful insight into mechanisms of neuron dynamics (Traub and Llinas, 1979;Traub et al, 1985Traub et al, , 1991Warman et al, 1994;Pinsky and Rinzel, 1994;Bernard et al, 1997). Based on the available voltage-clamp data and current-clamp data for HPCs in normal solution, isolated or coupled CA1 and CA3 HPCs have previously been simulated in detail.…”

Input-to-output transformation in a model of the rat hippocampal CA1 network

“…In the model, we used 23,500 CA1 principal cells. This is an estimate of the number of principal cells in a square millimeter patch given that there are approximately 320,000 principal cells in 13.6 square millimeters of the whole rat CA1 (Bernard and Wheal, 1994; Bernard et al, 1997). We assumed that at the beginning of a 20 ms gamma period, all CA1 principal cells were in the same state.…”