The Role of Constraints in Hebbian Learning

Models of unsupervised, correlation-based (Hebbian) synaptic plasticity are typically unstable: either all synapses grow until each reaches the maximum allowed strength, or all synapses decay to zero strength. A common method of avoiding these outcomes is to use a constraint that conserves or limits the total synaptic strength over a cell. We study the dynamic effects of such constraints. Two methods of enforcing a constraint are distinguished, multiplicative and subtractive. For otherwise linear learning rules, multiplicative enforcement of a constraint results in dynamics that converge to the principal eigenvector of the operator determining unconstrained synaptic development. Subtractive enforcement, in contrast, typically leads to a final state in which almost all synaptic strengths reach either the maximum or minimum allowed value. This final state is often dominated by weight configurations other than the principal eigenvector of the unconstrained operator. Multiplicative enforcement yields a “graded” receptive field in which most mutually correlated inputs are represented, whereas subtractive enforcement yields a receptive field that is “sharpened” to a subset of maximally correlated inputs. If two equivalent input populations (e.g., two eyes) innervate a common target, multiplicative enforcement prevents their segregation (ocular dominance segregation) when the two populations are weakly correlated; whereas subtractive enforcement allows segregation under these circumstances. These results may be used to understand constraints both over output cells and over input cells. A variety of rules that can implement constrained dynamics are discussed

Slowness: An Objective for Spike-Timing-Dependent Plasticity?

Slow Feature Analysis (SFA) is an efficient algorithm for learning input-output functions that extract the most slowly varying features from a quickly varying signal. It has been successfully applied to the unsupervised learning of translation-, rotation-, and other invariances in a model of the visual system, to the learning of complex cell receptive fields, and, combined with a sparseness objective, to the self-organized formation of place cells in a model of the hippocampus. In order to arrive at a biologically more plausible implementation of this learning rule, we consider analytically how SFA could be realized in simple linear continuous and spiking model neurons. It turns out that for the continuous model neuron SFA can be implemented by means of a modified version of standard Hebbian learning. In this framework we provide a connection to the trace learning rule for invariance learning. We then show that for Poisson neurons spike-timing-dependent plasticity (STDP) with a specific learning window can learn the same weight distribution as SFA. Surprisingly, we find that the appropriate learning rule reproduces the typical STDP learning window. The shape as well as the timescale are in good agreement with what has been measured experimentally. This offers a completely novel interpretation for the functional role of spike-timing-dependent plasticity in physiological neurons

Stochastic Synapses Enable Efficient Brain-Inspired Learning Machines

Recent studies have shown that synaptic unreliability is a robust and sufficient mechanism for inducing the stochasticity observed in cortex. Here, we introduce Synaptic Sampling Machines, a class of neural network models that uses synaptic stochasticity as a means to Monte Carlo sampling and unsupervised learning. Similar to the original formulation of Boltzmann machines, these models can be viewed as a stochastic counterpart of Hopfield networks, but where stochasticity is induced by a random mask over the connections. Synaptic stochasticity plays the dual role of an efficient mechanism for sampling, and a regularizer during learning akin to DropConnect. A local synaptic plasticity rule implementing an event-driven form of contrastive divergence enables the learning of generative models in an on-line fashion. Synaptic sampling machines perform equally well using discrete-timed artificial units (as in Hopfield networks) or continuous-timed leaky integrate & fire neurons. The learned representations are remarkably sparse and robust to reductions in bit precision and synapse pruning: removal of more than 75% of the weakest connections followed by cursory re-learning causes a negligible performance loss on benchmark classification tasks. The spiking neuron-based synaptic sampling machines outperform existing spike-based unsupervised learners, while potentially offering substantial advantages in terms of power and complexity, and are thus promising models for on-line learning in brain-inspired hardware

Molecular Players in Preserving Excitatory-Inhibitory Balance in the Brain

Information processing in the brain relies on a functional balance between excitation and inhibition, the disruption of which leads to network destabilization and many neurodevelopmental disorders, such as autism spectrum disorders. One of the homeostatic mechanisms that maintains the excitatory and inhibitory balance is called synaptic scaling: Neurons dynamically modulate postsynaptic receptor abundance through activity-dependent gene transcription and protein synthesis. In the first part of my thesis work, I discuss our findings that a chromatin reader protein L3mbtl1 is involved in synaptic scaling. We observed that knockout and knockdown of L3mbtl1 cause a lack of synaptic downscaling of glutamate receptors in hippocampal primary neurons and organotypic slice cultures. Genome-wide mapping of L3mbtl1 protein occupancies on chromatin identified Ctnnb1 and Gabra2 as downstream target genes of L3mbtl1-mediated transcriptional regulation. Importantly, partial knockdown of Ctnnb1 by itself prevents synaptic downscaling. Another aspect of maintaining E/I balance centers on GABAergic inhibitory neurons. In the next part of my thesis work, we address the role of the scaffold protein Shank1 in excitatory synapses onto inhibitory interneurons. We showed that parvalbumin-expressing interneurons lacking Shank1 display reduced excitatory synaptic inputs and decreased levels of inhibitory outputs to pyramidal neurons. As a consequence, pyramidal neurons in Shank1 mutant mice exhibit increased E/I ratio. This is accompanied by a reduced expression of an inhibitory synapse scaffolding protein gephyrin. These results provide novel insights into the roles of chromatin reader molecules and synaptic scaffold molecules in synaptic functions and neuronal homeostasis

Towards a Brain-inspired Information Processing System: Modelling and Analysis of Synaptic Dynamics: Towards a Brain-inspired InformationProcessing System: Modelling and Analysis ofSynaptic Dynamics

Biological neural systems (BNS) in general and the central nervous system (CNS) specifically exhibit a strikingly efficient computational power along with an extreme flexible and adaptive basis for acquiring and integrating new knowledge. Acquiring more insights into the actual mechanisms of information processing within the BNS and their computational capabilities is a core objective of modern computer science, computational sciences and neuroscience. Among the main reasons of this tendency to understand the brain is to help in improving the quality of life of people suffer from loss (either partial or complete) of brain or spinal cord functions. Brain-computer-interfaces (BCI), neural prostheses and other similar approaches are potential solutions either to help these patients through therapy or to push the progress in rehabilitation. There is however a significant lack of knowledge regarding the basic information processing within the CNS. Without a better understanding of the fundamental operations or sequences leading to cognitive abilities, applications like BCI or neural prostheses will keep struggling to find a proper and systematic way to help patients in this regard. In order to have more insights into these basic information processing methods, this thesis presents an approach that makes a formal distinction between the essence of being intelligent (as for the brain) and the classical class of artificial intelligence, e.g. with expert systems. This approach investigates the underlying mechanisms allowing the CNS to be capable of performing a massive amount of computational tasks with a sustainable efficiency and flexibility. This is the essence of being intelligent, i.e. being able to learn, adapt and to invent. The approach used in the thesis at hands is based on the hypothesis that the brain or specifically a biological neural circuitry in the CNS is a dynamic system (network) that features emergent capabilities. These capabilities can be imported into spiking neural networks (SNN) by emulating the dynamic neural system. Emulating the dynamic system requires simulating both the inner workings of the system and the framework of performing the information processing tasks. Thus, this work comprises two main parts. The first part is concerned with introducing a proper and a novel dynamic synaptic model as a vital constitute of the inner workings of the dynamic neural system. This model represents a balanced integration between the needed biophysical details and being computationally inexpensive. Being a biophysical model is important to allow for the abilities of the target dynamic system to be inherited, and being simple is needed to allow for further implementation in large scale simulations and for hardware implementation in the future. Besides, the energy related aspects of synaptic dynamics are studied and linked to the behaviour of the networks seeking for stable states of activities. The second part of the thesis is consequently concerned with importing the processing framework of the dynamic system into the environment of SNN. This part of the study investigates the well established concept of binding by synchrony to solve the information binding problem and to proposes the concept of synchrony states within SNN. The concepts of computing with states are extended to investigate a computational model that is based on the finite-state machines and reservoir computing. Biological plausible validations of the introduced model and frameworks are performed. Results and discussions of these validations indicate that this study presents a significant advance on the way of empowering the knowledge about the mechanisms underpinning the computational power of CNS. Furthermore it shows a roadmap on how to adopt the biological computational capabilities in computation science in general and in biologically-inspired spiking neural networks in specific. Large scale simulations and the development of neuromorphic hardware are work-in-progress and future work. Among the applications of the introduced work are neural prostheses and bionic automation systems

On the Role of Sensory Cancellation and Corollary Discharge in Neural Coding and Behavior

Studies of cerebellum-like circuits in fish have demonstrated that synaptic plasticity shapes the motor corollary discharge responses of granule cells into highly-specific predictions of self- generated sensory input. However, the functional significance of such predictions, known as negative images, has not been directly tested. Here we provide evidence for improvements in neural coding and behavioral detection of prey-like stimuli due to negative images. In addition, we find that manipulating synaptic plasticity leads to specific changes in circuit output that disrupt neural coding and detection of prey-like stimuli. These results link synaptic plasticity, neural coding, and behavior and also provide a circuit-level account of how combining external sensory input with internally-generated predictions enhances sensory processing. In addition, the mammalian dorsal cochlear nucleus (DCN) integrates auditory nerve input with a diverse array of sensory and motor signals processed within circuity similar to the cerebellum. Yet how the DCN contributes to early auditory processing has been a longstanding puzzle. Using electrophysiological recordings in mice during licking behavior we show that DCN neurons are largely unaffected by self-generated sounds while remaining sensitive to external acoustic stimuli. Recordings in deafened mice, together with neural activity manipulations, indicate that self-generated sounds are cancelled by non-auditory signals conveyed by mossy fibers. In addition, DCN neurons exhibit gradual reductions in their responses to acoustic stimuli that are temporally correlated with licking. Together, these findings suggest that DCN may act as an adaptive filter for cancelling self-generated sounds. Adaptive filtering has been established previously for cerebellum-like sensory structures in fish suggesting a conserved function for such structures across vertebrates