Topic: dendritic growth

Brain organoid technology is a pivotal tool for exploring human brain physiology and diseases. Despite its potential, current readout capabilities constrain brain organoid electrophysiological research. Classical microelectrode arrays (MEA) fall short in capturing data from intact organoids, which may flatten in the 2D-MEA surface, jeopardizing physiological responses and data validity. To overcome this, we pioneered a mesh MEA, preventing morphological deformations, fostering 3D growth, and facilitating electrical activity recording within intact organoids over an extended period. Electrophys

Early Life Stress (ELS) can result in enduring health consequences, highlighting the need for exploring timely intervention approaches. Our study aims to investigate whether metformin, a long-recognized diabetes medication with neuroprotective and neurotrophic potential, can mitigate ELS-induced disruptions in hippocampal neurogenesis and dendritic growth. To test this hypothesis, both male and female neonatal Wistar rats were allocated into four distinct groups: control, metformin treatment, ELS model, and ELS model with metformin treatment (ELS+M). During the initial two weeks, ELS model was

L-type voltage-gated calcium channels (L-VGCCs) are upstream of competing pathways that promote or inhibit dendritic growth. How L-VGCCs achieve signaling specificity remains unknown. We hypothesize that modulation of ICaL determines distinct processes controlling dendritic growth. To address this issue fluorescence imaging experiments were conducted on young murine cultured hippocampal neurons. Our findings show that dihydropyridine (DHP) blockers suppress dendritic growth and overexpression of DHP-insensitive CaV1.2 mutant prevented this effect, indicating that CaV1.2 is the channel isoform