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Oligodendrocyte precursor cells divide or differentiate in response to external stimuli to control their numbers and to form new myelin. Using zebrafish, we show that these two functions are accomplished by distinct subgroups of cells.
Wang et al. show that myelination is greatly inhibited in aged brains. Enhancing myelination by ablation of M1R in OPCs or clemastine treatment promotes oligodendroglial differentiation and consequently rescues spatial memory decline during aging.
Fear learning induces myelin formation. In the absence of new myelination, remote fear memory and neurophysiology of fear memory circuits are impaired. Conversely, administration of the pro-myelinating drug clemastine enhances remote fear memory.
The authors establish inducible Cxcr4-CreER-based fate mapping as a universal means to identify bone-marrow-derived myeloid cells in the injured brain and demonstrate that Cxcr4 deficiency affects the innate immune response and outcome after stroke.
Phase separation is emerging as a versatile means for cellular sub-compartment formation. Chen et al. review recent advances of dense synaptic assembly formation via phase separation and discuss implications of phase separation in synaptic physiology.
The authors identify an impaired myelination signature from the brains of mouse models of Pitt–Hopkins syndrome and show that it is shared in the postmortem brains of people with autism.
Microglia in the aging hippocampus accumulate lipid droplets, and are functionally impaired and inflamed. Lipid droplet formation in microglia is regulated by genes linked to neurodegeneration such as progranulin.
A chemogenetic approach was developed for cell-type-specific drug-inducible protein synthesis inhibition in mice. It was used to show that consolidation of long-term aversive memories requires rapid neuronal protein synthesis in the amygdala.
High concentrations of sodium are normally unpalatable. This study shows a neural population in the brainstem that suppresses appetite for sodium. Reducing the activity of these neurons can drive ingestion of high concentrations of sodium.
The authors measure evoked activity and perform dense reconstruction of the olfactory bulb wiring diagram in a zebrafish larva, uncovering a mechanism for whitening, a computation that decorrelates activity for pattern classification by memory networks.
Maes et al. use second-order conditioning, blocking and optogenetic inhibition to show that cue-evoked dopamine transients function as temporal-difference prediction errors rather than reward predictions.
Recent findings unveil a viral-like mechanism for the transmission of synaptic plasticity signals involving the activity-regulated cytoskeleton-associated protein (Arc). Arc forms capsid-like particles that package RNA and are transported across synapses. Here Erlendsson et al. present a high-resolution structural representation of Arc capsids, enabling deeper analysis of their function.
Rewards direct behavioral adaptation through midbrain dopamine signaling, though the timing of those effects is often ambiguous. Lee and colleagues find that different subpopulations of dopamine neurons obey similar constraints, indirectly regulating reward-related behavior through learning mechanisms restricted to a brief time window following reward.
Rees et al. show that de novo mutations in the gene SLC6A1, and more broadly across evolutionary constrained genes and genes implicated in neurodevelopmental disorders, increase the risk for developing schizophrenia.
Gao et al. provide evidence that two major classes of neurons exist in the paraventricular thalamus. One of these, termed type II PVT neurons, belongs to a previously ignored cell population that relays arousal information to the infralimbic cortex.
This resource comprises ultra-high-resolution MRI datasets and corresponding gray and white matter atlases of the marmoset brain to facilitate brain connectivity studies and the development of tractography algorithms in the primate brain.
In this study of protein-coding de novo mutations in schizophrenia, researchers found only a small contribution toward overall risk, coming predominantly from genes under negative selection and highly expressed in the brain.
In mice that have undergone Pavlovian reward conditioning, dopaminergic neurons regulate conditioned movements in a temporally restricted manner, consistent with a primary contribution to associative learning rather than online movement generation.