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Spike Response Model

 

The essentials of neuronal behavior are the absolute and relative refractory period, the response at the soma resulting from synaptic input (usually described by an alpha function), the omnipresent delays, and noise. All these ingredients have been incorporated in the spike response model (Gerstner and van Hemmen 1992, 1993; Gerstner et al. 1993) [5,7,6] . It presents a faithful but simplified description of the neurons themselves without taking recourse to differential equations. This is essential since we have to study the spatial activity of a large system of neurons (say ) over a long period of time.

We discretize time by units ms, the width of a spike, and label the neurons on a 2-dimensional square lattice by the index i. The state of a neuron is described by . If the potential at the hillock of neuron i reaches the threshold , then the neuron is expected to fire. We describe this stochastic behavior through a noise parameter in the transition probability

 

This is the conditional probability that neuron i fires at time given . In the noise-free limit we get where is the Heaviside step function: for and for x < 0. In the numerics to be described below we have taken and .

The spike response model describes the response of a neuron -- both the sender and the receiver -- to a spike. If a neuron has fired a spike, it exhibits refractory behavior for a while, i.e., it cannot or hardly spike. This is taken care of by the refractory function , which is during the absolute refractory period and negative but increasing to zero thereafter,

 

Here we take for and zero elsewhere.

The spike travels along an axon and reaches a synapse on the dendritic tree of neuron i after ms. Let the synaptic strength be and denote the alpha function by . Then we obtain for the total input at the hillock of neuron i

 

where so that ; here ms. For the sake of computational simplicity we have assumed that the delays depend on i (instead of, say, j). In this work the are taken from with equal probability. Furthermore, always vanishes.

The neurons considered so far are pyramidal cells. The stellate cells are modeled by an inhibitory loop which is assigned to each neuron,

 

where first assumes a strongly negative value during 5ms ( shunting inhibition) and then decays exponentially with a time constant ms. Moreover, is a uniformly distributed random variable. It is known that stellate cells operate locally. This we have simplified to a strictly local interaction; for details, see Gerstner et al. (1993) [6] . Putting things together we find

 

which is to be substituted into (1). What is left is specifying the in (3).

Since we are concerned with visual percepts such as hallucinations it seems natural, even imperative (Zeki 1993) [16] , to model the primary visual cortex. We will work with a simplified model of cortical connectivity. Inside a column the pyramidal cells experience an excitatory interaction. Different columns with strongly different direction preferences are expected to inhibit each other. The upshot is a ``mexican hat''gif,

 

with and . Here is the Euclidean distance between i and j. A second possibility, which has also been studied, is

 

with and, again, . We use free boundary conditions. In our numerical simulations we have seen no difference between (6) and (7). Alternatively and giving rise to the very same scenarios, one can replace in (3) by where with probability or ; otherwise vanishes. Typical values for the s are in the range between 2 and 5. The probabilities have been chosen in such a way that that nearest neighbors () are always connected. D is a drug parameter.

Summarizing, we have explicitly modeled the various interactions including the stellate cells, the delays which are abundantly present in the cortex, and the noise. We now turn to the network behavior itself.



next up previous
Next: Drug-induced collective excitations Up: Spontaneous excitations in the Previous: Introduction



Raphael Ritz
Fri Sep 22 16:19:19 PDT 1995