No Arabic abstract
We study the stable phases of an attractor neural network model, with binary units, for hippocampal place cells encoding 1D or 2D spatial maps or environments. Using statistical mechanics tools we show that, below critical values for the noise in the neural response and for the number of environments, the network activity is spatially localized in one environment. We calculate the number of stored environments. For high noise and loads the network activity extends over space, either uniformly or with spatial heterogeneities due to the cross-talk between the maps, and memory of environments is lost. Analytical predictions are corroborated by numerical simulations.
A study is made of an anisotropic Potts model in three dimensions where the coupling depends on both the Potts state on each site but also the direction of the bond between them using both analytical and numerical methods. The phase diagram is mapped out for all values of the exchange interactions. Six distinct phases are identified. Monte Carlo simulations have been used to obtain the order parameter and the values for the energy and entropy in the ground state and also the transition temperatures. Excellent agreement is found between the simulated and analytic results. We find one region where there are two phase transitions with the lines meeting in a triple point. The orbital ordering that occurs in $LaMnO_3$ occurs as one of the ordered phases.
The spontaneous transitions between D-dimensional spatial maps in an attractor neural network are studied. Two scenarios for the transition from on map to another are found, depending on the level of noise: (1) through a mixed state, partly localized in both maps around positions where the maps are most similar; (2) through a weakly localized state in one of the two maps, followed by a condensation in the arrival map. Our predictions are confirmed by numerical simulations, and qualitatively compared to recent recordings of hippocampal place cells during quick-environment-changing experiments in rats.
Artificial neural networks have diverged far from their early inspiration in neurology. In spite of their technological and commercial success, they have several shortcomings, most notably the need for a large number of training examples and the resulting computation resources required for iterative learning. Here we describe an approach to neurological network simulation, both architectural and algorithmic, that adheres more closely to established biological principles and overcomes some of the shortcomings of conventional networks.
The Topological Hypothesis states that phase transitions should be related to changes in the topology of configuration space. The necessity of such changes has already been demonstrated. We characterize exactly the topology of the configuration space of the short range Berlin-Kac spherical model, for spins lying in hypercubic lattices of dimension d. We find a continuum of changes in the topology and also a finite number of discontinuities in some topological functions. We show however that these discontinuities do not coincide with the phase transitions which happen for d >= 3, and conversely, that no topological discontinuity can be associated to them. This is the first short range, confining potential for which the existence of special topological changes are shown not to be sufficient to infer the occurrence of a phase transition.
Excessively high, neural synchronisation has been associated with epileptic seizures, one of the most common brain diseases worldwide. A better understanding of neural synchronisation mechanisms can thus help control or even treat epilepsy. In this paper, we study neural synchronisation in a random network where nodes are neurons with excitatory and inhibitory synapses, and neural activity for each node is provided by the adaptive exponential integrate-and-fire model. In this framework, we verify that the decrease in the influence of inhibition can generate synchronisation originating from a pattern of desynchronised spikes. The transition from desynchronous spikes to synchronous bursts of activity, induced by varying the synaptic coupling, emerges in a hysteresis loop due to bistability where abnormal (excessively high synchronous) regimes exist. We verify that, for parameters in the bistability regime, a square current pulse can trigger excessively high (abnormal) synchronisation, a process that can reproduce features of epileptic seizures. Then, we show that it is possible to suppress such abnormal synchronisation by applying a small-amplitude external current on less than 10% of the neurons in the network. Our results demonstrate that external electrical stimulation not only can trigger synchronous behaviour, but more importantly, it can be used as a means to reduce abnormal synchronisation and thus, control or treat effectively epileptic seizures.