Optically Tunable Threshold Switching and Thermally Activated Transport in Planar Ag/MAPbI(3) Thin Single-Crystal Devices.

The mammalian cerebral cortex exhibits evolutionary diversity in size and shape, most noticeably in the formation of cortical folds. The evolution of cortical gyrification arises from tightly coordinated neurodevelopmental processes, including neural progenitor proliferation, differentiation, and neuronal migration, that collectively shape cortical architecture. Although phylogenetic evidence suggests that gyrencephaly is the ancestral mammalian condition and that lissencephaly in some lineages reflects secondary loss (Lewitus et al. ; Llinares-Benadero and Borrell ; Kelava et al. ), the molecular mechanisms that govern the emergence and regional patterning of cortical folds remain poorly understood. While fundamental aspects of cortical development remain conserved across mammals, species-specific differences in gene expression, the timing of neurogenesis, and biomechanical influences drive substantial variation in cortical morphology, particularly in the emergence and patterning of gyri and sulci (Pinson and Huttner ). The roles of founder progenitor populations, including radial glial cells (RGCs) and intermediate progenitor cells (IPCs), are largely conserved across species (Barresi et al. ; Del-Valle-Anton and Borrell ). However, comparative analyses reveal that basal radial glial cells (bRGCs), a specialised glial progenitor subtype, are essential for gyrification (Heide et al. ; Matsumoto et al. ). This process relies on the presence of an expanded outer subventricular zone (oSVZ), a proliferative compartment enriched with bRGCs that is characteristic of gyrencephalic species (de Juan Romero et al. ; Hansen et al. ; Reillo et al. ). bRGCs possess district molecular and functional profiles compared with other neural progenitor cells (Pollen et al. ). Transcriptomic analyses in humans, ferrets, and macaques, provide compelling cellular and genetic evidence implicating bRGCs as key drivers of cortical folding (de Juan Romero et al. ; Florio et al. , ; Singh et al. ; Del-Valle-Anton et al. ). Dysregulated bRGC function contributes to cortical malformations such as microcephaly (Wang et al. ), and abnormal gyrification is increasingly recognised as a feature of neurodevelopmental disorders including schizophrenia, autism spectrum disorders, and epilepsies such as Rett Syndrome (Keidar et al. ; Sasabayashi et al. ). Malformations of cortical development and folding result in alterations to neuronal circuitry and network connectivity, leading to behavioural impairments that vary in severity and presentation depending on the affected brain regions. Patients often exhibit a combination of motor, language, and social deficits, as seen in conditions such as cerebral palsy, and frequently experience early-onset neonatal seizures that persist into adulthood (Russ et al. ). Dysregulation of the molecular mechanisms that regulate RGC function, reviewed extensively by our group (Barresi et al. ), contribute to adverse neurodevelopmental and psychiatric outcomes. Despite significant advances, the molecular drivers of cortical folding remain incompletely defined. Given their role in brain development, understanding bRGC biology in both normal and pathological contexts is critical for understanding mechanism underlying cortical malformation and associated behavioural outcomes.