About

Azahara Oliva is an Assistant Professor in the Department of Neurobiology and Behavior at Cornell University. She grew up in a small village in Castilla La Mancha, Spain, and initially majored in Physics at the Complutense University of Madrid, where she worked on modeling brain signals exhibiting chaotic dynamics. Her interest in the brain led her to pursue a Master's in Biomedical Physics and Neuroscience, focusing on developing biologically informed models of neuronal activity to reproduce brain patterns observed in the hippocampus. For her PhD at the University of Szeged in Hungary, she implanted electrodes in the hippocampus and entorhinal regions of rats to record neural activity during behavioral assays, analyzing how brain patterns related to learning and memory are coordinated. Her postdoctoral work at Columbia University and NYU involved developing experimental methods to detect and manipulate memory processes online, supporting theories of memory from a systems neuroscience perspective. Her research primarily aims to understand how global brain states modulate local network activity during learning, memory, and sleep, using rodents in behavioral assays combined with advanced electrophysiological and computational techniques. She investigates the neural transfer functions between neuronal ensembles across brain structures during different states and behaviors, utilizing large-scale electrodes, optogenetics, fiber photometry, and data mining tools to analyze neural dynamics.

Research topics

• Psychology
• Neuroscience
• Biology
• Physics
• Computer Science
• Communication
• Cognitive science

Selected publications

• Dynamic shifts in brain criticality support cognitive processing

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-14

  articleOpen accessSenior authorCorresponding

  Abstract Systems operating near their critical point, or close to a transition between order and disorder, have computational advantages. In the case of neural networks, proximity to criticality is proposed to support optimal brain function. However, different cognitive processes rely on disparate computational demands. Using large-scale electrophysiological recordings in behaving rodents, we examined how critical dynamics in the hippocampus are regulated during learning and sleep-dependent memory consolidation. We found that operating near criticality enables learning by facilitating hippocampal coordination with input regions and maximizing flexibility of neural representations. In contrast, the hippocampal network shifts toward a more ordered, subcritical regime during sleep memory replay, and recovers its proximity to criticality through cholecystokinin interneurons-mediated inhibition. Overall, our findings provide a biophysical substrate for understanding how critical dynamics in neuronal networks can support a variety of brain functions. Importantly, our results suggest that optimal learning systems, whether biological or artificial, may require a dynamic regulation between flexible and rigid states, and can offer biophysical constraints to guide the design of Large Language Models (LLM) tuned to criticality.

  PublisherOA PDFDOI

• A hippocampal population code for rapid generalization

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-16 · 5 citations

  preprintOpen accessCorresponding

  Abstract Generalizing from experience and applying prior knowledge to new situations is essential for intelligent behavior. Traditional models attribute this generalization to gradual statistical learning in the neocortex. However, such a slow process cannot account for animals’ rapid generalization from limited experience. Here, we demonstrate that the hippocampus supports rapid generalization in mice by generating disentangled memory representations, where different aspects of experience are encoded independently. This code enabled the transfer of prior knowledge to solve new tasks. We identify specific circuit mechanisms underlying this rapid generalization. We show that the seemingly random changes in individual neuronal activity over time and across environments result from structured circuit-level processes, governed by the dynamics of local inhibition and cross-regional cell assemblies, respectively. Our findings provide computational and mechanistic insights into how the geometric structure and underlying circuit organization of hippocampal population dynamics facilitate both memory discrimination and generalization, enabling efficient and flexible learning.

  PublisherOA PDFDOI

• Top-down regulation of subcortical regions by hippocampal long-range inhibition

  Current Biology · 2025-11-19

  articleOpen access
  PublisherOA PDFDOI

• Large sharp-wave ripples promote hippocampo-cortical memory reactivation and consolidation

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-29 · 3 citations

  preprintOpen access

  During sleep, ensemble activity patterns encoding recent experiences are reactivated in the hippocampus and cortex. This reactivation is coordinated by hippocampal sharp-wave ripples (SWRs) and is believed to support the early stages of memory consolidation. However, only a minority of sleep SWRs are associated with memory reactivation in the hippocampus and its downstream areas. Whether that subset of SWRs have specific physiological characteristics and directly contribute to memory performance is not known. We identified a specific subset of large SWRs linked to memory reactivation in both the hippocampus and prefrontal cortex (PFC) of mice, and found that their occurrence selectively increased during sleep following new learning. Closed-loop optogenetic SWR boosting during sleep was sufficient to enhance ensemble memory reactivation in hippocampus and PFC. This manipulation also improved subsequent memory retrieval and hippocampal-PFC coordination during waking, causally linking both phenomena to SWR-associated ensemble reactivation during sleep.

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• Goal-directed hippocampal theta sweeps during memory-guided navigation

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-08-26 · 4 citations

  preprintOpen access

  During navigation, animals continually sample their surrounding space and plan routes to distant goals. The brain mechanisms underlying these behaviors and how they coordinate to support memory-guided navigation in open environments are not understood. Using large-scale recordings in rats, we found two distinct types of place cell sequences within theta cycles that encoded trajectories sweeping beyond the animal's location: stereotypic left-right alternating sweeps and learning-dependent goal-directed sweeps. Goal-directed sweeps predicted upcoming trajectories to remembered goal locations, were coordinated with prefrontal cortex activity and preferentially replayed during sharp-wave ripples. We further describe a circuit mechanism in which a subpopulation of CA1 cells encodes egocentric goal direction, combined with reduced feedback inhibition, to generate goal-directed theta sweeps. These results indicate a flexible mechanism to support different behavioral demands during navigation.

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• Large sharp-wave ripples promote hippocampo-cortical memory reactivation and consolidation during sleep

  Neuron · 2025-11-07 · 5 citations

  articleOpen access
  PublisherOA PDFDOI

• Sleep microstructure organizes memory replay

  Nature · 2025-01-01 · 42 citations

  articleOpen accessSenior author

  Recently acquired memories are reactivated in the hippocampus during sleep, an initial step for their consolidation1–3. This process is concomitant with the hippocampal reactivation of previous memories4–6, posing the problem of how to prevent interference between older and recent, initially labile, memory traces. Theoretical work has suggested that consolidating multiple memories while minimizing interference can be achieved by randomly interleaving their reactivation7–10. An alternative is that a temporal microstructure of sleep can promote the reactivation of different types of memories during specific substates. Here, to test these two hypotheses, we developed a method to simultaneously record large hippocampal ensembles and monitor sleep dynamics through pupillometry in naturally sleeping mice. Oscillatory pupil fluctuations revealed a previously unknown microstructure of non-REM sleep-associated memory processes. We found that memory replay of recent experiences dominated in sharp-wave ripples during contracted pupil substates of non-REM sleep, whereas replay of previous memories preferentially occurred during dilated pupil substates. Selective closed-loop disruption of sharp-wave ripples during contracted pupil non-REM sleep impaired the recall of recent memories, whereas the same manipulation during dilated pupil substates had no behavioural effect. Stronger extrinsic excitatory inputs characterized the contracted pupil substate, whereas higher recruitment of local inhibition was prominent during dilated pupil substates. Thus, the microstructure of non-REM sleep organizes memory replay, with previous versus new memories being temporally segregated in different substates and supported by local and input-driven mechanisms, respectively. Our results suggest that the brain can multiplex distinct cognitive processes during sleep to facilitate continuous learning without interference. The temporal microstructure of the brain can multiplex distinct cognitive processes during sleep to support continuous learning.

  PublisherDOI

• A hippocampal circuit mechanism to balance memory reactivation during sleep

  Science · 2024-08-15 · 33 citations

  articleOpen accessSenior authorCorresponding

  Memory consolidation involves the synchronous reactivation of hippocampal cells active during recent experience in sleep sharp-wave ripples (SWRs). How this increase in firing rates and synchrony after learning is counterbalanced to preserve network stability is not understood. We discovered a network event generated by an intrahippocampal circuit formed by a subset of CA2 pyramidal cells to cholecystokinin-expressing (CCK+) basket cells, which fire a barrage of action potentials ("BARR") during non-rapid eye movement sleep. CA1 neurons and assemblies that increased their activity during learning were reactivated during SWRs but inhibited during BARRs. The initial increase in reactivation during SWRs returned to baseline through sleep. This trend was abolished by silencing CCK+ basket cells during BARRs, resulting in higher synchrony of CA1 assemblies and impaired memory consolidation.

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• Impaired mechanisms of context encoding in APP/PS1 mice are rescued by increasing cerebral blood flow

  Alzheimer s & Dementia · 2024-12-01

  articleOpen access

  BACKGROUND: Spatial disorientation is an early symptom of Alzheimer's disease (AD). The hippocampus creates a cognitive map, wherein cells form firing fields in specific locations within an environment, termed place cells. Critically, place cells remain stable across visits to an environment, but change their firing rate or field location in a different environment. In rodent models of AD-like pathology, place cells exhibit broadened tuning and altered responses to environmental changes. Additionally, events known as sharp wave ripples (SWRs), coordinate the firing of hippocampal neurons, including place cells, and are disrupted in mouse models of AD. Our lab found that increasing cerebral blood flow (CBF) with anti-Ly6G antibody treatment improved performance on spatial memory tasks. Here, we investigate the effect of increased CBF on neural mechanisms associated with cognitive map stability across contexts. METHOD: We investigated the association between CBF and cognitive map stability in 7-9-month-old APP/PS1 mice and wild-type controls by recording neural activity in hippocampus area CA1 using 64-channel silicon probes. Mice were recorded as they explored open field arenas with differing environmental contexts, A and B. Place cells were identified as neurons with significant spatial information in their firing rate maps. Local field potential recordings from pyramidal and stratum radiatum layers of CA1 were used to detect awake-SWRs (aSWRs). RESULT: Place cells from APP/PS1 mice did not exhibit higher place field correlations within contexts (AA' or BB'), as compared to between (AB) contexts, suggesting these different contexts are not differentially encoded (Figure 1). In contrast, wild-type control mice showed higher within context correlation (Figure 1). APP/PS1 mice also had a reduced rate and duration of aSWR compared to controls (Figure 2). Following treatment with anti-Ly6G antibodies, both context discrimination by place cells and duration of aSWR increased in APP/PS1 mice (Figure 2). CONCLUSION: These results highlight the association between place cell stability and subsequent aSWR dynamics as a potential mechanism contributing to an impaired cognitive map in AD. Importantly, the rescue of behavioral features and aSWR physiological properties following anti-Ly6G antibody treatment suggests that increasing CBF may be a candidate therapy to mitigate spatial memory impairments in AD.

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• Rescue of impaired hippocampal consolidation in the APP/PS1 mouse model of Alzheimer’s disease after increasing cerebral blood flow

  Alzheimer s & Dementia · 2024-12-01

  articleOpen access

  BACKGROUND: Alzheimer's disease (AD) manifests with early spatial memory impairment and is linked to the degeneration of hippocampal circuits. Hippocampal sharp wave ripples (SWRs) are high-frequency population-burst events that coordinate the reactivation of neural assemblies (groups of neurons that become correlated in their firing patterns during learning) in post-learning sleep, which is the neural basis of memory consolidation. SWRs are reduced in the APP/PS1 mouse model of AD-like pathology. Previously, we showed that cerebral blood flow (CBF) decreases and memory deficits were rescued following treatment with anti-Ly6G antibodies. Here, we examine the potential normalization of hippocampal circuit activity with CBF increase. METHOD: Male, 7-14-month-old APP/PS1 mice and wild-type controls were implanted with 64-channel silicon probes in hippocampal area CA1. Neural activity was recorded during sleep before and after the exploration of an open field. Putative cell types were identified using feature-based classification, and neural assemblies were detected using independent component analysis. RESULT: APP/PS1 mice had reduced magnitude and duration of assembly reactivation in post-task sleep SWRs. After treatment with anti-Ly6G antibodies, which increase CBF and improve memory performance, we found increased reactivation of these assemblies in post-task sleep SWRs, relative to no-treatment controls (Figure 1). CONCLUSION: We found that increasing CBF normalizes neural mechanisms of memory consolidation that are altered in AD mouse models, supporting the development of treatment approaches to increase CBF in AD.

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Frequent coauthors

• Antonio Fernández‐Ruiz

  Cornell University

  25 shared

• György Buzsáki

  NYU Langone Health

  15 shared

• Eliezyer Fermino de Oliveira

  Albert Einstein College of Medicine

  11 shared

• Antal Berényi

  11 shared

• Gergő Attila Nagy

  HUN-REN Institute of Experimental Medicine

  10 shared

• Florbela Rocha-Almeida

  Universidad Pablo de Olavide

  6 shared

• Gonzalo Martín-Vázquez

  University of Oulu

  4 shared

• Can Liu

  Ningxia Medical University

  3 shared

Education

• PhD, Physiology

  Szegedi Tudományegyetem

• Physics, Physics

  Universidad Complutense de Madrid

Awards & honors

• Suffrage Science Award