Zdbf2 is a paternally expressed gene that is mainly expressed in the hypothalamus and promotes appetite and body weight gain in neonates.

Both hand and face representations remain relatively stable after arm amputation in adulthood, with no link to phantom limb pain, whereas pre-natal limb loss triggers complex patterns of remapping that do not relate to cortical topography.

Advanced machine learning based brain signal decoding of grip-force as a proxy for movement vigor shows Parkinson's disease related performance reduction, suggestive of a loss of cortical vigor encoding in the absence of dopamine.

A novel co-translational mechanism continuously adjusts the expression levels of ribosomal proteins Rpl3 and Rpl4 to their consumption during ribosome synthesis by regulating the abundance of their mRNAs.

A critical re-evaluation of some of the quintessential examples given as evidence for cortical reorganisation argues that, contrary to the prevalent view, any opportunities for functional change in cortical organisation are incremental and constrained by the underlying structural ‘blueprint'.

The reconstruction of a sensorimotor pathway from the olfactory-sensory neurons down to the pre-motor system reveals a descending neuron that plays a critical role in the organization of larval chemotaxis.

Ts65dn mice exhibit structural, functional, molecular, and genetic alterations that are modulated but unrecovered by prenatal chronic GTE-EGCG, highlighting the importance of holistic studies to understand complex disorders and treatments.

Active zone release probability is correlated with calcium channel density and calcium influx at single release sites, with release strength increasing in an activity-dependent manner during synapse maturation.

Cd59 and developmental inflammation are key players in myelinating glial cell development, highlighting the collaboration between glia and the innate immune system to ensure normal neural development.

Loss of functional dystroglycan disrupts the formation and function of CCK⁺/CB₁R⁺ inhibitory synapses in hippocampal CA1, resulting in reduced seizure thresholds in mouse models of dystroglycanopathy.