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Eiselt et al. report limitations on the ability of mice to assess their hunger and thirst states under conditions that model human decisions. Incorrect food-seeking in thirst may contribute to overeating. The cover illustrates the uncertainty of a thirsty mouse deciding between food and water.
Gene replacement therapies have shown remarkable advances recently, including onasemnogene abeparvovec for treatment of symptomatic and presymptomatic patients with spinal muscular atrophy. A recent report by Van Alstyne and colleagues in a mouse model of spinal muscular atrophy raises concerns that such treatment can generate toxic overexpression of SMN protein.
Sensory information encoding in the mouse brain is more suboptimal when mice make correct decisions than when they make incorrect ones. These suboptimal encoding structures can help information flow between different brain regions, enhancing the ability of these brain regions to work together to make decisions.
For decades, researchers have wondered whether algorithms used by artificial neural networks might be implemented by biological networks. Payeur et al. have strengthened the connection between neuroscience and artificial intelligence by showing that biologically plausible mechanisms can approximate key features of an essential artificial intelligence learning algorithm.
Eiselt et al. report conditions under which mice confuse thirst for hunger, similar to some human decisions that lead to over-eating. Evaluation of physiological need state requires consuming food or water and depends on the prefrontal cortex.
Biglari et al. reveal subgroups of arcuate nucleus hypothalamic neurons that exhibit distinct molecular signatures and feeding-regulatory functions, thus uncovering new regulatory principles in body weight control.
AAV9-SMN is used to treat SMA. This study shows that AAV9-mediated SMN overexpression in mice causes late-onset motor dysfunction and synaptic and neuronal loss through protein aggregation, suggesting caution on the long-term safety of SMN gene therapy.
Cell-type-specific chromatin accessibility QTL during neurogenesis allow fine mapping of causal variants and more complete underlying of regulatory mechanisms underlying noncoding loci associated with gene expression and neuropsychiatric disorders.
This bi-ancestral genome-wide association study of major depressive disorder (MDD) identified 178 risk variants. The results advance understanding of the biology of MDD and hint at new treatment possibilities.
Silva et al. reveal distinct circuits for the extinction of remote fear memories, with the thalamic nucleus reuniens and its outputs to the basolateral amygdala taking center stage.
Correlations in neural activity in association cortex can benefit behavioral performance in perceptual tasks, even when decreasing sensory information, by facilitating the propagation and the readout of information carried by population activity.
Optimal decision making in a changing world requires non-linear evidence accumulation. Murphy et al. report signatures of this adaptive computation in recurrent dynamics of human parietal and motor cortices, accompanied by feedback to sensory cortex.
Detecting stimulus changes requires different strategies than encoding stationary stimuli. Młynarski and Hermundstad extend efficient coding theory to non-stationary environments and derive adaptive codes that best balance these competing objectives.
The authors propose a synaptic plasticity rule for pyramidal neurons based on postsynaptic bursting that captures experimental data and solves the credit assignment problem for deep networks.
Tian et al. conducted a genome-wide CRISPRi/CRISPRa screen in human neurons and uncovered a neuron-specific link among prosaposin, lipofuscin and ferroptosis. The CRISPRbrain data commons enables comparison of gene function across human cell types.
The authors introduce advanced technology for controlled wireless light delivery in optogenetics applications with real-time user programming capacity. The utility of the platform is highlighted by induction of neural synchrony to modify social behavior in mice.