Research articles

This study uses a new method of profiling cell type–specific gene expression to identify genes expressed in fruitfly clock neurons. Such profiling yields two novel circadian genes, in separate sets of clock neurons and with differing circadian functions.

Information flow in the cortex is usually thought to be subserved by direct, cortico-cortical connections. Using optical imaging in a thalmocortical slice preparation, this study demonstrates a potent corticothalamocortical pathway from layer 5 of the S1 barrel field to S2 of the mouse somatosensory cortex.

Recording from single neurons in awake macaque monkeys, the authors find that neurons of the frontal pole cortex encode decisions at the time of feedback, but do not carry signals typically seen in other prefrontal areas, such as information about sensory cues, strategies, working memory, future goals or movement plans.

The authors report that the spiking history of small, randomly sampled ensembles of human and nonhuman primate cortical neurons can predict subsequent single neuron spiking. Spiking could be predicted by both local ensemble spiking histories as well as those in other cortical areas. These results provide evidence for strong collective cortical dynamics at the level of neuronal spikes.

To keep track of input and output over a course of time, generation of rhythmic neuronal activity requires a form of spike counter. In this study, Pulver and Griffith show that electrogenic activity of Na⁺/K⁺ pump underlies afterhyperpolarization in Drosophila larval motor neuron, which can functions as an activity integrator and as an intrinsic mechanism of cellular short-term memory.

Simple cell receptive fields (RFs) consist of spatially segregated 'On' and 'Off' subregions. Previous work suggested that excitatory inputs underlie this segregation. This study uses voltage clamp recordings in mouse to reveal that actually inibitory inputs are responsible for RF organization.

Axonal pathfinding during development needs appropriate responses to various attractive and repulsive guidance cues. The exact mechanisms by which different attractant/repulsion machineries interact or how the switch is precisely regulated at appropriate location are unknown. Here, Parra and Zou find that Sonic Hedgehog (Shh) can turn on Semaphorin repulsion via Shh receptors Patched-1 and Smoothened via the PKA pathway.

Nardilysin (NRDc) enhances the shedding of ectodomains from neuronal membrane proteins. The null mutant described here reveals that nardilysin is necessary for myelination in both central and peripheral nervous system.

Major histocompatibility complex peptides function as olfactory cues for vomeronasal sensory neurons (VSNs) in the mammalian nose. Here, the authors report that individual VSNs expressing the receptor gene V2r1b have broad peptide responsiveness, but sufficient specificity to distinguish peptides differing by a single amino acid residue. Furthermore, they find that targeted disruption of V2r1b eliminates the VSN peptide response.

Even without the symptoms of Alzheimer's disease, normal brain releases a small amount of amyloid-β peptide (Aβ). Abramov and colleagues now show that endogenous Aβ that is produced and released from presynaptic terminals can alter synaptic transmission and short-term plasticity.

In cultured rat hippocampal neurons, thrombospondin 1 hastened synapse formation via interaction with neuroligin 1.

This study finds that excitatory neurons in cortical layer 2/3 can respond to their own firing with persistent hyperpolarization, termed slow self-inhibition or SSI. This process is mediated by endocannabinoids and regulates neuronal excitability.

Previous work has suggested that visual attention improves behavioral performance by increasing the firing rates of individual sensory neurons. Recording from populations of neurons in monkey visual area V4, this study finds that most of the attentional improvement in the population signal results from decreases in interneuronal correlations.

Nakazawa and colleagues describe a mouse strain in which the NR1 subunit of the NMDA receptor is selectively eliminated in cortical and hippocampal interneurons in early postnatal development. These mice have several behavioral deficits that are consistent with the theory that GABAergic dysfunction contributes to the pathology of several psychiatric disorders, including schizophrenia.

In Drosophila, the connections between olfactory receptor neurons and projection neurons are highly specific. Here, the authors report that two leucine-rich repeat transmembrane proteins (Capricious and Tartan) serve as a mechanism for projection neuron dendrite targeting in the olfactory map.

During development of the peripheral ganglia, 50% of neurons die by apoptosis. This study finds that satellite glial cell precursors clear these neuronal corpses in developing dorsal root ganglia and identifies some of the molecular components involved in this phagocytosis.

Cue-evoked activity of midbrain dopamine neurons is proposed to encode the magnitude, delay and uncertainty of predicted rewards. Here the authors report that this activity separates costs and benefits, as it does not encode the costs of the action required to obtain predicted rewards.

Dendritic excitability is a plastic property of neurons. This study shows that exposure to an enriched environment increases propagation of dendritic sodium spikes in a subset of dendritic branches in CA1 pyramidal neurons. This effect is mediated by localized downregulation of A-type potassium channel function.

Notch signaling is essential for the maintenance of adult neural stem cells in vivo. Here, Andreu-Agulló and colleagues show that PEDF, released from endothelial cells, enhances Notch signaling in the mouse subependymal zone by inactivating a repressor of Notch target genes.

Severe stress in early childhood can increase an individual's vulnerability to depression later in life. This study found that early-life stress in mice resulted in persistent elevation of the stress hormone arginine vasopressin (AVP), which was caused by persistent hypomethylation of CpG islands in the Avp promoter in the hypothalamus.