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In this study, the authors recorded from the cerebellum while monkeys experienced an illusory perception of self-motion, and found that the neurons encoded the erroneous linear acceleration. Their findings provide evidence that the cerebellum might be involved in the implementation of internal models, as previously hypothesized by theorists.
Using optogenetics and other methods in the zebrafish olfactory bulb, the authors explore the role of interneurons that are densely connected to mitral cells (MCs) by both electrical and chemical synapses. These interneurons maintain the mean and distribution of MC population activity within narrow limits as stimulus intensity changes.
The authors show that shortening of the basal process in neural progenitor cells by depletion of TAG-1 results in overcrowding in the periventricular space and, eventually, delamination and aberrant migration. These results suggest that one of the functions of interkinetic nuclear migration is to prevent progenitor congestion and mechanical stress.
The authors find that optogenetic stimulation of melanin-concentrating hormone (MCH)-expressing neurons in the lateral hypothalamus selectively extends the duration of paradoxical sleep episodes in mice. Activation of MCH fibers in the tuberomammillary nucleus leads to the release of GABA and a similar increase in paradoxical sleep stability.
There is currently no effective treatment for infantile neuronal ceroid lipofuscinosis, a neurodegenerative lysosomal storage disease that occurs in childhood. Here the authors show that a small molecule thioesterase-mimetic can alleviate neuropathology and extend lifespan in an animal model of the disease.
The authors use optogenetics to selectively activate single glomeruli in behaving mice. They find that mice can perceive the stimulation of a single glomerulus, even on an intense odor background. Different input intensities and the timing of input relative to sniffing can also be discriminated. This suggests that each glomerulus can transmit odor information using identity, intensity and temporal coding cues.
Fused-in-Sarcoma (FUS) gene encodes an RNA/DNA binding protein whose mutations are linked to amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). This study shows that FUS functions in the neuronal DNA damage response by its recruitment to the site of DNA double-stranded breaks and by its interaction with histone deacetylase 1. The study also shows ALS/FTLD-associated mutant FUS is defective in DNA repair mechanism and that ALS/FTLD patients with FUS mutations have greater DNA damage.
In this study, the authors document how SIRPα, a cell-adhesion molecule, participates in the late maturation of hippocampal excitatory synapses. They find that in response to activity, SIRPα sheds its ectodomain, which acts presynaptically to promote maturation in a process that requires CaM kinase, matrix metalloproteinases and the presynaptic receptor CD47.
Here the authors combine computational modeling, voltage-sensitive dye imaging (VSDI) in behaving monkeys, and behavioral measurements in humans, to investigate whether the large-scale topography of V1 population responses influences shape judgments. They find the judgments of human observers were systematically distorted as had been predicted based on the VSDI responses in monkey V1.
The authors describe a sensory context–dependent switch in a salt sensory circuit in C. elegans. In response to large changes in salt concentration, the ASE sensory neuron releases insulin-like peptides that switch the AWC olfactory sensory neuron into an interneuron in the salt circuit. Disrupting insulin signaling interferes with attraction to high concentrations of salt.
The authors show that long-term exposure of Drosophila to camphor, which is normally repulsive, leads to decreased repulsion. They identify the TRPL channel as the probable receptor for camphor in gustatory neurons and show that downregulation of TRPL, which requires the E3 ubiquitin ligase Ube3a, underlies this change in taste preference.
This study used fMRI repetition suppression to demonstrate that human subjects can represent and evaluate novel choice options by invoking multiple memories for previous experiences in hippocampus and medial prefrontal cortex.
Brain tumor initiating cells (BTICs) are self-renewing, tumorigenic cells that often reside in a necrotic and hypoxic niche in the brain. Here the authors show that BTICs can become more tumorigenic upon glucose restriction and compensate for this cellular stress by upregulating their capacity to take up glucose.
Polyamines such as spermidine and putrescine are known to promote autophagy and longevity in fruit flies. Similar to many other organisms, Drosophila also display age-induced memory impairment. Here, Gupta et al. find that a decrease in brain polyamines in aging Drosophila is correlated with age-dependent memory impairment. They also find that polyamines in flies' diet can alleviate this impairment, demonstrating a link between polyamines, autophagy and memory decline.
In this study, the authors show that depletion of the IL-17 signaling component, Act1, specifically from NG2+ glia led to a substantial reduction in the severity of pathology in an EAE mouse model. They also find that IL-17 induces apoptosis of NG2+ cells in an Act1-dependent manner.
To examine the nature of information encoded by prefrontal output signals, the authors simultaneously recorded neuronal activity in monkey prefrontal and parietal cortices during a rule-based spatial categorization task. They found that signals reflecting rule-dependent categories were selectively transmitted from prefrontal to parietal neurons.
The authors show that extinction of fear conditioning lowers the threshold for synaptic potentiation in the lateral amygdala (LA), and fear renewal-inducing stimuli induce phosphorylation of AMPAR subunit GluA1 at serine 831 in LA. Infusion of a peptide competing with Ser831-phosphorylated GluA1 into the LA blocks this low-threshold potentiation and attenuates fear renewal.
In this study, the authors show that overexpression/accumulation of the parkin substrate AIMP2 induces an age-dependent degeneration of dopaminergic neurons and results in motor dysfunction. This effect is dependent on AIMP2-induced activation of PARP1, which, in turn, induces cell death via parthanatos.
Using voltage sensitive–dye imaging in the cortices of anesthetized and awake mice, the authors show that spontaneous activity patterns contain similar motifs as those evoked by sensory stimulation. These motifs are also seen after optogenetic activation of the cortex, and they correlate with structural connectivity.
This study shows that associative reward learning produces dynamic experience-dependent alterations in DNA methylation and immediate-early gene expression in ventral tegmental area (VTA) dopamine neurons and that DNA methylation in the VTA is required for the formation of new reward-related memories.