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The first postnatal week ends with the development of perisomatic innervation and with an abrupt switch in the representation of self-motion in the region CA1 of the mouse hippocampus.

The calibration of decision thresholds will provide evidence for the optimal use of in silico predictors for the standardised classification of globin gene variants under the American College of Medical Genetics and Genomics/Association for Molecular Pathology framework.

Comparison of the intracellular activity of hippocampal neurons in novel and familiar environments reveals experience-dependent changes in inputs underlying the formation of stable representations of space.

Large-scale imaging analysis of CA1 reveals that distinct neural networks are involved in trace conditioning versus extinction learning, shedding light on how the hippocampus encodes different types of memory.

The majority of hippocampal neurons in CA3 experience inhibition before and during ripple buildup, while dentate and CA1 cells display depolarizing transients preceding and following ripple onset pointing to a long and orchestrated awake ripple initiation process.

Embryonic birthdate is a crucial determinant of heterogeneity among CA1 principal neurons, which include a previously overlooked subpopulation of pioneer neurons.

CA1 physiology is altered in the hippocampus of Down syndrome mice during both spatial exploration and rest, paralleled by an increase in populations of interneurons responsible for single cell and network synchronization.

Specific inhibition of cyclin-dependent kinase-like 5 (CDKL5), a kinase linked to a severe neurodevelopmental disorder, demonstrates an important role in the regulation of excitatory hippocampal synapses and synaptic plasticity that was not previously appreciated in rodent knock-out models.

Studies in a mouse model of spinocerebellar ataxia type 1 show that a protein called capicua stabilizes toxic ataxin-1 oligomers offering a possible explanation for regional patterns of neurodegeneration.

Latrophilin-2 G protein coupling is required in axons but not target neurons for neural circuit assembly in the mouse hippocampus.