Biology subjects

Miao, A.

Publications and source records attributed to Miao, A..

5 recordsLinked to original sources

bioRxiv2026

A Bidirectional Neural Interface With Direct On-Device Neuromorphic Decoding for Closed-Loop Optogenetics

Bidirectional interfaces combined with neural de-coding algorithms are essential for closed-loop (CL) neuromodulation, enabling simultaneous neural monitoring and responsive optogenetic stimulation. However, implementing these capabilities in compact wireless headstages for freely moving animals remains challenging, as most existing platforms rely on tethered setups and external processors to execute computationally intensive decoders. This work presents the design and optimization of a neural decoder integrated into a bidirectional wireless system for CL optogenetic experiments in rodents. The proposed platform combines 32-channel electrophysiological recording with neuromorphic feature extraction, dimensionality reduction, and a nonlinear support vector machine (NL-SVM) decoder implemented on a resource-constrained Spartan-6 FPGA. Temporal dynamics are captured using spike-count features and leaky integrators, while principal component analysis (PCA) reduces the feature space to six components, enabling sub-millisecond inference with minimal memory and power requirements. Model size is further reduced using k-means clustering during training to limit the number of support vectors. Decoder performance was validated using datasets from non-human primate and rat motor cortex recordings. The proposed decoder achieved accuracy comparable to convolutional neural networks (R2 =0.85 vs. 0.87) and outperformed Wiener filters (R2 = 0.81) while requiring significantly fewer computational resources. The full system was further demonstrated in vivo through wireless closed-loop optogenetic stimulation in rats, achieving a variance accounted for (VAF) of 0.9148. Overall, this work introduces a versatile, fully self-contained, and resource-efficient platform for real-time untethered closed-loop neuroscience experiments.

neuroscience↗

bioRxiv2023

Benchmarking nearest neighbor retrieval of zebra finch vocalizations across development

Vocalizations are highly specialized motor gestures that regulate social interactions. The reliable detection of vocalizations from raw streams of microphone data remains an open problem even in research on widely studied animals such as the zebra finch. A promising method for finding vocal samples from potentially few labelled examples (templates) is nearest neighbor retrieval, but this method has never been extensively tested on vocal segmentation tasks. We retrieve zebra finch vocalizations as neighbors of each other in the sound spectrogram space. Based on merely 50 templates, we find excellent retrieval performance in adults (F1 score of 0.93 {+/-} 0.07) but not in juveniles (F1 score of 0.64 {+/-} 0.18), presumably due to the larger vocal variability of the latter. The performance in juveniles improves when retrieval is based on fixed-size template slices (F1 score of 0.72 {+/-} 0.10) instead of entire templates. Among the several distance metrics we tested such as the cosine and the Euclidean distance, we find that the Spearman distance largely outperforms all others. We release our expert-curated dataset of more than 50000 zebra finch vocal segments, which will enable training of data-hungry machine-learning approaches.

animal behavior and cognition↗

bioRxiv2023

A REM-active basal ganglia circuit that regulates anxiety

REM sleep has been hypothesized to promote emotional resilience, but any neuronal circuits mediating this have not been identified. We find that in mice, somatostatin (Som) neurons in the entopeduncular nucleus (EPSom)/internal globus pallidus are predominantly active selectively during REM sleep. This unique REM activity is necessary and sufficient for maintaining normal REM sleep. Inhibiting or exciting EPSom neurons reduced or increased REM sleep duration, respectively. Activation of the sole downstream target of EPSom neurons, Vglut2 cells in the lateral habenula (LHb), increased sleep via the ventral tegmental area (VTA). A simple chemogenetic scheme to periodically inhibit the LHb over 4 days selectively removed a significant amount of cumulative REM sleep. Chronic REM reduction correlated with mice becoming anxious and more sensitive to aversive stimuli. Therefore, we suggest that REM sleep, in part generated by the EP[->]LHb[->]VTA circuit identified here, could contribute to stabilizing reactions to habitual aversive stimuli.

neuroscience↗

bioRxiv2020

Sleep deprivation triggers somatostatin neurons in prefrontal cortex to initiate nesting and sleep via the preoptic and lateral hypothalamus

Animals undertake specific behaviors before sleep. Little is known about whether these innate behaviors, such as nest building, are actually an intrinsic part of the sleep-inducing circuitry. We found, using activity-tagging genetics, that mouse prefrontal cortex (PFC) somatostatin/GABAergic (SOM/GABA) neurons, which become activated during sleep deprivation, induce nest building when opto-activated. These tagged neurons induce sustained global NREM sleep if their activation is prolonged metabotropically. Sleep-deprivation-tagged PFC SOM/GABA neurons have long-range projections to the lateral preoptic (LPO) and lateral hypothalamus (LH). Local activation of tagged PFC SOM/GABA terminals in LPO and the LH induced nesting and NREM sleep respectively. Our findings provide a circuit link for how the PFC responds to sleep deprivation by coordinating sleep preparatory behavior and subsequent sleep.

neuroscience↗

bioRxiv2019

Galanin neurons in the hypothalamus link sleep homeostasis, body temperature and actions of the alpha2 adrenergic agonist dexmedetomidine

Sleep deprivation induces a characteristic rebound in NREM sleep accompanied by an immediate increase in the power of delta (0.5 - 4 Hz) oscillations, proportional to the prior time awake. To test the idea that galanin neurons in the mouse lateral preoptic hypothalamus (LPO) regulate this sleep homeostasis, they were selectively genetically ablated. The baseline sleep architecture of LPO-{Delta}Gal mice became heavily fragmented, their average core body temperature permanently increased (by about 2{degrees}C) and the diurnal variations in body temperature across the sleep-wake cycle also markedly increased. Additionally, LPO-{Delta}Gal mice showed a striking spike in body temperature and increase in wakefulness at a time (ZT24) when control mice were experiencing the opposite - a decrease in body temperature and becoming maximally sleepy (start of "lights on"). After sleep deprivation sleep homeostasis was largely abolished in LPO-{Delta}Gal mice: the characteristic increase in the delta power of NREM sleep following sleep deprivation was absent, suggesting that LPO galanin neurons track the time spent awake. Moreover, the amount of recovery sleep was substantially reduced over the following hours. We also found that the 2 adrenergic agonist dexmedetomidine, used for long-term sedation during intensive care, requires LPO galanin neurons to induce both the NREM-like state with increased delta power and the reduction in body temperature, characteristic features of this drug. This suggests that dexmedetomidine over-activates the natural sleep homeostasis pathway via galanin neurons. Collectively, the results emphasize that NREM sleep and the concurrent reduction in body temperature are entwined at the circuit level. SignificanceCatching up on lost sleep (sleep homeostasis) is a common phenomenon in mammals, but there is no circuit explanation for how this occurs. We have discovered that galanin neurons in the hypothalamus are essential for sleep homeostasis as well as for the control of body temperature. This is the first time that a neuronal cell type has been identified that underlies sleep homeostasis. Moreover, we show that activation of these galanin neurons are also essential for the actions of the 2 adrenergic agonist dexmedetomidine, which induces both hypothermia together with powerful delta oscillations resembling NREM sleep. Thus, sleep homeostasis, temperature control and sedation by 2 adrenergic agonists can all be linked at the circuit level by hypothalamic galanin neurons.

neuroscience↗