arXiv subjects

Alejandro Rodriguez-Garcia

Publications and source records attributed to Alejandro Rodriguez-Garcia.

4 recordsLinked to original sources

arXiv2025

Dynamic gain neuromodulation attenuates the stability gap under joint training

Recent work in continual learning has highlighted the stability gap -- a temporary performance drop on previously learned tasks when new ones are introduced. This phenomenon reflects a mismatch between rapid adaptation and strong retention at task boundaries, underscoring the need for optimization mechanisms that balance plasticity and stability over abrupt distribution changes. While optimizers such as momentum-SGD and Adam introduce implicit multi-timescale behavior, they still exhibit pronounced stability gaps. Importantly, these gaps persist even under ideal joint training, making it crucial to study them in this setting to isolate their causes from other sources of forgetting. Motivated by how noradrenergic (neuromodulatory) bursts transiently increase neuronal gain under uncertainty, we introduce a dynamic gain scaling mechanism as a two-timescale optimization technique that balances adaptation and retention by transiently increasing the effective update magnitude while dynamically reparameterizing the weights governing the forward pass, thereby empirically mitigating transition-induced curvature amplification. Across domain- and class-incremental MNIST, CIFAR, and mini-ImageNet benchmarks under task-agnostic joint training, dynamic gain scaling effectively attenuates stability gaps while maintaining competitive accuracy, improving robustness at task transitions.

cs.LG↗

arXiv2025

The role of gain neuromodulation in layer-5 pyramidal neurons

Biological and artificial learning systems alike confront the plasticity-stability dilemma. In the brain, neuromodulators such as acetylcholine and noradrenaline relieve this tension by tuning neuronal gain and inhibitory gating, balancing segregation and integration of circuits. Fed by dense cholinergic and noradrenergic projections from the ascending arousal system, layer-5 pyramidal neurons in the cerebral cortex offer a relevant substrate for understanding these dynamics. When distal dendritic signals coincide with back-propagating action potentials, calcium plateaus turn a single somatic spike into a high-gain burst, and interneuron inhibition sculpts the output. These properties make layer-5 cells gain-tunable amplifiers that translate neuromodulatory cues into flexible cortical activity. To capture this mechanism we developed a two-compartment Izhikevich model for pyramidal neurons and single-compartment somatostatin (SOM) and parvalbumin (PV) interneurons, linked by Gaussian connectivity and spike-timing-dependent plasticity (STDP). The soma and apical dendrite are so coupled that somatic spikes back-propagate, while dendritic plateaus can switch the soma from regular firing to bursting by shifting reset and adaptation variables. We show that stronger dendritic drive or tighter coupling raise gain by increasing the likelihood of calcium-triggered somatic bursts. In contrast, dendritic-targeted inhibition suppresses gain, while somatic-targeted inhibition raises the firing threshold of neighboring neurons, thus gating neurons output. Notably, bursting accelerates STDP, supporting rapid synaptic reconfiguration and flexibility. This suggests that brief gain pulses driven by neuromodulators could serve as an adaptive two-timescale optimization mechanism, effectively modulating the synaptic weight updates.

q-bio.NC↗

arXiv2025

Improving the adaptive and continuous learning capabilities of artificial neural networks: Lessons from multi-neuromodulatory dynamics

Continuous, adaptive learning, the ability to adapt to the environment and keep improving performance, is a hallmark of natural intelligence. Biological organisms excel in acquiring, transferring, and retaining knowledge while adapting to volatile environments, making them a source of inspiration for artificial neural networks (ANNs). This study explores how neuromodulation, a building block of learning in biological systems, can help address catastrophic forgetting and enhance the robustness of ANNs in continual learning. Driven by neuromodulators including dopamine (DA), acetylcholine (ACh), serotonin (5-HT) and noradrenaline (NA), neuromodulatory processes in the brain operate at multiple scales, facilitating dynamic responses to environmental changes through mechanisms ranging from local synaptic plasticity to global network-wide adaptability. Importantly, the relationship between neuromodulators and their interplay in modulating sensory and cognitive processes is more complex than previously expected, demonstrating a "many-to-one" neuromodulator-to-task mapping. To inspire neuromodulation-aware learning rules, we highlight (i) how multi-neuromodulatory interactions enrich single-neuromodulator-driven learning, (ii) the impact of neuromodulators across multiple spatio-temporal scales, and correspondingly, (iii) strategies for approximating and integrating neuromodulated learning processes in ANNs. To illustrate these principles, we present a conceptual study to showcase how neuromodulation-inspired mechanisms, such as DA-driven reward processing and NA-based cognitive flexibility, can enhance ANN performance in a Go/No-Go task. Though multi-scale neuromodulation, we aim to bridge the gap between biological and artificial learning, paving the way for ANNs with greater flexibility, robustness, and adaptability.

q-bio.NC↗

arXiv2024

Augmenting learning in neuro-embodied systems through neurobiological first principles

Recent progress in artificial intelligence (AI) has been driven by insights from physics and neuroscience, particularly through the development of artificial neural networks (ANNs) capable of complex cognitive tasks such as vision and language processing. Despite these advances, they struggle with continual learning, adaptable knowledge transfer, robustness, and resource efficiency -- capabilities that biological systems handle seamlessly. Specifically, neuromorphic systems and artificial neural networks often overlook two key biophysical properties of neural circuits: neuronal diversity and cell-specific neuromodulation. These mechanisms, essential for regulating dynamic learning across brain scales, allow neuromodulators to introduce degeneracy in biological neural networks, ensuring stability and adaptability under changing conditions. In this article, we summarize recent bioinspired models, learning rules, and architectures, and propose a framework for augmenting ANNs, which has the potential to bridge the gap between neuroscience and AI through neurobiological first principles. Our proposed dual-framework approach leverages spiking neural networks to emulate diverse spiking behaviors and dendritic compartmental dynamics, thereby simulating the morphological and functional diversity of neuronal computations. Finally, we outline how integrating these biophysical principles into task-driven spiking neural networks and neuromorphic systems provides scalable solutions for continual learning, adaptability, robustness, and resource-efficiency. Additionally, this approach will not only provide insights into how emergent behaviors arise in neural networks but also catalyze the development of more efficient, reliable, and intelligent neuromorphic systems and robotic agents.

q-bio.NC↗