Research articles

Patches in primary visual cortex (V1) rich in cytochrome oxidase were thought to contain unoriented, color-opponent neurons. Here the authors measure orientation tuning in V1 neurons using acutely implanted 100-electrode arrays. Patch cells were nearly as well tuned as those in interpatches, suggesting that processing of form and color is not strictly segregated in primate V1. Patch cells had higher mean discharge rates, consistent with their enhanced metabolism.

The authors report that, in the extended amygdala, 2-arachidonoylglycerol and anandamide mediate retrograde short-term depression and long-term depression, respectively, via different signaling pathways. In contrast, in the striatum, 2-arachidonoylglycerol and cannabinoid receptor 1–mediated retrograde signaling mediated both forms of plasticity.

Here the authors identify NCKX4, a potassium-dependent Na⁺/Ca²⁺ exchanger as being necessary for rapid response termination and proper adaptation of vertebrate olfactory sensory neurons. They also report that Nckx4^−/− mice have a reduced ability to locate an odorous source and have lower body weights.

The authors report that GABA transporter 1 (GAT-1) cation currents directly increase GABAergic neuronal excitability and synaptic GABA release in the periaqueductal gray (PAG), and that these GAT-1 changes contribute to PAG-mediated signs of opioid withdrawal.

Loss of FMR1 gene function results in fragile X syndrome. Here, the authors demonstrate that the Drosophila fragile X homolog dFMR1 is involved in the RNA editing pathway via interaction with the enzyme dADAR and suggest that proper NMJ synaptic architecture requires modulation of dADAR activity by dFMR1.

The orbitofrontal cortex (OFC) has been hypothesized to carry information regarding the value of expected rewards. Such information could be used for generating instructive error signals conveyed by dopamine neurons. Here the authors report that this is indeed the case. However, contrary to the simplest hypothesis, OFC lesions did not result in the loss of all value information. Instead, lesions caused the loss of value information derived from model-based representations.

This study reports a double dissociation in the neuronal correlates of value-based decision making in monkey prefrontal cortex, with orbitofrontal cortex neurons encoding choice value relative to recent choice values, while anterior cingulate cortex neurons flexibly encode multiple decision parameters and reward prediction errors using a 'common valuation currency'.

DNA methylation in the context of epigenetics occurs on the 5' position of cytosine, which can be further oxidized by enzymes from the Ten-eleven translocation (Tet) family, resulting in 5-hydroxymethylcytosine (5-hmC). In the context of embryonic stem cells, Tet and 5-hmC DNA act in an alternate epigenetic state that regulates epigenetic programming and stem cell differentiation. Here, the authors describe the epigenomic profiling of 5-hmC in mouse and human brain across different time periods during development and aging.

In this behavioral study, the authors demonstrate how increased attention can sometimes lead to lower subject confidence, leading subjects to become more conservative in making decisions during a visual perception task.

This study examines the contribution of a specific phosphatidylinositol 3-kinase (PI3K) isoform, namely PI3Kγ, to hippocampal synaptic plasticity and behavior. The authors find that the loss of PI3Kγ can specifically impair NMDA receptor–mediated long-term depression and cognitive functions that rely on behavioral flexibility.

The authors find that the Avpr1a gene, encoding the vasopressin-1A receptor, is responsible for strain-dependent pain sensitivity of mice to formalin and capsaicin. In humans, a single nucleotide polymorphism in AVPR1A was found to affect capsaicin pain and desmopressin analgesia. In both species, the effects were male specific and dependent on stress levels at the time of testing.

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 generated knock-in mice of the AMPAR auxiliary subunit TARP that lack the C-terminal PDZ ligand. They found that synaptic transmission and AMPAR were reduced without changes in extrasynaptic AMPAR expression, but LTP was unaltered.

Using two-photon microscopy in mice, the authors find that the number of cortical spines increases in adolescent mice while they are awake and decreases while they are asleep.

Maturation of adult-born neurons in the dentate gyrus is known to require GABAergic input. Here the authors show that a subtype of interneurons, namely neurogliaform cells, acts as the primary source of GABA for newborn neurons in mouse dentate gyrus.

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.