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The authors show that synapses between rod bipolar cells and AII amacrine cells in the retina can encode luminance and compute contrast in the sustained and transient components of vesicle release, respectively. A release/replenishment model shows that a single, homogenous pool of vesicles is sufficient to generate this behavior.
The authors studied the dynamic regulation of Ca2+-permeable AMPARs (CP-AMPARs) in oligodendrocyte precursor cells. Group 1 mGluRs regulate CP-AMPARs via a pathway that requires intracellular Ca2+, PI3 kinase, PICK-1 and JNK. Purinergic receptor activation decreases CP-AMPAR expression.
This study reports that people are worse at incorporating negative information when updating their beliefs. Correspondingly, neural activity encodes desirable information updates, but there is weaker encoding of unexpectedly undesirable information.
Examining the role of ephrin-B3 in dendritic and synaptic development in vivo, this study finds that ephrin-B3 functions postsynaptically as a receptor to initiate reverse signaling events that organize dendritic branching complexity, spine maturation and formation of functional synapses.
The authors examine the neural circuitry causally involved in normative, fairness-related decisions by generating a temporarily diminished capacity for costly normative behavior through non-invasive brain stimulation. Their findings suggest that a prefrontal network, the activation of rDLPFC and pVMPFC and the connectivity between them, facilitates costly normative decisions.
Cocaine can easily cross the placental and fetal blood-brain barrier, and in utero exposure to cocaine can cause lasting behavioral changes in postnatal periods. Here, Bellone et al. studied the physiological and circuit level mechanism behind the consequence of in utero cocaine exposure and found a postnatal synaptic maturation defect of excitatory input to the dopaminergic neurons in the ventral tegmental area of mice. In particular, they found that late embryonic in utero cocaine exposure causes a delay in AMPAR/NMDAR switch in early postnatal mouse brain.
One mechanism by which medial prefontal cortex (mPFC) exerts cognitive control is thought to involve the subthalamic nucleus (STN), which acts as a temporary brake on behavior. Here the authors found increases in mPFC and STN theta power as a function of decision conflict. Increases in mPFC theta power predicted increased decision thresholds. STN deep brain stimulation reversed this relationship, resulting in impulsive choice.
Inserting a recording electrode into the nostrils of human volunteers allowed the authors to record neural activity directly from the olfactory epithelium, and measures of olfactory perception, all from the same individuals. This uncovered a non-uniform patchy organization of the receptive surface, which was organized in part according to the perception of odorant pleasantness.
The authors present a computational model based on standard learning rules that can simulate and account for a large range of known effects in the medial prefrontal cortex (mPFC), including dorsal anterior cingulate cortex (dACC). Their model suggests that this region is involved in learning and predicting the likely outcomes of actions and detecting when those predicted outcomes fail to occur.
Recording from primate retinal ganglion cells, the authors find that cone noise, traversing the retina through diverse pathways, accounts for most of the noise and correlations in the retinal output. This constrains how higher centers exploit signals carried by parallel visual pathways.
Mammalian grid cells have a spatially periodic pattern of responses to location, which is a puzzling feature. Here, the authors demonstrate that this pattern of activity is compatible with a coding scheme that allows for very accurate localization.
The authors show that retrieval of fear memory modifies the membrane expression of GluA2-containing AMPA receptors and synaptic strength in the dorsal hippocampus. This synaptic plasticity exerts an inhibitory constraint on memory strengthening and underlies the loss of fear response by reinterpretation of memory content during adaptive reconsolidation.
The authors characterize the endogenous local calcium dynamics in the processes of adult mouse hippocampal astrocytes, and find that the astrocytic Ca2+ activity is generated by synaptic events and contributes to basal synaptic transmission reliability.
Adaptation helps sensory neurons optimize in a steady environment, but can cause a failure in transmission when the environment changes suddenly. The authors report that the retina overcomes this limitation by complementing adaptation with an opposing process that sensitizes a separate population of neurons following a strong stimulus.
The authors determine the crystal structure of the extracellular domain of a receptor chimera constructed from the human α7 acetylcholine receptor (AChR) and acetylcholine binding protein (AChBP), as well as the structure with bound epibatidine, a potent AChR agonist. The structures provide a realistic template for structure-aided drug design and for defining structure-function relationships of α7 AChRs.
The authors use multivoxel pattern analysis of fMRI data to examine the role of lateral occipital (LO) cortex in the recognition of real-world visual scenes. They find that LO may support an object-based channel for scene recognition by combining information about multiple objects within a scene.
Homeobox proteins Engrailed-1 (En1) and Engrailed-2 (En2) are transcription factors that direct midbrain cell specification during development. Here, the authors show that exogenous En1 and En2 protect against dopaminergic cell death in several rodent models of Parkinson's disease.
The authors report that rat brain glutamatergic synaptic vesicles express monovalent cation/H+ exchangers that convert the Δψ of the proton electrochemical gradient into Δψ. They find that this K+/H+ exchange stimulates the accumulation of glutamate into vesicles, regulating glutamate release and thus synaptic transmission.
This study describes how the circadian clock and regulators of synaptic activity influence each other by identifying the ways in which oligophrenin-1 (a regulator of dendritic spine morphology) and Rev-erbA (a nuclear factor regulating circadian rhythms) interact.
The highwire (Hiw)/DFsn ubiquitin ligase complex regulates synaptic morphology during development and axonal regeneration on injury. The authors identify Drosophila Rae1 as a component of the Hiw/DFsn complex and show that it controls Hiw protein abundance during synaptic development.