Publications by authors named "Kelsey Tyssowski"

Despite dynamic inputs, neuronal circuits maintain relatively stable firing rates over long periods. This maintenance of firing rate, or firing rate homeostasis, is likely mediated by homeostatic mechanisms such as synaptic scaling and regulation of intrinsic excitability. Because some of these homeostatic mechanisms depend on transcription of activity-regulated genes, including and , we hypothesized that activity-regulated transcription would be required for firing rate homeostasis.

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Optogenetics is widely used to control diverse cellular functions with light, requiring experimenters to expose cells to bright light. Because extended exposure to visible light can be toxic to cells, it is important to characterize the effects of light stimulation on cellular function in the absence of optogenetic proteins. Here we exposed mouse cortical cultures with no exogenous optogenetic proteins to several hours of flashing blue, red, or green light.

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Neurons transcribe different genes in response to different extracellular stimuli, and these genes regulate neuronal plasticity. Thus, understanding how different stimuli regulate different stimulus-dependent gene modules would deepen our understanding of plasticity. To systematically dissect the coupling between stimulation and transcription, we propose creating a 'stimulation-transcription coupling map' that describes the transcription response to each possible extracellular stimulus.

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A vast number of different neuronal activity patterns could each induce a different set of activity-regulated genes. Mapping this coupling between activity pattern and gene induction would allow inference of a neuron's activity-pattern history from its gene expression and improve our understanding of activity-pattern-dependent synaptic plasticity. In genome-scale experiments comparing brief and sustained activity patterns, we reveal that activity-duration history can be inferred from gene expression profiles.

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Article Synopsis
  • - Neural precursor cells (NPCs) in the developing neocortex produce different types of neurons in a specific sequence, and the timing of these changes is crucial for proper cortical structure and function.
  • - The research identifies Ring1B, a component of polycomb group proteins, as a key factor that regulates the end of subcerebral projection neuron (SCPN) production by influencing the expression of Fezf2, which is vital for SCPN identity.
  • - When Ring1B is deleted from NPCs, it leads to prolonged Fezf2 expression and increased generation of SCPNs, highlighting Ring1B's role in timing neuron subtype production in the developing brain.
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During mammalian CNS development, when the neural precursor cells commit to the neuronal fate they must delaminate and migrate toward the pial surface in order to reach the appropriate final location. Thus, the coordination of delamination and fate commitment is important in creating the correct structure. Although previous studies have proposed that spindle orientation during mitosis plays a role in both delamination and fate commitment, thus coordinating these events, subsequent studies have challenged this model.

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