Alejandro Rodriguez-Garcia

Alejandro Rodriguez-Garcia, Anindya Ghosh, Jie Mei et al.

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.

Jie Mei, Alejandro Rodriguez-Garcia, Daigo Takeuchi et al.

Continuous, adaptive learning-the ability to adapt to the environment and improve performance-is a hallmark of both natural and artificial intelligence. Biological organisms excel in acquiring, transferring, and retaining knowledge while adapting to dynamic environments, making them a rich source of inspiration for artificial neural networks (ANNs). This study explores how neuromodulation, a fundamental feature of biological learning systems, can help address challenges such as catastrophic forgetting and enhance the robustness of ANNs in continuous learning scenarios. 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 the modulation of sensory and cognitive processes are more complex than expected, demonstrating a "many-to-one" neuromodulator-to-task mapping. To inspire the design of novel neuromodulation-aware learning rules, we highlight (i) how multi-neuromodulatory interactions enrich single-neuromodulator-driven learning, (ii) the impact of neuromodulators at multiple spatial and temporal scales, and correspondingly, (iii) strategies to integrate neuromodulated learning into or approximate it in ANNs. To illustrate these principles, we present a case study to demonstrate 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. By integrating multi-scale neuromodulation, we aim to bridge the gap between biological learning and artificial systems, paving the way for ANNs with greater flexibility, robustness, and adaptability.

Alejandro Rodriguez-Garcia, Anindya Ghosh, Srikanth Ramaswamy

Recent studies in continual learning have identified a transient drop in performance on mastered tasks when assimilating new ones, known as the stability gap. Such dynamics contradict the objectives of continual learning, revealing a lack of robustness in mitigating forgetting, and notably, persisting even under an ideal joint-loss regime. Examining this gap within this idealized joint training context is critical to isolate it from other sources of forgetting. We argue that it reflects an imbalance between rapid adaptation and robust retention at task boundaries, underscoring the need to investigate mechanisms that reconcile plasticity and stability within continual learning frameworks. Biological brains navigate a similar dilemma by operating concurrently on multiple timescales, leveraging neuromodulatory signals to modulate synaptic plasticity. However, artificial networks lack native multitimescale dynamics, and although optimizers like momentum-SGD and Adam introduce implicit timescale regularization, they still exhibit stability gaps. Inspired by locus coeruleus mediated noradrenergic bursts, which transiently enhance neuronal gain under uncertainty to facilitate sensory assimilation, we propose uncertainty-modulated gain dynamics - an adaptive mechanism that approximates a two-timescale optimizer and dynamically balances integration of knowledge with minimal interference on previously consolidated information. We evaluate our mechanism on domain-incremental and class-incremental variants of the MNIST and CIFAR benchmarks under joint training, demonstrating that uncertainty-modulated gain dynamics effectively attenuate the stability gap. Finally, our analysis elucidates how gain modulation replicates noradrenergic functions in cortical circuits, offering mechanistic insights into reducing stability gaps and enhance performance in continual learning tasks.

Alejandro Rodriguez-Garcia, Christopher J. Whyte, Brandon R. Munn et al.

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.