Biology subjects

Errington, S. P.

Publications and source records attributed to Errington, S. P..

9 recordsLinked to original sources

bioRxiv2026

Ordinal position in auditory sequences is encoded in population dynamics in macaque frontal cortex

The ability to extract structure from sensory sequences requires tracking not only stimulus identity but also ordinal position within a sequence. How and where ordinal information is represented in the primate brain remains unclear. Here, we recorded activity in populations of single neurons simultaneously from auditory cortex and ventrolateral prefrontal cortex in macaques passively listening to structured auditory sequences. Population-level analyses revealed that frontal cortex activity evolved progressively across the sequence, occupying distinct regions of neural state space for successive ordinal positions. In contrast, auditory cortex population activity reset with each element, producing stereotyped, stimulus-locked trajectories. Consistent with this dissociation, frontal cortex populations robustly decoded ordinal position independently of stimulus identity, whereas auditory cortex showed weak positional decoding despite strong identity representations. Frontal neurons further exhibited longer intrinsic timescales and reduced synchronization to element presentation, supporting integration of information across multiple elements. Together, these findings identify frontal activity as a key substrate for ordinal position encoding during auditory sequence processing, while auditory cortex primarily supports element-specific sensory representations.

neuroscience↗

bioRxiv2026

A prefrontal cortex-hypothalamus circuit for heart rate control in non-human primates

Humans exhibit changes in heart rate during cognitive and emotional events, and dysregulation of this brain-heart coupling is a hallmark of many psychiatric disorders. Yet, how circuits that regulate cognition exert direct control over heart physiology remains poorly understood, particularly in primates. Here, we identify a prefrontal-hypothalamic circuit that exerts powerful, bidirectional control over heart rate in monkeys. We show that electrical stimulation of a small ventral subregion within the ventrolateral prefrontal cortex (area 47/12; a12) evokes rapid and robust decreases in heart rate and increases heart rate variability, whereas neighboring prefrontal regions produce weaker or no effects. And a12 neurons are coupled to heart rate on a moment-by-moment basis. Anatomical tracing data reveal projections from a12 to a circumscribed region of lateral hypothalamus (LHA), and stimulation of this LHA target recapitulates the cardiac effects of prefrontal activation. Consistent with a prefrontal-to-hypothalamus system for heart rate control, stimulation of LHA produces faster, stronger, state-independent heart effects, whereas stimulation of a12 produces effects that are sensitive to internal states. Oppositely to its activation, chemogenetic inactivation of a12 or its projections to LHA increases heart rate, demonstrating that this pathway can provide tonic inhibitory control over cardiac function. To make steps towards a more cell-type-specific and minimally invasive causal control of this circuit, we developed a primate sonogenetic approach based on ultrasound activation of CaMKII+ neurons virally transduced with TRPV1. Sonogenetic stimulation of a12 produced increases in heart rate variability, and these effects were attenuated by inactivation of LHA. Finally, we found that sonogenetic and chemogenetic perturbation of the same prefrontal region during a value-based decision-making task bidirectionally alters risky decision making. Together, our work identifies how a12 regulates heart rate and cognition, revealing a mechanistic substrate for brain-body interactions and a potential therapeutic target for disorders of cognitive-autonomic dysregulation.

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bioRxiv2025

A preparatory cranial potential for saccadic eye movements in macaque monkeys

Response preparation is accomplished by gradual accumulation in neural activity until a threshold is reached. In humans, such a preparatory signal, referred to as the lateralized readiness potential, can be observed in the EEG over sensorimotor cortical areas before execution of a voluntary movement. Although well-described for manual movements, less is known about preparatory EEG potentials for saccadic eye movements in humans and nonhuman primates. Hence, we describe a lateralized readiness potential over the frontolateral cortex in macaque monkeys. Homologous to humans, we observed lateralized electrical potentials ramping before the execution of both rewarded and non-rewarded contralateral saccades. This potential parallels the neural spiking of saccadic movement neurons in the frontal eye field, suggesting that it may offer a non-invasive correlate of intracortical spiking activity. However, unlike neural spiking in the frontal eye field, polarization in frontolateral channels did not distinguish between saccade generation and inhibition. These findings provide new insights into non-invasive electrophysiological signatures of saccadic preparation in nonhuman primates, highlighting the potential of EEG measures to bridge invasive neural recordings and non-invasive studies of eye movement control in humans.

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bioRxiv2024

Conflict neurons in cingulate cortex of macaques

Conflict--the magnitude of co-activation of mutually incompatible response processes--was proposed to explain how cognitive control is invoked (Botvinick et al. 2001) and continues to engage debate (Becker et al. 2024). Original observations consistent with this construct emphasized the primary contribution of cingulate cortex (CC) based on human functional imaging (Botvinick et al., 1999; Carter et al., 2000) and electroencephalogram (Yeung, Botvinick, & Cohen, 2004). In countermanding tasks conflict arises through co-activation of competing GO and STOP processes (Boucher et al. 2007; Schall & Boucher 2007; Sajad et al. 2022). Single neuron activity representing conflict has been described in the supplementary motor cortex of human epilepsy patients (Fu et al., 2019; Sheth et al., 2012) and of macaque monkeys (Sajad, Errington, & Schall, 2022; Stuphorn, Taylor, & Schall, 2000) and in human cingulate cortex (Fu et al., 2019; Sheth et al., 2012) but not in monkey cingulate cortex (Ebitz & Platt, 2015; Ito, Stuphorn, Brown, & Schall, 2003; Nakamura, Roesch, & Olson, 2005). This lack of homology generated debate about the utility of macaques for investigation of cognitive control (Cole et al. 2009; Schall & Emeric 2010). With higher-resolution, less-biased samples, we re-examined the presence of a conflict signal in cingulate cortex of monkeys. Neurons modulating specifically when response conflict was maximal were found in cingulate cortex-- more commonly in the dorsal than the ventral bank. However, such neurons were much more common in supplementary motor cortex. These data confirm the presence of a conflict signal in medial frontal cortex and demonstrate that it can be found in a small fraction of neurons in cingulate cortex. Further research is needed to determine if the weak response conflict signal in cingulate cortex is sufficient or negligible.

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bioRxiv2023

Cortical Origin of Theta Error Signals

A multi-scale approach elucidated the origin of the error-related-negativity (ERN), with its associated theta-rhythm, and the post-error-positivity (Pe) in macaque supplementary eye field (SEF). Using biophysical modeling, synaptic inputs to layer-3 (L3) and layer-5 (L5) pyramidal cells (PCs) were optimized to account for error-related modulation and inter-spike intervals. The intrinsic dynamics of dendrites in L5 but not L3 PCs generate theta rhythmicity with random phase. Saccades synchronized the phase of this theta-rhythm, which was magnified on errors. Contributions from L5 PCs to the laminar current source density (CSD) observed in SEF were negligible. The CSD derived from L3 PCs could not explain the observed association between their error-related spiking modulation and scalp-EEG. Laminar CSD comprises multipolar components, with dipoles explaining ERN features, and quadrupoles reproducing those for Pe. The presence of monopoles indicates diffuse activation. These results provide the most advanced explanation of the cellular mechanisms generating the ERN.

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bioRxiv2022

Cortical Contributions to Medial Frontal β-Bursts during Executive Control

EEG {beta}-bursts observed over the medial frontal cortex are claimed to mediate response inhibition despite their infrequent occurrence. The weak association with stopping behavior is supposed to be a by-product of the low signal-to-noise ratio of EEG recordings. We tested the premise that {beta}-bursts are more common within the cerebral cortex and more directly associated with response inhibition. We sampled simultaneously EEG and intracortical local field potentials (LFP) within the medial frontal cortex (MFC) of two macaque monkeys performing a response inhibition task. Intracortical {beta}-bursts were just as infrequent as those in EEG and did not parallel the likelihood of canceling a planned response. Cortical {beta}-bursts were more prevalent in upper layers but were not synchronized across a cortical column or with EEG {beta}-bursts. These findings contradict claims for a causal contribution of {beta}-bursts during response inhibition, provide important constraints for biophysical and cortical circuit models, and invite further considerations of {beta}-burst function in cognitive control.

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bioRxiv2021

Cortical Microcircuitry of Executive Control and Source of Associated Event-Related Potentials

Medial frontal cortex enables executive control by monitoring relevant information and using it to adapt behavior. In macaques performing a saccade countermanding (stop-signal) task, we recorded EEG over and neural spiking across all layers of the supplementary eye field (SEF). We report the laminar organization of concurrently activated neurons monitoring the conflict between incompatible responses and the timing of events serving goal maintenance and executive control. We also show their relation to coincident event-related potentials (ERP). Neurons signaling response conflict were largely broad-spiking found across all layers. Neurons signaling the interval until specific task events were largely broad-spiking neurons concentrated in L3 and L5. Neurons predicting the duration of control and sustaining the task goal until the release of operant control were a mix of narrow- and broad-spiking neurons confined to L2/3. We complement these results with the first report of a monkey homologue of the N2/P3 ERP complex associated with response inhibition. N2 polarization varied with error likelihood and P3 polarization varied with the duration of expected control. The amplitude of the N2 and P3 were predicted by the spike rate of different classes of neurons located in L2/3 but not L5/6. These findings reveal important, new features of the cortical microcircuitry supporting executive control and producing associated ERP.

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bioRxiv2020

Dissociation of Medial Frontal β-Bursts and Executive Control

The neural mechanisms of executive and motor control concern both basic researchers and clinicians. In human studies, preparation and cancellation of movements are accompanied by changes in the {beta}-frequency band (15-29 Hz) of EEG. Previous studies with human participants performing stop signal (countermanding) tasks have described reduced frequency of transient {beta}-bursts over sensorimotor cortical areas before movement initiation and increased {beta}-bursting over medial frontal areas with movement cancellation. This modulation has been interpreted as contributing to the trial-by-trial control of behavior. We performed identical analyses of EEG recorded over the frontal lobe of macaque monkeys performing a saccade countermanding task. Whilst, we replicate the occurrence and modulation of {beta}-bursts associated with initiation and cancellation of saccades, we found that {beta}-bursts occur too infrequently to account for the observed stopping behavior. We also found {beta}-bursts were more common after errors, but their incidence was unrelated to response time adaptation. These results demonstrate the homology of this EEG signature between humans and macaques but raise questions about the current interpretation of {beta}-band functional significance.

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bioRxiv2020

Express saccades during a countermanding task

Express saccades are unusually short latency, visually guided saccadic eye movements. They are most commonly observed when the fixation spot disappears at a consistent, short interval before a target spot appears at a repeated location. The saccade countermanding task includes no fixation-target gap, variable target presentation times, and the requirement to withhold saccades on some trials. These testing conditions should discourage production of express saccades. However, two macaque monkeys performing the saccade countermanding task produced consistent, multimodal distributions of saccadic latencies. These distributions consisted of a longer mode extending from 200 ms to as much as 600 ms after target presentation and another consistently less than 100 ms after target presentation. Simulations revealed that by varying express saccade production, monkeys could earn more reward. If express saccades were not rewarded, they were rarely produced. The distinct mechanisms producing express and longer saccade latencies were revealed further by the influence of regularities in the duration of the fixation interval preceding target presentation on saccade latency. Temporal expectancy systematically affected the latencies of regular but not of express saccades. This study highlights that cognitive control can integrate information across trials and strategically elicit intermittent very short latency saccades to acquire more reward.

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