LRRK2 G2019S knock-in mice are a genetically faithful model that recapitulates the slow disease progression of familial PD, with initial alterations to behaviour and neurotransmission providing early pathophysiological targets for neuroprotective interventions.
Individual neurons can adjust the strength of their synapses by using spontaneous calcium influx through NMDA receptors to trigger the release of additional calcium from intracellular stores, which can in turn be used to regulate protein synthesis.
Virus infection of the central nervous system disrupts the homeostasis of the immune-neural-synaptic axis via induction of pleiotropic genes with an unintended off-target negative impact on the neurotransmission.
Genetic and electrophysiological analyses reveal that the mechanisms orchestrating the induction and expression of homeostatic plasticity are compartmentalized and operate with exquisite specificity on both sides of the synapse.
Placing the PACAP/PAC1 signaling within glutamate/GABA cell type and subregional contexts in mouse brain reveals its conspicuous role for sensorimotor circuit interaction through modulating neuronal plasticity.
Axonal arborisation growth is regulated by dynamic, focal localisations of Neurexin and Neuroligin that provide stability for filopodia, enabling a 'stick and grow'-based mechanism, wholly independent of synapse formation.