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Claudia Clopath

Publications and source records attributed to Claudia Clopath.

26 records · Page 2Linked to original sources

Chaos in Homeostatically Regulated Neural Systems

Low-dimensional yet rich dynamics often emerge in the brain. Examples include oscillations and chaotic dynamics during sleep, epilepsy, and voluntary movement. However, a general mechanism for the emergence of low dimensional dynamics remains elusive. Here, we consider Wilson-Cowan networks and demonstrate through numerical and analytical work that a type of homeostatic regulation of the network firing rates can paradoxically lead to a rich dynamical repertoire. The dynamics include mixed-mode oscillations, mixed-mode chaos, and chaotic synchronization. This is true for single recurrently coupled node, pairs of reciprocally coupled nodes without self-coupling, and networks coupled through experimentally determined weights derived from functional magnetic resonance imaging data. In all cases, the stability of the homeostatic set point is analytically determined or approximated. The dynamics at the network level are directly determined by the behavior of a single node system through synchronization in both oscillatory and non-oscillatory states. Our results demonstrate that rich dynamics can be preserved under homeostatic regulation or even be caused by homeostatic regulation.

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Supervised Learning in Spiking Neural Networks with FORCE Training

Populations of neurons display an extraordinary diversity in the behaviors they affect and display. Machine learning techniques have recently emerged that allow us to create networks of model neurons that display behaviours of similar complexity. Here, we demonstrate the direct applicability of one such technique, the FORCE method, to spiking neural networks. We train these networks to mimic dynamical systems, classify inputs, and store discrete sequences that correspond to the notes of a song. Finally, we use FORCE training to create two biologically motivated model circuits. One is inspired by the zebra-finch and successfully reproduces songbird singing. The second network is motivated by the hippocampus and is trained to store and replay a movie scene. FORCE trained networks reproduce behaviors comparable in complexity to their inspired circuits and yield information not easily obtainable with other techniques such as behavioral responses to pharmacological manipulations and spike timing statistics.

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Gap junction plasticity can lead to spindle oscillations

Patterns of waxing and waning oscillations, called spindles, are observed in multiple brain regions during sleep. Spindle are thought to be involved in memory consolidation. The origin of spindle oscillations is ongoing work but experimental results point towards the thalamic reticular nucleus (TRN) as a likely candidate. The TRN is rich in electrical synapses, also called gap junctions, which promote synchrony in neural activity. Moreover, gap junctions undergo activity-dependent long-term plasticity. We hypothesized that gap junction plasticity can modulate spindle oscillations. We developed a computational model of gap junction plasticity in recurrent networks of TRN and thalamocortical neurons (TC). We showed that gap junction coupling can modulate the TRN-TC network synchrony and that gap junction plasticity is a plausible mechanism for the generation of sleep-spindles. Finally, our results are robust to the simulation of pharmacological manipulation of spindles, such as the administration of propofol, an anesthetics known to generate spindles in humans.

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Acetylcholine-modulated plasticity in reward-driven navigation: a computational study

Neuromodulation plays a fundamental role in the acquisition of new behaviours. Our experimental findings show that, whereas acetylcholine biases hippocampal synaptic plasticity towards depression, the subsequent application of dopamine can retroactively convert depression into potentiation. We previously demonstrated that incorporating this sequentially neuromodulated Spike-Timing-Dependent Plasticity (STDP) rule in a network model of navigation yields effective learning of changing reward locations. Here, we further characterize the effects of cholinergic depression on behaviour. We find that acetylcholine, by allowing learning from negative outcomes, influences exploration in a non-trivial manner that highly depends on the specifics of the model, the environment and the task. Interestingly, sequentially neuromodulated STDP also yields flexible learning, surpassing the performance of other reward-modulated plasticity rules.

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Gap junction plasticity as a mechanism to regulate network-wide oscillations

Cortical oscillations are thought to be involved in many cognitive functions and processes. Several mechanisms have been proposed to regulate oscillations. One prominent but understudied mechanism is gap-junctional coupling. Gap junctions are ubiquitous in cortex between GABAergic interneurons. Moreover, recent experiments indicate their strength can be modified in an activity-dependent manner, similar to chemical synapses. We hypothesized that activity-dependent gap junction plasticity acts as a mechanism to regulate oscillations in the cortex. We developed a computational model of gap junction plasticity in a recurrent cortical network. We showed that gap junction plasticity can serve as a homeostatic mechanism for oscillations by maintaining a tight balance between two network states: asynchronous irregular activity and synchronized oscillations. This homeostatic mechanism allows for robust communication between neuronal assemblies through two different mechanisms: transient oscillations and frequency modulation. This implies a direct functional role for gap junction plasticity in information transmission in cortex.

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Overcoming catastrophic forgetting in neural networks

The ability to learn tasks in a sequential fashion is crucial to the development of artificial intelligence. Neural networks are not, in general, capable of this and it has been widely thought that catastrophic forgetting is an inevitable feature of connectionist models. We show that it is possible to overcome this limitation and train networks that can maintain expertise on tasks which they have not experienced for a long time. Our approach remembers old tasks by selectively slowing down learning on the weights important for those tasks. We demonstrate our approach is scalable and effective by solving a set of classification tasks based on the MNIST hand written digit dataset and by learning several Atari 2600 games sequentially.

cs.LG↗

Balanced activation in a simple embodied neural simulation

In recent years, there have been many computational simulations of spontaneous neural dynamics. Here, we explore a model of spontaneous neural dynamics and allow it to control a virtual agent moving in a simple environment. This setup generates interesting brain-environment feedback interactions that rapidly destabilize neural and behavioral dynamics and suggest the need for homeostatic mechanisms. We investigate roles for both local homeostatic plasticity (local inhibition adjusting over time to balance excitatory input) as well as macroscopic task negative activity (that compensates for task positive, sensory input) in regulating both neural activity and resulting behavior (trajectories through the environment). Our results suggest complementary functional roles for both local homeostatic plasticity and balanced activity across brain regions in maintaining neural and behavioral dynamics. These findings suggest important functional roles for homeostatic systems in maintaining neural and behavioral dynamics and suggest a novel functional role for frequently reported macroscopic task-negative patterns of activity (e.g., the default mode network).

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Local inhibitory plasticity tunes global brain dynamics and allows the emergence of functional brain networks

Rich, spontaneous brain activity has been observed across a range of different temporal and spatial scales. These dynamics are thought to be important t for efficient neural functioning. Experimental evidence suggests that these neural dynamics are maintained across a variety of different cognitive states, in response to alterations of the environment and to changes in brain configuration (e.g., across individuals, development and in many neurological disorders). This suggests that the brain has evolved mechanisms to stabilize dynamics and maintain them across a range of situations. Here, we employ a local homeostatic inhibitory plasticity mechanism, balancing inhibitory and excitatory activity in a model of macroscopic brain activity based on white-matter structural connectivity. We demonstrate that the addition of homeostatic plasticity regulates network activity and allows for the emergence of rich, spontaneous dynamics across a range of brain configurations. Furthermore, the presence of homeostatic plasticity maximises the overlap between empirical and simulated patterns of functional connectivity. Therefore, this work presents a simple, local, biologically plausible inhibitory mechanism that allows stable dynamics to emerge in the brain and which facilitates the formation of functional connectivity networks.

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