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Biology subjects

Slezak, M.

Publications and source records attributed to Slezak, M..

5 recordsLinked to original sources

Homecage-Like Monitoring Reveals Domain-Specific Rescue of Central SPTAN1 R1098Q Phenotypes by Wild-Type Partner Co-Housing

Neurodegenerative disorders manifest with markedly different phenotypes, with motor- and memory impairments dominating both clinical and preclinical phenotyping efforts. However, neurodegeneration in unlikely to be confined to these two functional domains alone, and its broader behavioral consequences, including social alterations remain underexplored. Here, we present a non-invasive, high-content home-cage phenotyping framework to investigate social and exploratory dysfunction in SPTAN1 R1098Q mice, a model of early infantile epileptic encephalopathy (EIEE5). Our pipeline integrates three open-source AI engines: SLEAP.ai for markerless multi-animal pose estimation, DeepOF for automated classification of autonomous and social behaviors, and SAM2 for segmentation and quantification of nest-building material usage. Long-term monitoring revealed that SPTAN1 R1098Q mutants exhibit impaired spatial habituation in mutant-mutant (MUT - MUT) pairs. Mutants also displayed persistent, unreciprocated trailing (following) of cage mates and a pronounced reduction of nest-building behavior alongside. Notably, co-housing with a wild-type littermate (MUT - WT) attenuated mutant hyperactivity and restored more typical rest pattern, suggesting that social context can partially buffer these behavioral abnormalities. By revealing social and exploratory alterations that expand conventional phenotyping, this computational ethology pipeline advances 3R principles while revealing that intrinsic executive state-switching failures in neurodegenerative models can be functionally buffered by social dynamics.

animal behavior and cognition↗

Glucocorticoid receptors mediate reprogramming of astrocytes in depression.

Psychiatric disorders are among the most pressing problems of the modern society, with various forms of depression affecting more than 300 millions of people worldwide. Dysfunction of glial cells has consistently been reported in major depressive disorder (MDD); however, no comprehensive resource detailing glial dysfunction is available. To provide insight into neurobiological mechanisms behind severe psychiatric symptoms, we performed transcriptional analysis of post-mortem samples from a subpopulation of suicide completers with previously reported glial abnormalities. We focused on BA25, a subregion of the prefrontal cortex prioritized for targeted medical interventions, due to its metabolic aberrations in disease. We found that a significant portion of genes deregulated in MDD is enriched in glia, with astrocyte-specific genes representing the highest fraction. Then we employed a novel protocol for enriching astrocytic nuclei to provide a detailed molecular signature of astrocytes in MDD. The analysis of the gene set revealed the glucocorticoid receptor (GR) as a key regulatory transcription factor. We found that astrocyte-specific elimination of the GR in mice largely prevented transcriptional, metabolic and behavioral changes elicited by chronic stress. We also demonstrated that regional manipulation of glutamate turnover in astrocytes suffices to elicit discrete traits of depressive-like behavior. Our data points to astrocytes as a key cellular site of convergence of multiple traits of depression and provide a resource for exploring novel targets for glia-focused therapeutic approaches.

neuroscience↗

Impact of Fkbp5 x Early Life Adversity x Sex in Humanized Mice on Multidimensional Stress Responses and Circadian Rhythmicity

The cumulative load of genetic predisposition, early life adversity (ELA) and lifestyle shapes the prevalence of psychiatric disorders. Single nucleotide polymorphisms (SNPs) in the human FKBP5 gene were shown to modulate disease risk. To enable investigation of disease-related SNPs in behaviorally relevant context, we generated humanized mouse lines carrying either the risk (AT) or the resiliency (CG) allele of the rs1360780 locus and exposed litters of these mice to maternal separation. Behavioral and physiological aspects of their adult stress responsiveness displayed interactions of genotype, early life condition and sex. In humanized females carrying the CG-but not the AT-allele, ELA led to altered HPA-axis functioning, exploratory behavior and sociability. These changes correlated with differential expression of genes in the hypothalamus, where synaptic transmission, metabolism, and circadian entrainment pathways were deregulated. Our data suggest an integrative role of FKBP5 in shaping the sex-specific outcome of ELA in adulthood.

neuroscience↗

Flexible, fast and selective genetic manipulation of the vertebrate CNS with misPiggy

In utero electroporation is increasingly used for manipulation of gene expression in the mammalian central nervous system. Here we created a transposon-based single plasmid system, that allows long-term conditional loss- and gain-of-function experiments across major CNS cell types. The system is widely applicable across species, allowing fast, flexible and cheap cell manipulation in previously non-transgenic species.

neuroscience↗

Astrocytes integrate local sensory and brain-wide neuromodulatory signals.

Astrocytes play multiple functions in the central nervous system, from control of blood flow through to modulation of synaptic activity. Transient increases in intracellular Ca2+ are thought to control these activities. The prevailing concept is that these Ca2+ transients are triggered by distinct pathways, with little mechanistic and functional overlap. Here we demonstrate that astrocytes in visual cortex of mice encode local visual signals in conjunction with arousal state, functioning as multi-modal integrators. Such activity adds an additional layer of complexity to astrocyte function and may enable astrocytes to specifically and subtly regulate local network activity and plasticity.

neuroscience↗