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Lacagnina et al. show that extinction training suppresses the associated hippocampal fear engram and generates a distinct extinction engram. Reactivation of extinction engram cells reduces fear, while reactivation of fear engram cells causes fear relapse.
The Alzheimer’s disease (AD) amyloid-beta peptide causes oligodendrocyte progenitor cells to undergo senescence, contributing to neuroinflammation and cognitive impairment. Treatment of AD mice with senolytic drugs ameliorates AD neuropathologies and cognitive deficits.
The authors have identified a subpopulation of astrocytes that is enriched in cortical layer V of the mouse cortex and is also present in the human cortex. These cells express Norrin, a protein mutated in a rare neurological degenerative disease called Norrie disease. Norrin acts on neurons to modify their morphology and activity.
Sensory stimuli are recognized faster when they are expected. Comparing a spiking network model to cortical recordings from behaving animals, Mazzucato et al. show that expectation accelerates sensory processing by modulating the intrinsically generated activity preceding stimulation.
Using a novel assay, Ellis et al. show that stem cell-derived neurons from individuals with autism carrying SHANK2 mutations are hyperconnected, have impaired activity-dependent dendrite extension, and have perturbed transcription of ASD gene modules.
How grid cells’ geometric firing patterns arise remains unknown. This study shows preserved grid cell co-activity patterns across sleep that reflect grid field overlap during waking, suggesting that grid firing emerges from specific connectivity patterns.
Recording from cell ensembles in the medial entorhinal cortex, Gardner et al. show that the correlation structure of the grid cell system is preserved between awake and sleep states. This rigidity is a signature of continuous attractor networks.
Using a behaviorally obtained reference point to compute social value, Ma et al. show that social-value distance is encoded by the amygdala in prosocials. Oxytocin amplifies this amygdala representation and increases prosociality in individualists.
Apical tuft dendrites of pyramidal neurons in retrosplenial cortex receive inhibition from a class of CA1 GABAergic neurons with long-range layer 1-targeting axons; this inhibition opposes matrix-type thalamocortical excitation from anterior thalamus.
Clancy et al. investigated the relationship between individual neuron activity and cortex-wide dynamics. Neurons were diversely coupled to distal areas, and locomotion affected how neurons in different areas coupled with distal activity.
Animals must determine quickly whether any given environmental stimuli are beneficial or detrimental. This work reveals a novel strategy to encode opposing valences by a single population of CRF neurons in the hypothalamus.
A simple behavioral task identifies two qualitatively different groups within the general population, according to their speech-to-speech synchronization abilities. Group pertinence predicts brain function and anatomy, as well as word-learning performance.
Causal manipulations combined with simultaneous recordings of both interneurons and medium spiny neurons in the striatum reveal dissociable contributions of cholinergic and parvalbumin interneurons in movement initiation and termination.
Miller et al. show that subpopulations of D1 receptor-expressing neurons in the medial amygdala modulate approach–avoidance responses to threats through inhibitory and excitatory projections to the extended amygdala and hypothalamus, respectively.
The cellular origin of glioblastoma is controversial. Alcantara Llaguno et al. examine the tumor-initiating capacity of adult neuronal cells and find that increasing lineage commitment is accompanied by decreasing susceptibility to transformation.
Li et al. have discovered a necessary role for the DNA modification N6-methyldeoxyadenosine (m6dA) in regulating experience-dependent gene expression and the formation of fear extinction memory. These findings expand the scope of DNA modifications in the adult brain.
The authors report that mitophagy is impaired in Alzheimer’s disease. Stimulation of mitophagy reverses cognitive deficits in nematode and mouse models of Alzheimer’s disease, suggesting a potential therapeutic intervention.
Shen et al. show that FMRP promotes mitochondrial fusion through HTT. FMRP loss caused fragmented mitochondria and oxidative stress in immature neurons, and enhancing mitochondrial fusion rescued neuronal and behavioral deficits in Fmr1-mutant mice.
The authors found that white blood cells plug about 2% of capillaries in the brains of Alzheimer’s disease mouse models. When the adhesion of these cells was blocked, cerebral blood flow immediately increased and cognitive performance rapidly improved.
An interaction between UTX and 53BP1, which occurs in humans but not mice, promotes neurogenic gene expression that underlies neuronal differentiation and cortical development, perhaps providing insight into human-specific neurodevelopment.