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Search indexed bioRxiv preprints in genomics, neuroscience, cell biology and bioinformatics. Read source abstracts and check manuscript versions; preprints are not peer reviewed.

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At least 415 records · Page 23Linked to original sources

A unifying model to predict multiple object orienting behaviors in tethered flies

Individual visual processing circuits for Drosophila locomotor control have been studied in detail, but contributions of specific pathways to multiple behaviors remain unclear. To address how both flexible and stereotyped visual object response behaviors potentially share neural circuit components, we investigated models of asymmetric motion responses. Such models have predicted that object fixation without explicit neural encoding of position is possible. Here we investigated what neural circuits and behaviors are consistent with such models. In behavioral experiments on tethered flying flies, we found close correspondence between T4/T5-neuron dependent turning responses to objects and model output for high frequency perturbations. Furthermore, we found that the model predicts key results from several published accounts of stereotyped object tracking. The concurrence of experiment and theory suggests a neural substrate and algorithmic basis for stereotyped object tracking and informs future studies of flexible visual behaviors and their neural bases.

neuroscience↗

Functional divergence of Plexin B structural motifs in distinct steps of Drosophila olfactory circuit assembly

Plexins exhibit multitudinous, evolutionarily conserved functions in the development of nervous systems. However, how Plexins employ their diverse structural motifs in vivo to perform distinct roles in the stepwise assembly of neural circuits is unclear. Here, we systematically mutagenized structural motifs of Drosophila Plexin B (PlexB) and examined the function of these variants at multiple PlexB-mediated neurodevelopmental processes in olfactory receptor neurons: axon fasciculation, trajectory choice, and synaptic partner selection. We found that the extracellular Sema domain is essential for all three processes, the catalytic site of the intracellular RapGAP is engaged in none, and the intracellular GTPase-binding motifs are essential for trajectory choice and synaptic partner selection, but are dispensable for fasciculation. Moreover, extracellular PlexB cleavage serves as a regulatory mechanism of PlexB signaling. Thus, PlexB structural motifs have divergent roles in distinct steps of neural development, altogether contributing to the functional versatility of PlexB in neural circuit assembly.

neuroscience↗

The female-specific VC neurons are mechanically activated, feed-forward motor neurons that facilitate serotonin-induced egg laying in C. elegans

Successful execution of behavior requires coordinated activity and communication between multiple cell types. Studies using the relatively simple neural circuits of invertebrates have helped to uncover how conserved molecular and cellular signaling events shape animal behavior. To understand the mechanisms underlying neural circuit activity and behavior, we have been studying a simple circuit that drives egg-laying behavior in the nematode worm C. elegans. Here we show that the sex-specific, Ventral C (VC) motor neurons are important for vulval muscle contractility and egg laying in response to serotonin. Ca2+ imaging experiments show the VCs are active during times of vulval muscle contraction and vulval opening, and optogenetic stimulation of the VCs promotes vulval muscle Ca2+ activity. Blocking VC neurotransmission inhibits egg laying in response to serotonin and increases the failure rate of egg-laying attempts, indicating that VC signaling facilitates full vulval muscle contraction and opening of the vulva for efficient egg laying. We also find the VCs are mechanically activated in response to vulval opening. Optogenetic stimulation of the vulval muscles is sufficient to drive VC Ca2+ activity and requires muscle contractility, showing the presynaptic VCs and the postsynaptic vulval muscles can mutually excite each other. Together, our results demonstrate that the VC neurons facilitate efficient execution of egg-laying behavior by coordinating postsynaptic muscle contractility in response to serotonin and mechanosensory feedback. Significance StatementMany animal motor behaviors are modulated by the neurotransmitters serotonin and acetylcholine. Such motor circuits also respond to mechanosensory feedback, but how neurotransmitters and mechanoreceptors work together to coordinate behavior is not well understood. We address these questions using the egg-laying circuit in C. elegans where we can manipulate presynaptic neuron and postsynaptic muscle activity in behaving animals while recording circuit responses through Ca2+ imaging. We find that the cholinergic VC motoneurons are important for proper vulval muscle contractility and egg laying in response to serotonin. Muscle contraction also activates the VCs, forming a positive feedback loop that promotes full contraction for egg release. In all, mechanosensory feedback provides a parallel form of modulation that shapes circuit responses to neurotransmitters.

neuroscience↗

Neuronal functional connectivity is impaired in a layer dependent manner near the chronically implanted microelectrodes

ObjectiveThis study aims to reveal longitudinal changes in functional network connectivity within and across different brain structures near the chronically implanted microelectrode. While it is well established that the foreign-body response (FBR) contributes to the gradual decline of the signals recorded from brain implants over time, how does the FBR impact affect the functional stability of neural circuits near implanted Brain-Computer Interfaces (BCIs) remains unknown. This research aims to illuminate how the chronic FBR can alter local neural circuit function and the implications for BCI decoders. ApproachThis study utilized multisite Michigan-style microelectrodes that span all cortical layers and the hippocampal CA1 region to collect spontaneous and visually-evoked electrophysiological activity. Alterations in neuronal activity near the microelectrode were tested assessing cross-frequency synchronization of LFP and spike entrainment to LFP oscillatory activity throughout 16 weeks after microelectrode implantation. Main ResultsThe study found that cortical layer 4, the input-receiving layer, maintained activity over the implantation time. However, layers 2/3 rapidly experienced severe impairment, leading to a loss of proper intralaminar connectivity in the downstream output layers 5/6. Furthermore, the impairment of interlaminar connectivity near the microelectrode was unidirectional, showing decreased connectivity from Layers 2/3 to Layers 5/6 but not the reverse direction. In the hippocampus, CA1 neurons gradually became unable to properly entrain to the surrounding LFP oscillations. SignificanceThis study provides a detailed characterization of network connectivity dysfunction over long-term microelectrode implantation periods. This new knowledge could contribute to the development of targeted therapeutic strategies aimed at improving the health of the tissue surrounding brain implants and potentially inform engineering of adaptive decoders as the FBR progresses. Our studys understanding of the dynamic changes in the functional network over time opens the door to developing interventions for improving the long-term stability and performance of intracortical microelectrodes.

bioengineering↗

The inhibition of automatic imitation: a meta-analysis and synthesis of fMRI studies

Humans copy other people without their conscious awareness, a behaviour known as automatic imitation. Although automatic imitation forms a key part of daily social interactions, we do not copy other people indiscriminately. Instead, we control imitative tendencies by prioritising some actions and inhibiting others. To date, neuroimaging studies investigating the control of automatic imitation have produced inconsistent findings. Some studies suggest that imitation control relies on a domain-specific neural circuit related to social cognition (the theory-of-mind network). In contrast, other studies show engagement of a domain-general neural circuit that is engaged during a diverse range of cognitive control tasks (the multiple demand network). Given the inconsistency of prior findings, in the current paper we avoided problems associated with interpreting individual studies by performing a meta-analysis. To do so, we used a multi-level kernel density analysis to quantitatively identify consistent patterns of activation across functional magnetic resonance imaging studies investigating the control of imitation. Our results show clear and consistent evidence across studies that the control of automatic imitation is guided by brain regions in the multiple demand network including dorsolateral frontoparietal cortex. In contrast, there was only limited evidence that regions in the theory of mind network were engaged. Indeed, medial prefrontal cortex showed no consistent engagement and right temporoparietal junction engagement may reflect spatial rather than imitative control. As such, the current meta-analysis reinforces the role of domain-general control mechanisms and provides limited evidence in support of the role of domain-specific processes in regulating imitative tendencies. Consequently, neurocognitive models of imitation need updating to place more emphasis on domain-general control mechanisms, as well as to consider more complex organisational structures of control, which may involve contributions from multiple cognitive systems.

neuroscience↗

Recording and neural circuit-based manipulation of the maternal oxytocin pulses in mice

Pulsatile release of the hormone oxytocin (OT) mediates uterine contraction during parturition and milk ejection during lactation1-3. These pulses are generated by unique activity patterns of the central neuroendocrine OT neurons located in the paraventricular and supraoptic hypothalamus. Classical studies have characterized putative OT neurons by in vivo extracellular recording techniques in rats and rabbits under anesthesia1, 4-7 or awake8-10. Due to technical limitations, however, the identity of OT neurons in these previous studies was speculative based on their electrophysiological characteristics and axonal projection to the posterior pituitary, not on OT gene expression. To pinpoint OT neural activities among other hypothalamic neurons that project to the pituitary11, 12 and make better use of cell-type-specific neuroscience toolkits13, a mouse model needs to be developed for studies of parturition and lactation. We herein introduce viral genetic approaches in mice to characterize the maternal activities of OT neurons by fiber photometry. During lactation, a sharp photometric peak of OT neurons appeared at approximately 520 s following simultaneous suckling stimuli from three pups. The amplitude of the peaks increased as the mother mice experienced lactation, irrespective of the age of the pups, suggesting the intrinsic plasticity of maternal OT neurons. Based on a mono-synaptic input map to OT neurons, we pharmacogenetically activated the inhibitory neurons in the bed nucleus of the stria terminalis and found suppression of the activities of OT neurons. Collectively, our study illuminates temporal dynamics in the maternal neural activities of OT neurons and identifies one of its modulatory circuits. Highlights- Pulsatile activities of genetically-defined OT neurons in mother mice were recorded in vivo. - The maternal experience-dependent plasticity of the OT neural activities was found. - Input-mapping of OT neurons in mother mice was performed by rabies-mediated trans-synaptic tracing. - Photometric peaks of OT neurons were suppressed by the activation of BST inhibitory neurons.

neuroscience↗

Connectome-constrained deep mechanistic networks predict neural responses across the fly visual system at single-neuron resolution

We can now measure the connectivity of every neuron in a neural circuit, but we are still blind to other biological details, including the dynamical characteristics of each neuron. The degree to which connectivity measurements alone can inform understanding of neural computation is an open question. Here we show that with only measurements of the connectivity of a biological neural network, we can predict the neural activity underlying neural computation. We constructed a model neural network with the experimentally determined connectivity for 64 cell types in the motion pathways of the fruit fly optic lobe but with unknown parameters for the single neuron and single synapse properties. We then optimized the values of these unknown parameters using techniques from deep learning, to allow the model network to detect visual motion. Our mechanistic model makes detailed experimentally testable predictions for each neuron in the connectome. We found that model predictions agreed with experimental measurements of neural activity across 24 studies. Our work demonstrates a strategy for generating detailed hypotheses about the mechanisms of neural circuit function from connectivity measurements. We show that this strategy is more likely to be successful when neurons are sparsely connected--a universally observed feature of biological neural networks across species and brain regions.

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An Intra-brainstem Circuit for Pain-induced Inhibition of Itch

Pain and itch are unpleasant and distinct sensations that give rise to behaviors such as reflexive withdrawal and scratching in humans and mice. Interestingly, it has been observed that pain modulate itch through the neural circuits housed in the brain and spinal cord. However, we are yet to fully understand the identities of and mechanisms by which specific neural circuits mediate pain-induced modulation of itch. Independent studies indicate that brainstem nuclei such as the lateral parabrachial nucleus (LPBN) and rostral ventromedial medulla (RVM) are important for the suppression of itch by painful stimuli. Here, using mouse and viral genetics, rabies tracing, chemogenetics, and calcium imaging, we show that the synaptic connections between LPBN and RVM plays an instrumental role in the interactions between pain and itch. Notably, we found that the LPBN neurons that express the gene encoding the substance P receptor, Tacr1 (LPBNTacr1), synapse onto Tacr1-expressing RVM neurons (RVMTacr1). The RVMTacr1 neurons were found to be nociceptive, sufficient for inhibiting itch, and necessary for pain-induced itch suppression. Moreover, through brain-wide anterograde and retrograde viral tracing studies, we found that the RVMTacr1 neurons are bidirectionally connected with LPBN, periaqueductal gray (PAG), and lateral hypothalamic area (LHA). Thus, together, our data indicate that the RVMTacr1 neurons integrate nociceptive information to mediate itch-induced scratching and can mediate the physiological effects of itch through their downstream targets.

neuroscience↗

Long-term editing of brain circuits in mice using an engineered electrical synapse

Electrical signaling across distinct populations of brain cells underpins cognitive and emotional function; however, approaches that selectively regulate electrical signaling between two cellular components of a mammalian neural circuit remain sparse. Here, we engineered an electrical synapse composed of two connexin proteins found in Morone americana (white perch fish) - connexin34.7 and connexin35 - to accomplish mammalian circuit modulation. By exploiting protein mutagenesis, devising a new in vitro system for assaying connexin hemichannel docking, and performing computational modeling of hemichannel interactions, we uncovered a structural motif that contributes to electrical synapse formation. Targeting these motifs, we designed connexin34.7 and connexin35 hemichannels that dock with each other to form an electrical synapse, but not with other major connexins expressed in the mammalian central nervous system. We validated this electrical synapse in vivo using C. elegans and mice, demonstrating that it can strengthen communication across neural circuits composed of pairs of distinct cell types and modify behavior accordingly. Thus, we establish Long-term integration of Circuits using connexins (LinCx) for precision circuit-editing in mammals.

neuroscience↗

Memory consolidation and improvement by synaptic tagging and capture in recurrent neural networks

The synaptic-tagging-and-capture (STC) hypothesis formulates that at each synapse the concurrence of a tag with protein synthesis yields the maintenance of changes induced by synaptic plasticity. This hypothesis provides a biological principle underlying the synaptic consolidation of memories that is not verified for recurrent neural circuits. We developed a theoretical model integrating the mechanisms underlying the STC hypothesis with calcium-based synaptic plasticity in a recurrent spiking neural network. In the model, calcium-based synaptic plasticity yields the formation of strongly interconnected cell assemblies encoding memories, followed by consolidation through the STC mechanisms. Furthermore, we find that the STC mechanisms have an up to now undiscovered effect on memories - with the passage of time they modify the storage of memories, such that after several hours memory recall is significantly improved. This kind of memory enhancement can provide a new principle for storing information in biological and artificial neural circuits.

neuroscience↗

Insulin-Producing Cells Monitor the Temperature and Compensate for Cold-Induced Sleep in Drosophila

Sleep is regulated by environmental factors including temperature, but the neural circuits that receive the sensory signal and mediate the regulation remain unclear. We examined how cold could influence Drosophila sleep patterns and its neural mechanism. The results showed that Drosophila has more sleep duration, less sleep latency and deeper sleep depth under cold condition. We identified the Insulin-producing Cells (IPCs) can be activated by cold, and receive the cold signal from the 11216 cold-sensing neuron without a direct synaptic connection. Elevation of IPCs sensitivity to cold impairs the sleep-promoting effect of cold while blocking of IPCs enhance the effect mostly on sleep circadian, suggesting that the cold activated IPCs have a compensative role in sleep regulation. Our finding revealed a potential neural circuit that help maintain sleep circadian in detrimental environment and may give new insight to the complicated sleep regulation mechanism.

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Untuned But Not Irrelevant: A Role For Untuned Neurons In Sensory Information Coding

To study sensory representations, neuroscientists record neural activities while presenting different stimuli to the animal. From these data, we identify neurons whose activities depend systematically on each aspect of the stimulus. These neurons are said to be \"tuned\" to that stimulus feature. It is typically assumed that these tuned neurons represent the stimulus feature in their firing, whereas any \"untuned\" neurons do not contribute to its representation. Recent experimental work questioned this assumption, showing that in some circumstances, neurons that are untuned to a particular stimulus feature can contribute to its representation. These findings suggest that, by ignoring untuned neurons, our understanding of population coding might be incomplete. At the same time, several key questions remain unanswered: Are the impacts of untuned neurons on population coding due to weak tuning that is nevertheless below the threshold the experimenters set for calling neurons tuned (vs untuned)? Do these effects hold for different population sizes and/or correlation structures? And could neural circuit function ever benefit from having some untuned neurons vs having all neurons be tuned to the stimulus? Using theoretical calculations and analyses of in vivo neural data, I answer those questions by: a) showing how, in the presence of correlated variability, untuned neurons can enhance sensory information coding, for a variety of population sizes and correlation structures; b) demonstrating that this effect does not rely on weak tuning; and c) identifying conditions under which the neural code can be made more informative by replacing some of the tuned neurons with untuned ones. These conditions specify when there is a functional benefit to having untuned neurons.\n\nAuthor SummaryIn the visual system, most neurons firing rates are tuned to various aspects of the stimulus (motion, contrast, etc.). For each stimulus feature, however some neurons appear to be untuned: their firing rates do not depend on that stimulus feature. Previous work on information coding in neural populations ignored untuned neurons, assuming that only the neurons tuned to a given stimulus feature contribute to its encoding. Recent experimental work questioned this assumption, showing that neurons with no apparent tuning can sometimes contribute to information coding. However, key questions remain unanswered. First, how do the untuned neurons contribute to information coding, and could this effect rely on those neurons having weak tuning that was overlooked? Second, does the function of a neural circuit ever benefit from having some neurons untuned? Or should every neuron be tuned (even weakly) to every stimulus feature? Here, I use mathematical calculations and analyses of data from the mouse visual cortex to answer those questions. First, I show how (and why) correlations between neurons enable the untuned neurons to contribute to information coding. Second, I show that neural populations can often do a better job of encoding a given stimulus feature when some of the neurons are untuned for that stimulus feature. Thus, it may be best for the brain to segregate its tuning, leaving some neurons untuned for each stimulus feature. Along with helping to explain how the brain processes external stimuli, this work has strong implications for attempts to decode brain signals, to control brain-machine interfaces: better performance could be obtained if the activities of all neurons are decoded, as opposed to only those with strong tuning.

neuroscience↗

Two Parallel Pathways Mediate Olfactory-Driven Backward Locomotion

Although animals switch to backward walking upon sensing an obstacle or danger in their path, the initiation and execution of backward locomotion is poorly understood. The discovery of Moonwalker Descending Neurons (MDNs), made Drosophila useful to study neural circuits underlying backward locomotion. MDNs were demonstrated to receive visual and mechanosensory inputs. However, whether other modalities converge onto MDNs and what are the neural circuits activating MDNs are unknown. We show that aversive but not appetitive olfactory input triggers MDN-mediated backward locomotion. We identify in each hemisphere, a single Moonwalker Subesophageal Zone neuron (MooSEZ), which triggers backward locomotion. MooSEZs act both upstream and in parallel to MDNs. Surprisingly, MooSEZs also respond mostly to aversive odor. Contrary to MDNs, blocking MooSEZs activity has little effect on odor-evoked backward locomotion. Thus, this work reveals another important modality input to MDNs in addition to a novel olfactory pathway and MDN-independent backward locomotion pathway.

neuroscience↗

From sequences to schemas: low-rank recurrent dynamics underlie abstract relational representations

A hallmark of intelligent behavior is the ability to extract abstract relational structure from temporal sequences -- recognizing, for instance, that aab, ccd, and eef all follow the same underlying pattern, regardless of the specific elements involved. This capacity, observed across species and sensory modalities, is thought to underlie the formation of cognitive schemas: compressed internal models that support rapid generalization to novel experiences. Yet the neural circuit mechanisms by which such abstract, identity-independent representations emerge from sequential experience remain largely unknown. Here, we investigate this question using Recurrent Neural Networks (RNNs) as mechanistic models of neural circuits, trained to classify sequences based on their latent algebraic patterns (e.g., aab, aad [->] AAB; aba, aca [->] ABA) without supervision on intermediate transitions. We demonstrate that RNNs spontaneously learn low-dimensional representations that mirror the hierarchical generative structure of the sequences, and that this abstraction is mechanistically supported by the emergence of low-rank recurrent connectivity. The leading singular component of the recurrent weight matrix integrates relational transition information -- whether consecutive tokens are the same or different -- across time, driving the formation of a structured, tree-like geometry in the population state space. Through singular vector ablation, we establish a causal role for this component: removing it selectively erases memory for earlier transitions while leaving local, single-step sensitivity intact. Finally, while RNNs trained on next-token prediction do not spontaneously acquire these abstract representations, transferring the low-rank scaffold learned from classification significantly accelerates learning and improves generalization -- an effect specific to the abstract structure of the scaffold rather than generic statistical pretraining. These findings offer a computational account of how task demands shape recurrent connectivity to support temporal abstraction, with direct implications for understanding schema formation in biological brains.

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Revisiting Chemoaffinity Theory: Chemotactic Implementation Of Topographic Axonal Projection

Neural circuits are wired by chemotactic migration of growth cones guided by extracellular guidance cue gradients. How growth cone chemotaxis builds the macroscopic structure of the neural circuit is a fundamental question in neuroscience. I addressed this issue in the case of the ordered axonal projections called topographic maps in the retinotectal system. In the retina and tectum, the erythropoietin-producing hepatocellular (Eph) receptors and their ligands, the ephrins, are expressed in gradients. According to Sperrys chemoaffinity theory, gradients in both the source and target areas enable projecting axons to recognize their proper terminals, but how axons chemotactically decode their destinations is largely unknown. To identify the chemotactic mechanism of topographic mapping, I developed a mathematical model of intracellular signaling in the growth cone that focuses on the growth cones unique chemotactic property of being attracted or repelled by the same guidance cues in different biological situations. The model presented mechanism by which the retinal growth cone reaches the correct terminal zone in the tectum through alternating chemotactic response between attraction and repulsion around a preferred concentration. The model also provided a unified understanding of the contrasting relationships between receptor expression levels and preferred ligand concentrations in EphA/ephrinA- and EphB/ephrinB-encoded topographic mappings. Thus, this study redefines the chemoaffinity theory in chemotactic terms.\n\nAuthor SummaryThis study revisited the chemoaffinity theory for topographic mapping in terms of chemotaxis. According to this theory, the axonal growth cone projects to specific targets based on positional information encoded by chemical gradients in both source and target areas. However, the mechanism by which the chemotactic growth cone recognizes its proper terminal site remains elusive. To unravel this mystery, I mathematically modeled a growth cone exhibiting concentration-dependent attraction and repulsion to chemotactic cues. The model identified a novel growth cone guidance mechanism in topographic mapping, highlighting the importance of the growth cones unique ability to alternate between attraction and repulsion. Furthermore, an extension of the model provided possible molecular mechanisms for contrasting two types of topographic mappings observed in the retinotectal system.

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Neonatal immune challenge induces female-specific changes in social behavior and somatostatin cell number, independent of microglial inflammatory signaling

Decreases in social behavior are a hallmark aspect of acute "sickness behavior" in response to infection. However, immune insults that occur during the perinatal period may have long-lasting consequences for adult social behavior by impacting the developmental organization of underlying neural circuits. Microglia, the resident immune cells of the central nervous system, are sensitive to immune stimulation and play a critical role in the developmental sculpting of neural circuits, making them likely mediators of this process. Here, we investigated the impact of a postnatal day (PND) 4 lipopolysaccharide (LPS) challenge on social behavior in adult mice. Somewhat surprisingly, neonatal LPS treatment decreased sociability in adult female, but not male mice. LPS-treated females also displayed reduced social interaction and social memory in a social discrimination task as compared to saline-treated females. Somatostatin (SST) interneurons within the anterior cingulate cortex (ACC) have recently been suggested to modulate a variety of social behaviors. Interestingly, the female-specific changes in social behavior observed here were accompanied by an increase in SST interneuron number in the ACC. Finally, these changes in social behavior and SST cell number do not appear to depend on microglial inflammatory signaling, because microglia-specific genetic knock-down of myeloid differentiation response protein 88 (MyD88; the removal of which prevents LPS from increasing proinflammatory cytokines such as TNF and IL-1{beta}) did not prevent these LPS-induced changes. This study provides novel evidence for enduring effects of neonatal immune activation on social behavior and SST interneurons in females, independent of microglial inflammatory signaling.

neuroscience↗

Bidirectional modulation of pain-related behaviors in the zona incerta

Central amygdala neurons expressing protein kinase C-delta (CeA-PKC{delta}) are sensitized following nerve injury and promote pain-related responses in mice. The neural circuits underlying modulation of pain-related behaviors by CeA-PKC{delta} neurons, however, remain unknown. In this study, we identified a functional monosynaptic inhibitory neural circuit that originates in CeA-PKC{delta} neurons and terminates in the ventral region of the zona incerta (ZI), a subthalamic structure previously linked to pain processing. Behavioral experiments further show that chemogenetic inhibition of GABAergic ZI neurons is sufficient to induce bilateral hypersensitivity in uninjured mice as well as contralateral hypersensitivity after nerve injury. In contrast, chemogenetic activation of GABAergic ZI neurons reverses nerve injury-induced hypersensitivity, demonstrating that silencing of the ZI is required for injury-induced behavioral hypersensitivity. Our results identify a previously unrecognized inhibitory efferent pathway from CeA-PKC{delta} neurons to the ZI and demonstrate that ZI-GABAergic neurons can bidirectionally modulate pain-related behaviors in mice.

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Daily light-induced transcription in visual cortex neurons drives downward Firing Rate Homeostasis and stabilizes sensory processing

Balancing plasticity and stability in neural circuits is essential for an animals ability to learn from its environment while preserving the 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 2-photon imaging, we find that the daily appearance of light induces in excitatory neurons a large gene program along with rapid and transient shifts in the ratio of excitation and inhibition (E/I-ratio) and ongoing neural activity. Furthermore, we find that the light-induced transcription factor NPAS4 drives these daily normalizations of E/I-ratio and neural activity rates and that it stabilizes the neurons response properties. These findings indicate that daily sensory-induced transcription normalizes E/I-ratio and drives downward Firing Rate Homeostasis to maintain proper sensory processing and perception.

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