Updated January 5th, 2025
Research Spotlight
Disturbances in sleep are noted across a plethora of neuropsychiatric conditions. Many pharmaceuticals targeting mental illnesses also produce sleep side effects. Walder-Christensen et al. show that sleep states are reflected by the neural dynamics of canonical emotional encoding regions in mice. The sleep architecture reflected by these regions is altered by sleep-promoting drugs and chronic stress. These findings support the interconnected construction of sleep and affective internal state at the network level.
Dopaminergic neurotransmission is implicated in the extinction of fear memories. Gunduz-Cinar et al. show that the activity of midbrain dopamine neurons fails to show normal dynamic changes during fear extinction in a rodent model of impaired extinction. This finding could have translational relevance for understanding the neural basis of extinction-deficiency in various psychiatric disorders.
Neuroinflammation damages neurons and can contribute to diseases like Alzheimer’s. Cannabidiol (CBD) has anti-inflammatory properties, which suggests that it could combat neuroinflammation in Alzheimer’s. Babak Baban and colleagues, from Augusta University, explored whether CBD can be leveraged as an anti-inflammatory treatment in an established Alzheimer’s disease mouse model. The researchers assessed two distinct mechanisms for shaping immune responses and regulating neuroinflammation in the central nervous system following CBD treatment via inhalation. With several molecular and genetic measures, they discovered that CBD reduced expression of key regulators for neuroinflammation in Alzheimer’s mice, which was associated with less proinflammatory molecules. Baban et al. also identified distinct regulators of the immune response and neuroinflammation with which CBD interacted. “Alzheimer’s work has long centered on plaques and tangles,” says Baban. “But our study shows that chronic autoinflammation is also a core driver of the disease. What’s exciting is that CBD not only calms this immune overactivation but, in earlier work, we’ve shown it can also help clear plaques and tangles through a different mechanism. Together, this points to a multitarget approach with real therapeutic potential."
Using psychedelics to treat psychiatric diseases has become less controversial as scientists continue to reveal their underlying mechanisms. Researchers led by Pavel Ortinski, from the University of Kentucky, used male rats to assess how psychedelic drugs target the claustrum, a brain region with many receptors that psychedelics interact with. The researchers found that activating claustrum neurons targeting a cognitive area implicated in psychiatric diseases (the anterior cingulate cortex) under psychedelic drug exposure strengthened projections onto these claustrum neurons. This did not occur when activating the neurons in normal conditions. Says Ortinski, “One idea is that the intensely memorable experience common during psychedelic ‘trips’ is critical for success in psychiatric treatment. Neurons are thought to encode memories by strengthening their connections with other neurons, so this pathway may be the mechanism through which psychedelics intensify memories.” Ortinski hopes to continue exploring whether this mechanism contributes to the success of psychedelics in alleviating psychiatric disease symptoms.
Brian Kai Loong Man, from the Technical University of Denmark, led a study to explore effort during listening in noisy environments. Study participants performed listening tasks hearing sounds alone, seeing speakers and listening to their words, or only seeing the speakers with no audio. The researchers found that pupil size was an effective measure of effort, and that visual perception reduced the amount of effort needed to comprehend speech.
Most-Discussed Research Published in November and December
Below are five Early Release articles that generated the most online discussion in November and December of 2025, as measured by Altmetric. Altmetric data is available for all articles published in eNeuro on the Info & Metrics tab. Learn more about how the Altmetric score is calculated.
RNA localization establishes compartment-specific gene expression that is critical for synapse function. Thousands of mRNAs localize to the hippocampal synaptic neuropil; however, whether mRNAs are spatially organized as similar or distinctly composed ribonucleoprotein particles for delivery to synapses is unknown. Using multiplexed smFISH to assess the spatial organization of 15 neuropil localized mRNAs, we find that these mRNAs are present in variably sized puncta suggestive of heterogeneous transcript copy number states. RNA colocalization analyses in multiple hippocampal cell types suggest that the spatial relationship of these mRNAs is best described by their abundance in the neuropil. Stochastic RNA–RNA interactions based on neuropil abundance are consistent with models indicating that global principles, such as energy minimization, influence population localization strategies.
ADAP1/Centaurin-α1 (CentA1) is highly enriched in the brain, and an increased CentA1 level has been linked to Alzheimer's disease (AD). However, the precise role of CentA1 in the pathogenesis of AD is poorly understood. We found that genetic deletion of CentA1 in the AD model mice rescues the pathological hallmarks of AD, including loss of dendritic spines in the hippocampus, amyloid plaque deposition, neuroinflammation, and spatial memory deficits. Transcriptome analysis of the forebrain demonstrated that gene expression changes caused by APP overexpression were restored in J20 mice lacking CentA1. These findings support the role of CentA1 in AD progression.
Altered Dopamine Signaling in Extinction-Deficient Mice
This study investigated VTA-DA neuronal function in mice exhibiting deficient fear extinction.
Mirror-invariance is a perceptual bias to recognize mirrored objects as identical. Letters constitute a unique category of object: for example, ‘b’ and ‘d’ share identical shape yet must be identified as distinct entities to enable efficient reading. In our study, we investigated the neural underpinnings of tactile mirror-invariance in congenitally blind individuals and whether it was affected by tactile reading acquisition. We showed engagement of the parietal, occipital, and ventral visual regions in mirror-invariant tactile object recognition, indicating that this perceptual bias extends beyond the visual modality. Moreover, we found that unlike in the sighted, it was the parietal and lateral occipital cortex that showed neural signatures of breaking mirror-invariance for Braille letters in congenitally blind individuals, demonstrating, how following congenital visual deprivation, neural computations can be repurposed to meet novel task requirements.
Anxiety-associated behaviors following ablation of Miro1 from cortical excitatory neurons
Neuropsychological disorders such as autism spectrum disorder, schizophrenia, and bipolar disorder have overlapping endophenotypes. While the mechanisms underlying these disorders are poorly understood, recent evidence implicates mitochondrial dysfunction and cellular mis-localization playing a role. Mitochondria support energy requirements and other physiological functions in cells. Previous research from our lab has shown distinct dynamic localization patterns within migrating excitatory and inhibitory neurons during development. To further examine the importance of mitochondrial localization, we ablated MIRO1, a protein important for coupling mitochondria to motor proteins, in excitatory neurons. The mis-localization of mitochondria in migrating excitatory neurons is associated with diminished motor skills and anxiety-like behavior in post-natal mice.
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