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Purpose: This study aimed to validate the new DormoTech Vlab device's performance, usability, and validity as a sleep test and physiological data recorder. The novel device has been designed for patient comfort, ease of use, and home-based assessment of sleep disordered breathing and other sleep-related measurements., Methods: Forty-seven adults (mean age = 52 years, 42% female, body mass index 29.4 kg/m 2 ) underwent simultaneous testing with the DormoTech Vlab device and routine full polysomnography (PSG) using the Nox A1 system (K192469, Nox Medical). The sleep studies were manually and independently scored according to recommended guidelines. The primary outcome measure was the apnea-hypopnea index (AHI) and its corresponding conventional severity level (i.e., normal, mild, moderate, severe). Secondary endpoints included other standard PSG parameters., Results: The AHI was 21.7 ± 24.2 events/h (mean ± standard deviation) using the Vlab device versus 21.5 ± 23.9 events/h for gold standard PSG Nox A1 (p = 0.7). When AHI was grouped by severity, inter-test agreement was high (Cohen's kappa = 0.97). Results between the two systems were largely similar in the secondary endpoints, with high correlation between the two systems, and statistically significant (p < 0.05) differences only in REM latency measurements. The Vlab device provides similar sleep study data to conventional gold standard PSG and clinically near-identical test interpretation in almost all cases., Conclusion: Based on these results, the Vlab device can be considered substantially equivalent to the reference Nox A1 system in terms of usability, efficacy, and validity., Clinical Trial Registration: Trial name: Evaluation of the Usability and Performance Assessment of the DormoTech VLAB Device as a Home Sleep Test Identification number: NCT06224972. Date of Registration: 2023-12-06., Competing Interests: Declarations. Ethical approval: All procedures performed in this study involving human participants were in accordance with the ethical standards of the 1965 Helsinki Declaration. Approval was granted by the IEC committee on ethics of Shamir Medical Center on April 24, 2023, study number 0067-23-ASF. Consent to participate: Informed consent was obtained from all participants included in the study. Competing interest: Financial support for this study was provided by DormoTech Medical. All Vlab devices used in the study were supplied by DormoTech Medical under a collaborative research agreement. Benjamin D. Fox, Murad Shihab, and Asher Tal received support in the form of Vlab devices to perform this study, provided by DormoTech Medical. Asher Tal reports a relationship with DormoTech Medical that includes: board membership. Ofer Barnea reports a relationship with DormoTech Medical that includes: equity or stocks. Abed Nassir reports a relationship with DormoTech that includes: employment and equity or stocks. Abed Nassir, Ofer Barnea has patent #EP3457938B1. Dahlia Kushinsky reports a relationship with DormoTech Medical that includes: employment., (© 2025. The Author(s).)

Balancing plasticity and stability in neural circuits is essential for an animal's ability to learn from its environment while preserving proper processing and perception of sensory information. However, unlike the mechanisms that drive plasticity in neural circuits, the activity-induced molecular mechanisms that convey functional stability remain poorly understood. Focusing on the visual cortex of adult mice and combining transcriptomics, electrophysiology, and in vivo calcium imaging, we find that the daily appearance of light induces, in excitatory neurons, a large gene program along with rapid and transient increases in the ratio of excitation and inhibition (E/I ratio) and neural activity. Furthermore, we find that the light-induced transcription factor NPAS4 drives these daily normalizations of the E/I ratio and neural activity rates and that it stabilizes the neurons' response properties. These findings indicate that daily sensory-induced transcription normalizes the E/I ratio and drives downward firing rate homeostasis to maintain proper sensory processing and perception., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

Neural circuits are characterized by genetically and functionally diverse cell types. A mechanistic understanding of circuit function is predicated on linking the genetic and physiological properties of individual neurons. However, it remains highly challenging to map the transcriptional properties to functionally heterogeneous neuronal subtypes in mammalian cortical circuits in vivo . Here, we introduce a high-throughput two-photon nuclear phototagging (2P-NucTag) approach optimized for on-demand and indelible labeling of single neurons via a photoactivatable red fluorescent protein following in vivo functional characterization in behaving mice. We demonstrate the utility of this function-forward pipeline by selectively labeling and transcriptionally profiling previously inaccessible 'place' and 'silent' cells in the mouse hippocampus. Our results reveal unexpected differences in gene expression between these hippocampal pyramidal neurons with distinct spatial coding properties. Thus, 2P-NucTag opens a new way to uncover the molecular principles that govern the functional organization of neural circuits.

Processing of sensory information in neural circuits is modulated by an animal's behavioral state, but the underlying cellular mechanisms are not well understood. Focusing on the mouse visual cortex, here we analyze the role of GABAergic interneurons that are located in layer 1 and express Ndnf (L1 NDNF INs) in the state-dependent control over sensory processing. We find that the ongoing and sensory-evoked activity of L1 NDNF INs is strongly enhanced when an animal is aroused and that L1 NDNF INs gain-modulate local excitatory neurons selectively during high-arousal states by inhibiting their apical dendrites while disinhibiting their somata via Parvalbumin-expressing interneurons. Because active NDNF INs are evenly spread in L1 and can affect excitatory neurons across all cortical layers, this indicates that the state-dependent activation of L1 NDNF INs and the subsequent shift of inhibition in excitatory neurons toward their apical dendrites gain-modulate sensory processing in whole cortical columns., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2021 Elsevier Inc. All rights reserved.)

The heart and pyloric rhythms of crustaceans have been studied separately and extensively over many years. Local and hormonal neuromodulation and sensory inputs into these central pattern generator circuits play a significant role in an animal's response to perturbations, but are usually lost or removed during in vitro studies. To examine simultaneously the in vivo motor output of the crustacean heart and pyloric rhythms, we used photoplethysmography. In the population measured ( n =49), the heart rhythm frequency ranged from 0.3 to 2.3 Hz. The pyloric rhythm varied from 0.2 to 1.6 Hz. We observed a weak correlation between the frequencies of the heart and pyloric rhythms. During multiple hour-long recordings, many animals held at a controlled temperature showed strong inhibitory bouts in which the heart decreased in frequency or become quiescent and the pyloric rhythm decreased in frequency. We measured the simultaneous responses of the rhythms to temperature ramps by heating or cooling the saline bath while recording both the heart and pyloric muscle movements. Q 10 , critical temperature (temperature at which muscle function is compromised) and changes in frequency were calculated for each of the rhythms tested. The heart rhythm was more robust to high temperature than the pyloric rhythm., Competing Interests: Competing interestsThe authors declare no competing or financial interests., (© 2019. Published by The Company of Biologists Ltd.)

A wealth of data has elucidated the mechanisms by which sensory inputs are encoded in the neocortex, but how these processes are regulated by the behavioral relevance of sensory information is less understood. Here, we focus on neocortical layer 1 (L1), a key location for processing of such top-down information. Using Neuron-Derived Neurotrophic Factor (NDNF) as a selective marker of L1 interneurons (INs) and in vivo 2-photon calcium imaging, electrophysiology, viral tracing, optogenetics, and associative memory, we find that L1 NDNF-INs mediate a prolonged form of inhibition in distal pyramidal neuron dendrites that correlates with the strength of the memory trace. Conversely, inhibition from Martinotti cells remains unchanged after conditioning but in turn tightly controls sensory responses in NDNF-INs. These results define a genetically addressable form of dendritic inhibition that is highly experience dependent and indicate that in addition to disinhibition, salient stimuli are encoded at elevated levels of distal dendritic inhibition. VIDEO ABSTRACT., (Copyright © 2018 The Authors. Published by Elsevier Inc. All rights reserved.)