Biology subjects

Guang, J.

Publications and source records attributed to Guang, J..

5 recordsLinked to original sources

bioRxiv2026

REM Sleep Disengagement of β Oscillations Permits Rapid Dream Movements in Parkinsonism

REM sleep behavior disorder is a hallmark of prodromal -synucleinopathies, yet why patients with Parkinsons disease can generate rapid, coordinated movements during REM sleep despite daytime bradykinesia remains unknown. Here we combined recordings of eye movements, cortical electroencephalography, and basal ganglia-thalamic neuronal activity across vigilance states in non-human primates before and after MPTP-induced parkinsonism. Parkinsonism enhanced {beta} oscillations and impaired movement-related neural dynamics during wakefulness and NREM sleep, whereas both pathological {beta} activity and motor impairments were attenuated during REM sleep. {beta} suppression preceded the onset of REM sleep, indicating that network reconfiguration begins before REM becomes behaviorally apparent. These findings demonstrate that Parkinsonian network dysfunction is dynamically gated by brain state rather than continuously imposed by dopamine depletion. REM sleep is a natural physiological condition in which {beta} oscillations are disengaged, uncovering a latent capacity, normally masked by REM atonia, for rapid movement even in the dopamine-depleted motor network.

neuroscience↗

bioRxiv2025

Basal ganglia-independent thalamic bursts do not wake cortex during sleep

The thalamus is a key forebrain structure that gates peripheral, subcortical, and cortico-cortical communication1,2. Awake thalamic bursts provide the cortex with a "wake-up" signal2-4. Paradoxically, thalamic neurons discharge tonically during cellular depolarization and activated brain states (wakefulness, REM sleep) but burst during hyperpolarization and NREM sleep5-9. It has been proposed that NREM thalamic bursts do not awaken the cortex because of their periodic and synchronized nature2-4; however, this has never been tested in vivo during natural sleep. We simultaneously recorded polysomnographic signals, local field potentials, and spiking activity from multiple thalamic neurons in the ventral anterior and centromedian nuclei of two female non-human primates during naturally occurring vigilance states. These nuclei receive GABAergic output from the basal ganglia10,11, with discharge rate and GABA outflow decreasing during NREM sleep12. We found that despite the expected thalamic depolarization, bursting increased significantly. NREM bursts were neither periodic nor highly synchronized. However, EEG activity time-locked to burst onset during NREM sleep differed markedly from that observed during wakefulness and REM sleep. These results support a modulatory, rather than a driving, relationship between the basal ganglia and thalamus. NREM thalamic bursts do not awaken the cortex, probably due to unique state-dependent thalamocortical dynamics.

neuroscience↗

bioRxiv2024

An AI-Driven Model of Consciousness, Its Disorders, and Their Treatment

Understanding disorders of consciousness (DOC) remains one of the most challenging problems in neuroscience, hindered by the lack of experimental models for probing mechanisms or testing interventions [1]. To address this, we introduce a generative adversarial AI framework [2] that pits deep neural networks--trained to detect consciousness across over 680,000 neuroelectro-physiology samples and validated on 565 patients, healthy volunteers, and animals--against interpretable, machine learning-driven neural field models [3]. This adversarial architecture produces biologically realistic simulations of both conscious and comatose brains that recapitulate empirical neurophysiological features across humans, monkeys, rats, and bats. Without explicit programming, the AI model retrodicts known DOC responses to brain stimulation and generates testable predictions about unconsciousness mechanisms. Two such predictions are validated here: selective disruption of the basal ganglia indirect pathway, supported by diffusion MRI in 51 DOC patients; and increased cortical inhibitory-to-inhibitory synaptic coupling, supported by RNA sequencing from resected brain tissue in six human coma patients and a rat stroke model. The model also identifies high-frequency subthalamic nucleus stimulation as a promising DOC intervention, supported here using electrophysiology data from human patients. This work introduces an AI framework for causal inference and therapeutic discovery in consciousness research and complex systems more broadly.

neuroscience↗

bioRxiv2023

Non-linear input-output relationships in the subthalamic nucleus of Parkinson's patients

Both local field potentials (LFP) and spiking (SPK) activity in the subthalamic nucleus (STN) are related to Parkinsons disease (PD) symptoms; however, their relationship is poorly understood. We explore it by separating STN signals of 146 PD patients (308 trajectories, >25,000 recording sites) into aperiodic and periodic components and whitening these signals using their corresponding aperiodic parameters. The LFP aperiodic exponents resemble Brown noise ( = 2.20 {+/-} 0.40) and are significantly higher than SPK aperiodic exponents ( = 0.11 {+/-} 0.22, White noise). The periodic oscillations of LFP are overwhelmingly distributed in the high beta frequency domain while those of SPK are in both low and high beta domains. Beta oscillation center frequencies were downshifted in SPK relative to simultaneously recorded LFP. This demonstrates that the STN synaptic input (LFP) undergoes significant modifications when transformed into STN output (SPK) of PD patients, and may explain the critical role of STN in PD physiology and STN-Deep-Brain-Stimulation therapeutic efficacy.

neuroscience↗

bioRxiv2020

Toward asleep DBS: Cortico basal-ganglia neural activity during interleaved propofol/ketamine sedation mimics NREM/REM sleep activity

Deep brain stimulation (DBS) is currently a standard long-term treatment for advanced motor symptoms in Parkinsons disease (PD). In an effort to enable DBS under sedation, asleep DBS, we characterized the cortico-basal ganglia neuronal network of two non-human primates under propofol, ketamine and interleaved propofol-ketamine (IPK) sedation. Further, we compared these sedation states in the healthy and Parkinsonian condition to those of healthy sleep. Ketamine increases high frequency power and synchronization while propofol increases low frequency power and synchronization in polysomnography and neuronal activity recordings. Thus, ketamine does not mask the low frequency oscillations used for physiological navigation toward basal ganglia DBS targets. The brain state under ketamine and propofol mimicked rapid eye movement (REM) and Non-REM (NREM) sleep activity, respectively, and the IPK protocol imitates the NREM-REM sleep cycle. These promising results are the first step towards asleep DBS with non-distorted physiological navigation.

neuroscience↗