# Beyond Hebb: Exclusive-OR and Biological Learning∗

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## Abstract

A learning algorithm for multilayer neural networks based on biologically plausible mechanisms is studied. Motivated by findings in experimental neurobiology, we consider synaptic averaging in the induction of plasticity changes, which happen on a slower time scale than firing dynamics. This mechanism is shown to enable learning of the exclusive-OR (XOR) problem without the aid of error backpropagation, as well as to increase robustness of learning in the presence of noise.   
PACS numbers: 87.17.Aa, 82.20.Wt, 87.19.La   

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Since the early days of neurophysiology we have evidence of biological mechanisms serving as the basis for learning and information processing in the brain. Cajal’s pictures showing networks of intertwined nerve cells readily lead to the hypothesis of information flow and processing in these networks . Subsequently formulated theoretical models of the neuron, as by McCulloch and Pitts , and the Hebbian learning rule, postulating synaptic strengthening for simultaneous pre- and postsynaptic activity , sparked the development of algorithms for neuronal learning and memory. The development of learning algorithms, however, took place almost decoupled from biological validation, partly due to lack of detailed knowledge of the neurophysiology of learning, but also due to their success in applied fields (“connectionism”, “machine learning”). Among the first models were layered assemblies of formal neurons (Perceptrons) combined with gradient rules defining the synaptic weights . Later, combining Hebb’s strictly local rule with symmetrically connected formal neurons defined the Hopfield model of simple associative learning . However, only a complicated non-local learning rule, now known as error backpropagation, finally was able to solve simple non-linear learning problems as the learning of the exclusive-or (XOR) function . This complicated form of reverse information transfer, however, has not been observed in biological circuits .

For computation in biological nervous systems the question remains, which underlying biological processes are capable of the most general form of learning , including problems of the XOR class. A more biologically plausible learning concept is learning by reinforcement and recently a number of models along this line have been formulated . One such model by Barto and Anandan combines a local mechanism of synaptic plasticity changes with a global feedback signal indicating information worth memorizing . A remaining problem in these models is the regulation of mean activity level in large networks which has been attacked by Alstrøm and Stassinopoulos  and Stassinopoulos and Bak . An even more elegant mechanism has been proposed by Chialvo and Bak  with reinforcement through negative feedback which is motivated by the observed long-term depression (LTD) in biological networks. In this algorithm, the dynamics of synaptic plasticity comes to a halt when learning reaches its goal, just by definition. While we think that this is a very interesting approach to formulating a biologically plausible learning mechanism, this model suffers a severe restriction in learning capabilities. It has been shown to work well on simple tasks as non-overlapping pattern sets, however, it is not able to learn tasks as the XOR function, at least not without unreasonably large numbers of neurons and very long learning times. It is, therefore, nearly as limited as the early single layer perceptron models that, for this reason, nearly paralyzed the research in neural networks in the seventies (mainly following the sobering analysis of perceptron capabilities by Minsky and Papert ).

In the following we will study a model in this spirit which, however, does not exhibit this restriction. Let us first define the model, then report numerical results on its learning capabilities. We will then discuss the robustness of our model in the presence of noise. The letter concludes with a discussion of the motivation of our model from current findings in neurobiology.

Consider a layered network of binary formal neurons $`x_i\{0,1\}`$, with $`I`$ input sites $`x_0,\mathrm{},x_{I1}`$, $`J`$ hidden sites $`x_I,\mathrm{},x_{I+J1}`$, and $`K`$ output units $`x_{I+J},\mathrm{},x_{I+J+K1}`$. The adjacent layers are completely connected by weights $`w_{ji}`$ from each input to each hidden unit and from each hidden unit to each output unit. In addition, each weight is assigned an internal degree of freedom, acknowledging the finite time scale of synaptic plasticity induction as will be discussed below. In the model this is represented by an additional discrete variable $`c_{ji}`$ associated to each weight $`w_{ji}`$ serving as a synaptic memory during learning.

The network dynamics is defined by the following steps. The input sites are activated with external stimuli $`x_0,\mathrm{},x_{I1}`$. Each hidden node $`j`$ then receives a weighted input $`h_j=_{i=0}^{I1}w_{ji}x_i`$. Its state is chosen according to a probabilistic rule s.t. each hidden neuron fires with probability $`p_j=a^1\mathrm{exp}(\beta h_j)`$ with the normalization $`a=_j\mathrm{exp}(\beta h_j)`$. We consider the low activity limit of the network where only one hidden neuron fires at a time. Each output neuron $`k`$ now receives an input sum $`h_k=_{j=I}^{I+J1}w_{kj}x_j`$ with the only non-zero contribution from the firing hidden neuron $`j^{}`$ such that $`h_k=w_{kj^{}}`$. The above probabilistic rule applies to the output layer as well, determining one firing output neuron $`x_k^{}`$ which represents the output of the network corresponding to a given input pattern. Note that in the low activity limit used here, the probabilistic rule is a stochastic approximation of the winner-take-all rule . We think our variant based on local dynamics is biologically more realistic than supplying global information of which neuron has the highest input sum within a layer. In the limit $`\beta \mathrm{}`$, the neuronal activity in our model follows exact winner-take-all dynamics, since then $`\mathrm{max}_jp_j=a^1\mathrm{exp}(\beta \mathrm{max}_jh_j)1`$. This deterministic case has been used in the network model of Chialvo and Bak . Here, however, we consider stochastic models with finite values of $`\beta `$.

Now it remains to specify the learning dynamics of the network weights $`w_{ji}`$ themselves. For each activation pattern, the network output is compared to the target output and a feedback signal $`r`$ returned to the network, with $`r=+1`$, if its output neurons represent the predefined target output, given the current input, and $`r=1`$ otherwise. Depending on this binary feedback, connections and corresponding counter values are updated. All “active” synapses $`w`$ (and corresponding counter values $`c`$) for which pre- and postsynaptic sites have been simultaneously active are updated as follows. The feedback signal is subtracted from the memory $`c`$ of each active synapse according to:

$$cc^{}=\{\begin{array}{ccccc}\mathrm{\Theta },\hfill & \mathrm{if}\hfill & & cr& >\mathrm{\Theta }()\hfill \\ cr,\hfill & \mathrm{if}\hfill & \hfill \mathrm{\Theta }& cr& 0\hfill \\ 0,\hfill & \mathrm{if}\hfill & \hfill 0>& cr.& \end{array}$$
(1)   
Thus, each counter $`c`$ is an error account of the corresponding synapse. The capacity of the account is given by the memory size $`\mathrm{\Theta }`$. In case this threshold is exceeded \[marked by $`()`$ in equation (1)\] the synapse is penalized, i. e., it is weakened by a constant amount $`\delta `$:

$$ww^{}=w\delta .$$
(2)   
(Alternatively, a multiplicative penalty combined with a constant growth of weights has been successfully checked, too.) Therefore, the counter averages over the record of a synapse, instead of penalizing each single error at the moment it occurs. Note that the model by Chialvo and Bak  is just this latter case and is obtained by setting $`\mathrm{\Theta }=0`$ and $`\beta =\mathrm{}`$. After these changes to weights and counters the learning cycle is iterated by presenting another—possibly different—pattern of stimuli to the network.

Note that $`\beta `$ and $`\delta `$ are not independent parameters; changing the value of $`\delta `$ does not affect the dynamics, as long as the product $`\beta \delta `$ is kept constant and the weights are rescaled correspondingly. Furthermore, the firing probabilities are conserved under transformations that add the same value to all outgoing connections of one neuron. We could therefore keep the values of the weights in a bounded domain without changing the model dynamics.

Let us next demonstrate the learning capability and robustness of the model by simulating an XOR learning task. The network used has $`I=3`$ input sites $`x_0`$, $`x_1`$, and $`x_2`$, with the input site $`x_01`$ serving as bias. The hidden layer has $`J=3`$ neurons, the minimum number necessary to represent the XOR function in the present architecture. $`K=2`$ output neurons represent the two possible outcomes with only one of them active at a time. The initial values of the weights $`w`$ are uniformly chosen random numbers $`[0,1]`$, all counters $`c`$ are set to $`0`$, and $`\delta =1`$. The four patterns of the XOR function are presented with equal probability. Fig. 1 shows learning curves for memory sizes $`\mathrm{\Theta }=0,1,2`$ with $`\beta =10`$ and averaged over 10000 independent runs each.

The displayed error $`E`$ is the fraction of simulation runs that have produced an incorrect output at the considered time step. We find that learning takes place with $`\mathrm{\Theta }1`$ only, where the error quickly converges to zero, whereas with $`\mathrm{\Theta }=0`$ as in the model of Chialvo and Bak  no learning takes place at all. The error remains constant hardly below the “default” of $`0.5`$ (this holds for the whole simulation time of 100,000 trials, not shown here).

The obviously dramatic effect of the synaptic memory can be understood in the following way: Any synapse that is involved in failure—meaning that pre- and postsynaptic firings have occured prior to unsuccessful output of the network—is a candidate for decrement. In the case $`\mathrm{\Theta }=0`$ all such “failing” synapses are weakened, such that on repeated presentation of the same stimuli the activity is likely to be lead to a different output neuron. This is a simple and reasonable principle as long as our learning goal is the mapping of just one pattern of stimuli or a set of non-overlapping patterns. However, the task of learning a non-trival logical operation as the one we are facing here, requires a more elaborate mechanism: The immediate weakening of all synapses, that are involved in failure for a certain pattern, eventually destroys a useful structure for the successful mapping of other patterns. This is avoided by the synaptic memory considered here: Only if a synapse is repeatedly involved in failure, its efficacy is reduced.

The idea of averaging over errors and updating the weights on a slower time scale than sample presentation is well known from batch learning methods . In those methods, errors are determined over a whole sweep through the pattern set and subsequently weights are updated synchronously. However, those algorithms fail to explain learning in biological neural systems as they rely on biologically implausible mechanisms as, for example, back-propagating errors. In fact, what we wish to define here is a learning method based on purely local dynamics, where weight changes are based only on information that is locally available (the two adjacent neurons of a synapse) with nothing more than a single global reinforcement signal—exactly the information that is available to a biological synapse. A first step in this direction would be a trivial “localized” version of batch learning where weight changes are based on the global reinforcement signal, only. Indeed, this works for single layer networks, however, fails for learning XOR-type problems in multi-layer networks. Here, our work proposes a solution, using a synaptic error account combined with asynchronous updating of the synaptic weights. It can be viewed as a generalization of the Hebbian learning rule: While the Hebb rule alone is not able to make a network learn the XOR, the above extension does so. The resulting network is a self-contained dynamical system with local dynamical rules defined in a way that the overall network dynamics results in adaptive learning of general logical functions including the XOR problem. Besides learning XOR as shown here, the algorithm also proved to learn logical functions of higher dimensions and complexity.

The aspect of protecting synapses from too quick changes has further implications with regard to the network’s robustness against noise. Fig. 2 demonstrates the effect of the inverse noise level $`\beta `$ on the mean residual error after 90,000 trials.

For fixed memory length $`\mathrm{\Theta }`$ we find a sharp transition from a regime of non-learning, characterized by $`E=0.5`$, to a regime of effective learning with $`E0`$. We conclude that the network is able to learn just as long as the information gain provided by the feedback signal is larger than the information loss caused by the uncertainty of the stochastic neural dynamics. The effect of increasing the memory length $`\mathrm{\Theta }`$ is obvious: The critical point between the two regimes is shifted to lower values of $`\beta `$, i. e., higher noise. Synapses with larger memory can average out the uncertainty and therefore enable stochastically firing networks to adapt to their environment.

Now let us briefly discuss the biological motivations for the choice of mechanisms used in the model above. First, observations in experimental neurobiology show clear evidence that modulation of long-term potentiation (LTP) and depression (LTD) via external signals occurs (i.e., modulation of plasticity of weights). In one example from the hippocampus CA1 region, which is involved in learning and memory formation, modulation mediated by dopamine has been verified . In particular, when dopamine is applied during or shortly after LTD activity, one observes that LTD is suppressed (and LTP can appear instead). Learning activity can thereby receive feedback via dopamine which then modulates synaptic plasticity, in particular LTD. Indeed, hormone signals are widely known to interfere with learning and memory formation. For example adrenal hormones have been shown to enhance susceptibility for LTD , an effect which has even been found following behavioral stress in living animals . A broad class of other factors that modulate synaptic plasticity have been classified, sometimes summarized as “metaplasticity” . We believe that further research in this area will provide new insights in the computational mechanics of biological nervous systems.

Furthermore, progress has been made in exploring the mechanisms of retrograde feedback in LTP and LTD. Evidence accumulates in favor of some physiological mechanisms that feed back the postsynaptic activity to the presynaptic site. A possible mechanism recently proposed for LTD is the messenger nitric oxide evoking a specific presynaptic biochemical cascade which, eventually, interacts with the intracellular mechanisms for vesicle formation and loading . The subsequently reduced transmitter release establishes a long term depression of this synaptic pathway. An interesting observation is the long time scale of this process of the order of 15 minutes , especially when compared to that of neuronal firing packages. This opens up the possibility that considerable time averaging may occur in the course of inducing LTD. The effect of such a synaptic averaging on learning has been simulated above by an internal counter associated with each synaptic weight. Further experimental research on the timing of externally induced LTD and the lifetimes of the biochemical agents involved in the retrograde signaling cascade may show to what extent synaptic averaging in the induction of plasticity changes is established in nature.

To summarize, we studied a biologically motivated model for goal-directed learning in multilayer neural networks. In contrast to existing models, synaptic plasticity is based on a time-averaged individual failure rate of each synapse. Thereby, learning of general logical functions (including XOR) is possible on the basis of local synaptic plasticity alone, combined with homogeneous failure feedback. In particular, no error backpropagation is needed. The presented algorithm also works in the presence of noise, where internal errors are compensated for by the averaging of each synapse: only persistent failure is punished.