Felix Lankester, Tito J Kibona ... Sarah Cleaveland
Livestock abortion surveillance can capture valuable information on important livestock pathogens, including those that are zoonotic and with epidemic potential, revealing importance of timely collection of diagnostic samples for attribution.
Maryam Rahimi-Balaei, Shayan Amiri ... Hassan Marzban
A distinct subset of cerebellar nuclei neurons originates from a previously unrecognized germinal zone within the cerebellar primordium, independent of Atoh1 influence, highlighting new cellular origins in cerebellar development.
Co-release of the functionally opposing fast neurotransmitters, glutamate and GABA, from distinct synaptic vesicles within the same supramammillary synaptic terminal modulates dentate granule cell firing in a frequency-dependent manner.
An accurate and efficient biologically plausible statistical model of the spiking activity of neural populations shows computational benefits of homeostatic synaptic scaling in learning large neural population codes.
In astrocytes, there exists an intrinsic spatial threshold of subcellular calcium levels that triggers an astrocyte calcium surge throughout the cell, demonstrating cellular astrocyte calcium integration of time and space.
Neurodegeneration driven by pathogenic aggregating proteins reorganizes the actin cytoskeleton, causing cellular stiffening and abolishing force generation required for endocytic events.
Kiss1ARH neurons transition from synchronous to burst firing under preovulatory levels of E2, causing a shift from peptidergic to glutamatergic transmission that drives the GnRH surge through enhanced glutamate neurotransmission.
Subhradip Das, Sushmitha Hegde ... Girish S Ratnaparkhi
During Drosophila primordial germ cells (PGCs) specification, the centrosome and germplasm are subject to regulation, during the maternal zygotic transition, by Caspar/TER94-dependent degradative pathways that influence PGC determinants.
Studies with mice and brain organoids models reveals that dysregulation of GTF2IRD1-TTR-ERK pathway significantly contributes to neuronal deficits of Williams syndrome.
