Melanie Holmgren, Michael E Ravicz ... Lavinia Sheets
Mechanically induced injury of zebrafish lateral-line organs shares key features of damage observed in noise-exposed mammalian ears, such as inflammation and synapse loss, yet, unlike mammals, rapidly repairs following damage.
Mechanically activated Piezo1 ion channels, at physiologically relevant densities, behave as independent mechanotransducers, which we propose is essential for homogenous transduction of forces across the entire cell membrane.
People use vmPFC-dependent forward thinking to guide social choices and exploit the controllability of social environments, expanding the role of this neurocomputational mechanism beyond spatial and cognitive mapping.
Fast network oscillations in the mammalian main olfactory bulb emerge from the dense synchronization of gamma-frequency firing among resonant tufted cells.
Jakob Jordan, Maximilian Schmidt ... Mihai A Petrovici
Artificial evolution discovers biophysically plausible plasticity rules for spiking networks that perform competitively with and even outperform labor-intensive human-designed models in various learning scenarios, while providing new views on experimental data.
Striatal cholinergic interneurons and astrocytes lose cilia and show dysregulation of Hedgehog signaling in mice with a Parkinson's disease-associated, G2019S LRRK2 mutation or upon loss of PPM1H phosphatase specific for LRRK2-phosphorylated Rab GTPases.
Excitatory and inhibitory postsynaptic receptors are maintained at corresponded postsynaptic sites with the different dependency of presynaptic neurons in the mature mammalian brain.
Timothy T Rogers, Christopher R Cox ... Matthew A Lambon Ralph
Signals recorded directly from human anterior temporal cortex reveal that the brain represents animacy information using a distributed code that changes radically as a stimulus is processed, as predicted by an artificial neural network model.
Genetic disruption of sodium-hydrogen exchanger 6 (NHE6) reduces amyloid plaques in humanized Alzheimer's disease mouse models and restores normal synaptic responses to neuromodulatory input in humanized ApoE4-expressing animals.
