Biology subjects

Tripathy, S.

Publications and source records attributed to Tripathy, S..

At least 19 recordsLinked to original sources

bioRxiv2026

Choriodecidual Ureaplasma parvum infection induces fetal lung inflammation prior to intra-amniotic infection in a nonhuman primate model

Preterm birth before 28 weeks remains a leading cause of neonatal mortality and long-term morbidity. Intrauterine infection-driven chorioamnionitis is strongly associated with preterm labor, fetal inflammatory response syndrome, and neonatal lung disease. Ureaplasma species are among the most common organisms isolated in chorioamnionitis and are frequently detected in the placenta, amniotic fluid, and respiratory tract of preterm infants. Clinical and experimental data implicate Ureaplasma exposure in early lung inflammation, impaired alveolar development, and bronchopulmonary dysplasia (BPD), yet the pathogenic events preceding microbial invasion of the amniotic cavity or fetal tissues remain poorly defined. To characterize early intrauterine and fetal lung inflammatory responses to localized choriodecidual U. parvum infection, we used a chronically catheterized pregnant rhesus macaque (Macaca mulatta) model. Time-mated animals underwent surgical placement of maternal, amniotic, and choriodecidual catheters and were inoculated with low-passage U. parvum serovar 1 or vehicle control at approximately 117 days gestational age. Placenta, fetal membranes, fetal plasma, and fetal lungs were assessed by qRT-PCR, multiplex cytokine assays, immunoblotting, immunohistochemistry, and trichrome staining to evaluate inflammatory signaling, inflammasome activation, prostaglandin pathways, immune cell infiltration, fibrosis, and lung maturation markers. Choriodecidual infection was confirmed in all inoculated animals. Amniotic fluid remained culture-and PCR-negative, and fetal lungs were largely free of detectable bacterial DNA. Despite the absence of intra-amniotic infection, fetal lung cytokine profiling revealed broad pro-inflammatory activation, with elevated GM-CSF, IL-1{beta}, IL-6, IL-8, MIP-1/{beta}, MCP-1, VEGF and reduced IL-10 contrasting with a modest systemic response limited to elevated plasma IL-18. Fetal lungs showed increased immune cell infiltration, upregulation of NLRP3, PYCARD, and CASP1, and activation of SAPK/JNK and NF-{kappa}B signaling. Histopathology demonstrated increased alveolar macrophages and intra-alveolar neutrophils with minimal fibrosis. Surfactant gene expression was altered (increased SFTPA, decreased SFTPB), and elevated -SMA indicated early myofibroblast activation. Localized choriodecidual U. parvum infection induces fetal lung inflammation prior to detectable intra-amniotic infection, demonstrating that direct infection of the amniotic fluid or fetal lung is not required for the initiation of fetal pulmonary inflammation. These findings suggest that subclinical ascending infection may initiate fetal lung injury and increase susceptibility to postnatal respiratory morbidity associated with preterm birth.

physiology↗

bioRxiv2026

Impacts of heminode disruption on auditory processing of noisy sound stimuli

Hidden hearing loss (HHL) is an auditory neuropathy characterized by altered auditory nerve responses despite normal hearing thresholds. Recent experimental and computational studies suggest that permanent disruptions to heminode positions in spiral ganglion neuron (SGN) fibers can contribute to these deficits. However, the interaction between heminode disruption and noisy backgrounds ubiquitous in daily listening remains unexplored. This study investigates how background noise affects auditory processing with these peripheral disorders and how deficits propagate to downstream sound localization circuits in the superior olivary complex. We developed computational models of SGN fibers with mild and severe degrees of heminode disruption, subjected to sinusoidal tone stimuli in the presence of background noise with varying spectral characteristics. We analyzed the phase-locking of SGN fiber responses to the stimulus tone and modeled the subsequent effects on interaural time difference (ITD) sensitivity in the medial superior olive (MSO) using a binaural localization network. We found that near-tone-frequency noise disrupted SGN phase locking through cycle-to-cycle variability in spike phases, with effects consistent across tone frequencies. Mild heminode disruption produced frequency-dependent degradation in SGN phase locking, with effects observed only at higher frequencies tested (600-1000 Hz), without reducing overall firing rates. Critically, the effects of noise and heminode disruption were additive, with combined exposure leading to reduced ITD sensitivity and large temporal fluctuations in MSO responses. Severe heminode disruption, which additionally reduced firing rates at the SGN fibers and subsequent stages, produced profound localization deficits across all frequencies tested. Thus, our model results suggest that noisy environments exacerbate auditory deficits from peripheral disorders implicated in HHL and could potentially impair speech intelligibility through degradation in localization ability. This model may be useful for understanding the downstream impacts of SGN neuropathies.

neuroscience↗

bioRxiv2026

Spatial dynamics of cellular and molecular plasticity in the maternal and postpartum mouse brain

Pregnancy is a critical window for neuroplasticity and maternal mental health, yet our understanding of the molecular and cellular changes underlying this adaptation remains incomplete. Here we profile the female mouse brain in nulliparous, late-pregnant and postpartum states with three single-cell spatial technologies (Slide-tags, MERFISH and Xenium). Together these assays resolve 1.5 million cells in one coronal plane spanning the cortex, striatum, lateral septum and preoptic area. Pregnancy is associated with changes in gene expression in most cell types, beyond the circuits previously established to govern maternal behavior. These changes resolve into three programs that are reproducible across platforms: synaptic pathways increase in neurons as growth and plasticity pathways decrease; immune and angiogenic pathways increase in glia and vascular cells; and cholesterol synthesis decreases as uptake increases across both neurons and glia. Finally, mapping human depression genetics onto these data, we find risk genes concentrated almost entirely in neurons, and this concentration changes with reproductive state in the preoptic area, basal forebrain and ventral striatum. These results place the neurons carrying depression risk among the circuits remodeled during pregnancy, providing a possible cellular substrate for peripartum vulnerability.

genomics↗

bioRxiv2025

Linking age changes in human cortical microcircuits to impaired brain function and EEG biomarkers

Human brain aging involves a variety of cellular and synaptic changes, but how these changes affect brain function and signals remains poorly understood due to experimental limitations in humans, meriting the use of detailed computational models. We identified key human cellular and synaptic changes occurring with age from previous studies, including a loss of inhibitory cells, NMDA receptors, and spines. We integrated these changes into our detailed human cortical microcircuit models and simulated activity in middle-age ([~]50 yrs) and older ([~]70 yrs) microcircuits, and linked the altered mechanisms to reduced spike rates and impaired signal detection. We then simulated EEG potentials arising from the microcircuit activity and found that the emergent power spectral changes due to these aging cellular mechanisms reproduced most of the resting-state EEG biomarkers seen in human aging, including reduced aperiodic offset, exponent, and periodic peak center frequency. Using machine learning, we demonstrated that the changes to the cellular and synaptic aging mechanisms can be estimated accurately from the simulated EEG aging biomarkers. Our results link cellular and synaptic mechanisms of aging with impaired cortical function and physiological biomarkers in clinically-relevant brain signals.

neuroscience↗

bioRxiv2024

Molecular architecture of human dermal sleeping nociceptors

Human dermal sleeping nociceptors display ongoing activity in neuropathic pain, affecting 10% of the population. Despite advances in rodents, a molecular marker for these mechano-insensitive C-fibers (CMis) in human skin remains elusive, preventing targeted therapy. In this translational Patch-seq study, we combine single-cell transcriptomics following electrophysiological characterization with single-nucleus and spatial transcriptomics from pigs and humans. We functionally identified CMis in pig sensory neurons with patch-clamp using adapted protocols from human microneurography. We identified oncostatin-M-receptor (OSMR) and somatostatin (SST) as marker genes for CMis. Following dermal injection in healthy human volunteers, oncostatin-M, the ligand of OSMR, exclusively modulates CMis. We identified the entire molecular architecture of human dermal sleeping nociceptors, providing new therapeutic targets and the basis for a mechanistic understanding of neuropathic pain. One Sentence SummaryWe identify the molecular architecture and specifically OSMR and SST as molecular markers for human dermal sleeping nociceptors, key players in the generation of neuropathic pain. Short versionIn this Patch-seq study, we identify OSMR and SST as molecular markers for human dermal sleeping nociceptors, key players in the generation of neuropathic pain.

neuroscience↗

bioRxiv2024

Single neuron diversity supports area functional specialization along the visual cortical pathways

Humans and other primates have specialized visual pathways composed of interconnected cortical areas. The input area V1 contains neurons that encode basic visual features, whereas downstream in the lateral prefrontal cortex (LPFC) neurons acquire tuning for novel complex feature associations. It has been assumed that each cortical area is composed of repeatable neuronal subtypes, and variations in synaptic strength and connectivity patterns underlie functional specialization. Here we test the hypothesis that diversity in the intrinsic make-up of single neurons contributes to area specialization along the visual pathways. We measured morphological and electrophysiological properties of single neurons in areas V1 and LPFC of marmosets. Excitatory neurons in LPFC were larger, less excitable, and fired broader spikes than V1 neurons. Some inhibitory fast spiking interneurons in the LPFC had longer axons and fired spikes with longer latencies and a more depolarized action potential trough than in V1. Intrinsic bursting was found in subpopulations of both excitatory and inhibitory LPFC but not V1 neurons. The latter may favour temporal summation of spikes and therefore enhanced synaptic plasticity in LPFC relative to V1. Our results show that specialization within the primate visual system permeates the most basic processing level, the single neuron.

neuroscience↗

bioRxiv2024

Spike frequency adaptation in primate lateral prefrontal cortex neurons results from interplay between intrinsic properties and circuit dynamics

Recordings of cortical neurons isolated from brain slices and dissociated from their networks, display intrinsic spike frequency adaptation (I-SFA) to a constant current input. Interestingly, extracellular recordings in behaving subjects also show extrinsic-SFA (E-SFA) in response to sustained visual stimulation. Because neurons are isolated from brain networks in slice recordings, it is challenging to infer how I-SFA contributes to E-SFA in interconnected brains during behavior. To investigate this, we recorded responses of macaque lateral prefrontal cortex neurons in vivo during a visually guided saccade task and in acute brain slices in vitro. Broad spiking (BS) putative pyramidal cells and narrow spiking (NS) putative inhibitory interneurons exhibited E-SFA in vivo. In acute brain slices, both cell types displayed I-SFA though their magnitudes differed. To investigate how in vitro I-SFA contributes to in vivo E-SFA, we developed a data-driven hybrid circuit model in which local NS neurons are driven by BS input. We observed that model NS cell responses show longer SFA than observed in vivo. Introducing inhibition of NS cells to the model circuit removed this discrepancy. Our results indicate that both I-SFA and inhibitory circuit dynamics contribute to E-SFA in LPFC neurons. They highlight the contribution of single neuron and network dependent computations to neural activity underlying behavior.

neuroscience↗

bioRxiv2024

Perinatal Brain Injury Triggers Niche-Specific Changes to Cellular Biogeography

Preterm infants are at risk for brain injury and neurodevelopmental impairment due, in part, to white matter injury following chronic hypoxia exposure. However, the precise molecular mechanisms by which perinatal hypoxia disrupts early neurodevelopment are poorly understood. Here, we constructed a brain-wide map of the regenerative response to newborn brain injury using high-resolution imaging-based spatial transcriptomics to analyze over 1.3 million cells in a mouse model of chronic neonatal hypoxia. Additionally, we developed a new method for inferring condition-associated differences in cell type spatial proximity, enabling the identification of niche-specific changes in cellular architecture. We observed hypoxia-associated changes in region-specific cell states, cell type composition, and spatial organization. Importantly, our analysis revealed mechanisms underlying reparative neurogenesis and gliogenesis, while also nominating pathways that may impede circuit rewiring following perinatal hypoxia. Altogether, our work provides a comprehensive description of the molecular response to newborn brain injury.

neuroscience↗

bioRxiv2023

Fetal Membrane Inflammasome Activation by Choriodecidual Ureaplasma parvum Infection without Intra-Amniotic Infection in an NHP Model

Intrauterine infection is a significant cause of preterm labor and neonatal morbidity and mortality. Ureaplasma parvum is the micro-organism most commonly isolated from cases of preterm birth and preterm premature rupture of membranes (pPROM). However, the mechanisms during the early stages of ascending reproductive tract infection that initiate maternal-fetal inflammatory pathways, preterm birth and pPROM remain poorly understood. To examine inflammation in fetal (chorioamnionic) membranes in response to Ureaplasma parvum infection, we utilized a novel in vivo non-human primate model of early choriodecidual infection. Eight chronically catheterized pregnant rhesus macaques underwent maternal-fetal catheterization surgery at 105-112 days gestation and choriodecidual inoculation with Ureaplasma parvum (105cfu/mL of a low passaged clinical isolate, serovar 1; n=4) or saline/sterile media (Controls; n=4) starting at 115-119 days gestation, repeated every 5 days until scheduled cesarean-section at 136-140d gestation (term=167d). The average inoculation to delivery interval was 21 days and Ureaplasma infection of the amniotic fluid was undetectable by culture and PCR in all animals. Inflammatory mediators in amniotic fluid (AF) were assessed by Luminex, ELISA and multiplex assays. RNA was extracted from the chorion and amnionic membranes for single gene analysis (qRT-PCR) and protein expression was determined by Western blot and immunohistochemistry. Our NHP model of choriodecidual Ureaplasma infection, representing an early-stage ascending reproductive tract infection without microbial invasion of the amniotic cavity, resulted in increased fetal membrane protein and gene expression of MMP-9 and PTGS2, but did not result in preterm labor (no increase in uterine contractility) or increased concentrations of amniotic fluid pro-inflammatory cytokines (IL-1{beta}, IL-6, IL-8, IL-18, TNF-). However, membrane expression of inflammasome sensor molecules, NLRP3, NLRC4, AIM2 and NOD2, and the adaptor protein ASC (PYCARD) gene expression were significantly increased in the Ureaplasma group when compared to non-infected controls. Gene expression of IL-1{beta}, IL-18, the IL-18R1 receptor, CASPASE-1 and pro-CASPASE-1 protein were also increased in the fetal membranes with Ureaplasma infection. Downstream inflammatory signaling genes MYD88 was also significantly upregulated in both the amnion and chorion, along with a significant increase in NFKB in the chorion. These results demonstrate that even at the early stages of ascending reproductive tract Ureaplasma infection, activation of inflammasome complexes and pathways associated with degradation of chorioamnionic membrane integrity are present. This study therefore provides experimental evidence for the importance of the early stages of ascending Ureaplasma infection in initiating processes of pPROM and preterm labor. These findings have implications for the identification of intrauterine inflammation before microbes are detectable in the amniotic fluid (sterile inflammation) and the timing of potential treatments for preterm labor and fetal injury caused by intrauterine infection.

physiology↗

bioRxiv2022

Chrna5 is a marker of acetylcholine super-responder subplate neurons with specialized expression of nicotinic modulator proteins

Attention depends on cholinergic excitation of prefrontal neurons but is sensitive to perturbation of 5-containing nicotinic receptors encoded by Chrna5. However, Chrna5-expressing (Chrna5+) neurons remain enigmatic, despite their potential as a target to improve attention. Here, we generate complex transgenic mice to probe Chrna5+ neurons and their sensitivity to endogenous acetylcholine. Through opto-physiological experiments, we discover that Chrna5+ neurons contain a distinct population of acetylcholine super-responders. Leveraging single-cell transcriptomics, we discover molecular markers conferring subplate identity on this subset. We determine that Chrna5+ super-responders express a unique complement of GPI-anchored lynx prototoxin genes (Lypd1, Ly6g6e, and Lypd6b), predicting distinct nicotinic receptor regulation. To manipulate lynx regulation of endogenous nicotinic responses, we developed a pharmacological strategy guided by transcriptomic predictions. Overall, we reveal Chrna5-Cre mice as a transgenic tool to target the diversity of subplate neurons in adulthood, yielding new molecular strategies to manipulate their cholinergic activation relevant to attention disorders.

neuroscience↗

bioRxiv2022

Common genetic variants in CHRNA5 alter β-amyloid neuropathology and highlight chandelier cells in human aging and Alzheimer's disease

Changes in high-affinity nicotinic acetylcholine receptors are intricately connected to neuropathology in Alzheimers Disease (AD). Protective and cognitive-enhancing roles for the nicotinic 5 subunit have been identified, but this gene has not been closely examined in the context of human aging and dementia. Therefore, we investigate the nicotinic 5 gene CHRNA5 and the impact of relevant single nucleotide polymorphisms (SNPs) in prefrontal cortex from 922 individuals with matched genotypic and post-mortem RNA sequencing in the Religious Orders Study and Memory and Aging Project (ROS/MAP). We find that a genotype robustly linked to increased expression of CHRNA5 (rs1979905A2) predicts significantly reduced cortical {beta}-amyloid load. Intriguingly, co-expression analysis suggests CHRNA5 has a distinct cellular expression profile compared to other nicotinic receptor genes. Consistent with this prediction, single nucleus RNA sequencing from 22 individuals reveals CHRNA5 expression is disproportionately-elevated in chandelier neurons, a distinct subtype of inhibitory neuron known for its role in excitatory/inhibitory (E/I) balance. We show that chandelier neurons are enriched in amyloid-binding proteins compared to basket cells, the other major subtype of PVALB-positive interneurons. Consistent with the hypothesis that nicotinic receptors in chandelier cells normally protect against {beta}-amyloid, cell-type proportion analysis from 549 individuals reveals these neurons show amyloid-associated vulnerability only in individuals with impaired function/trafficking of nicotinic 5-containing receptors due to homozygosity of the missense CHRNA5 SNP (rs16969968A2). Taken together, these findings suggest that CHRNA5 and its nicotinic 5 subunit exert a neuroprotective role in aging and Alzheimers disease centered on chandelier interneurons.

neuroscience↗

bioRxiv2021

In-vitro Reconstitution of Membrane Contact Sites between the Endoplasmic Reticulum and Lipid Droplets

Coordinated cell function requires inter-organelle communication across Membrane Contact Sites (MCS). Here we deposit ER-enriched microsomes purified from rat liver or from cultured cells on a coverslip in the form of a continuous planar membrane. We visualize real-time protein and lipid exchanges across MCS that form between this ER-mimicking membrane and lipid droplets purified from rat liver. An Optical trap is used to demonstrate physical tethering of individual lipid droplets to the ER-mimicking membrane at MCS, and to directly measure the strength of this tether. In-vitro MCS formation changes dramatically in response to metabolic state and immune activation in the animal. Surprisingly, we find that the Rab18 GTPase and Phosphatidic acid are common molecular factors to control both of these pathways. This assay could possibly be adapted to interrogate MCS formation between other membranes (e.g. mitochondria, peroxisomes, endosomes etc.), and abnormalities therein that cause neurological, metabolic and pathogenic diseases.

cell biology↗

bioRxiv2020

The Neuron Phenotype Ontology: A FAIR Approach to Proposing and Classifying Neuronal Types

The challenge of defining and cataloging the building blocks of the brain requires a standardized approach to naming neurons and organizing knowledge about their properties. The US Brain Initiative Cell Census Network, Human Cell Atlas, Blue Brain Project, and others are generating vast amounts of data and characterizing large numbers of neurons throughout the nervous system. The neuroscientific literature contains many neuron names (e.g. parvalbumin-positive interneuron or layer 5 pyramidal cell) that are commonly used and generally accepted. However, it is often unclear how such common usage types relate to the many proposed evidence-based types that are based on the results of new techniques. Further, comparing different models across labs remains a significant challenge. Here, we propose an interoperable knowledge representation, the Neuron Phenotype Ontology (NPO) that provides a standardized and machine computable approach for naming and normalizing phenotypes in cell types by using community ontology identifiers as a common language. The NPO provides a framework for systematically organizing knowledge about cellular properties and enables interoperability with existing neuron naming schemes. We evaluate the NPO by populating a knowledge base with three independent cortical neuron classifications derived from published data sets that describe neurons according to molecular, morphological, electrophysiological and synaptic properties. Competency queries to this knowledge base demonstrate that this knowledge model enables interoperability between the three test cases and common usage neuron names from the literature.

neuroscience↗

bioRxiv2019

Sag currents are a major contributor to human pyramidal cell intrinsic differences across cortical layers and between individuals

In the human neocortex coherent interlaminar theta oscillations are driven by deep cortical layers, suggesting neurons in these layers exhibit distinct electrophysiological properties. To characterize this potential distinctiveness, we use in vitro whole-cell recordings from cortical layers 2 and 3 (L2&3), layer 3c (L3c) and layer 5 (L5) of the human cortex. Across all layers we observe notable heterogeneity, indicating human cortical pyramidal neurons are an electrophysiologically diverse population. L5 pyramidal cells are the most excitable of these neurons and exhibit the most prominent sag current (abolished by blockade of the hyperpolarization activated cation current, Ih). While subthreshold resonance is more common in L3c and L5, we rarely observe this resonance at frequencies greater than 2Hz. However, the frequency dependent gain of L5 neurons reveals they are most adept at tracking both delta and theta frequency inputs, a unique feature that may indirectly be important for the generation of cortical theta oscillations.

neuroscience↗

bioRxiv2019

Transcriptomic correlates of electrophysiological and morphological diversity within and across neuron types

In order to further our understanding of how gene expression contributes to key functional properties of neurons, we combined publicly accessible gene expression, electrophysiology, and morphology measurements to identify cross-cell type correlations between these data modalities. Building on our previous work using a similar approach, we distinguished between correlations which were \"class-driven,\" meaning those that could be explained by differences between excitatory and inhibitory cell classes, and those that reflected graded phenotypic differences within classes. Taking cell class identity into account increased the degree to which our results replicated in an independent dataset as well as their correspondence with known modes of ion channel function based on the literature. We also found a smaller set of genes whose relationships to electrophysiological or morphological properties appear to be specific to either excitatory or inhibitory cell types. Next, using data from Patch-seq experiments, allowing simultaneous single-cell characterization of gene expression and electrophysiology, we found that some of the gene-property correlations observed across cell types were further predictive of within-cell type heterogeneity. In summary, we have identified a number of relationships between gene expression, electrophysiology, and morphology that provide testable hypotheses for future studies.

neuroscience↗

bioRxiv2018

Macrophage-induced rifampin tolerance across Mycobacterium tuberculosis lineages is Rv1258c-dependent

The Mycobacterium tuberculosis (Mtb) Lineage 4 strains CDC1551 and H37Rv develop tolerance to multiple antibiotics upon macrophage residence. Genetic mutation of the efflux pump Rv1258c in CDC1551 abolishes rifampin tolerance but not isoniazid tolerance. Here we show that clinical isolates from the other predominant Mtb lineages developed macrophage-induced isoniazid tolerance. Furthermore, all lineages developed rifampin tolerance except Lineage 2 Beijing strains, which are natural Rv1258c mutants. Thus macrophage-induced antibiotic tolerance is featured across the majority of Mtb lineages. Our findings further link Rv1258c to rifampin tolerance among clinical isolates.

microbiology↗

bioRxiv2018

Data-driven approaches for improving the interpretability of patch-seq data

Patch-seq, enabling simultaneous measurement of a transcriptomic, electrophysiological, and morphological features, has recently emerged as a powerful tool for neuronal characterization. However, we show the method is susceptible to technical artifacts, including the presence of mRNA contaminants from multiple cells, that limit the interpretability of the data. We present a straightforward marker gene-based approach for controlling for these artifacts and show that our method improves the correspondence between gene expression and electrophysiological features.

neuroscience↗

bioRxiv2016

NeuroExpresso: A cross-laboratory database of brain cell-type expression profiles with applications to marker gene identification and bulk brain tissue transcriptome interpretation

The identification of cell type marker genes, genes highly enriched in specific cell types, plays an important role in the study of the nervous system. In particular, marker genes can be used to identify cell types to enable studies of their properties. Marker genes can also aid the interpretation of bulk tissue expression profiles by revealing cell type specific changes.\n\nWe assembled a database, NeuroExpresso, of publicly available mouse brain cell type-specific gene expression datasets. We then used stringent criteria to select marker genes highly expressed in individual cell types. We found a substantial number of novel markers previously unknown in the literature and validated a subset of them using in silico analyses and in situ hybridization. We next demonstrate the use of marker genes in analysis of whole tissue data by summarizing their expression into \"cell type profiles\" that can be thought of as surrogates for the relative abundance of the cell types across the samples studied.\n\nFurther analysis of our cell type-specific expression database confirms some recent findings about brain cell types along with revealing novel properties, such as Ddc expression in oligodendrocytes. To facilitate further use of this expanding database, we provide a user-friendly web interface for the visualization of expression data.\n\nSignificance StatementCell type markers are powerful tools in the study of the nervous system that help reveal properties of cell types and acquire additional information from large scale expression experiments. Despite their usefulness in the field, known marker genes for brain cell types are few in number. We present NeuroExpresso, a database of brain cell type specific gene expression profiles, and demonstrate the use of marker genes for acquiring cell type specific information from whole tissue expression. The database will prove itself as a useful resource for researchers aiming to reveal novel properties of the cell types and aid both laboratory and computational scientists to unravel the cell type specific components of brain disorders.

neuroscience↗