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Bronstein, H.

Publications and source records attributed to Bronstein, H..

2 recordsLinked to original sources

Developmental time course of social touch, parvalbumin interneurons, perineuronal nets and Mef2c expression reveals a sensitive period of somatosensory cortex development in prairie voles

Social touch facilitates our attachment to others, especially early in life, which may be linked to the maturation of parvalbumin interneurons (PVI) in the somatosensory cortex (S1). These neurons respond to social touch, mature in a sensory experience-dependent manner, and influence both somatosensory processing and social behavior in models of Autism Spectrum Disorder. Prairie voles (Microtus ochrogaster) are an ideal rodent model for studying these concepts since they engage in a species-typical social touch called "huddling". This study first showed that over development from juvenile to adult, same-sex siblings huddled less and explored more. Next, we tracked two markers of plasticity indicative of PVI maturation, extracellular perineuronal nets (PNNs) and nuclear transcription factor Myocyte enhancing factor 2C (Mef2c) - across seven developmental timepoints. We found that, while PV expression in S1 was stable by P21, PNNs and Mef2c continued to shift afterwards, indicating a protracted development. Four unique clusters of PVIs converge during development between P14-P21, suggesting a sensitive period of PVI development. Finally, to determine environmental factors affecting these processes, environmental enrichment between P21-P28 led to accelerated PVI maturation. This developmental mapping provides a particularly salient model to investigate the molecular underpinnings of cortical and social development.

neuroscience↗

Loss of cell cycle control renders cells nonresponsive to local extrinsic differentiation cues

Objective and approachesAberrantly proliferating cells are linked to a number of diseases including cancers and developmental defects.To determine the extent to which local extrinsic signals contribute to or ameliorate mutant cell behaviors, we examined survival and differentiation of mutant cells in wild-type retinal environments by generating chimeric zebrafish embryos comprised of unlabeled host cells and GFP-labeled neural progenitor donor cells. In addition, we examined the fate of retinal progenitor cells when cdkn1c, a cyclin dependent kinase inhibitor, was induced in clones within wild-type and hdac1 mutant retinae.\n\nResultsWe found that seven of the ten mutants examined exhibited apoptosis when grafted into wild-type tissue, with cells from two slowly cycling mutants, elys and emi1, noticeably differentiating in a wild-type environment. Observations of the one hyperproliferative mutant, hdac1, revealed that these mutant cells did not appear to die or differentiate but instead survived and formed tumor-like rosettes in a wild-type environment. Ectopic expression of cdkn1c was unable to force cell cycle exit and differentiation of the majority of hdac1 mutant cells.\n\nConclusionsTogether, these results suggest that although a wild-type environment rarely encourages cell cycle exit and differentiation of neural progenitors with cell cycle defects, wild-type survival signals may enable hyperproliferative progenitor cells to persist instead of die.

developmental biology↗