Research articles

Midbrain dopaminergic neuron activity is associated with reward signaling and aversive stimuli. Using genetic models in which excitatory response of dopaminergic neurons are reduced, the authors find that the imbalance of dopaminergic neuronal response following aversive stimuli is manifested in generalized anxiety.

This study uses subjects with newly removed congenital occlusions to demonstrate that object matching between touch and vision is not innate. Formerly blind subjects, when they had their sight restored, were initially unable to visually match an object to a sample they had previously touched, but rapidly developed such cross-modal matching.

Secreted frizzled-related proteins (SFRPs) are putative Wnt antagonists. Here, Esteve et al. show that SFRPs during eye development can also serve as inhibitors of Notch signaling by acting on ADAM10 metalloprotease activity.

The authors report that radial glia–like (oRG) progenitor cells are present in the mouse embryonic cortex and that these cells arise from asymmetric divisions of radial glia. In turn, they undergo asymmetric divisions to generate neurons.

Chen and colleagues show that visual deprivation drives structural remodeling of the dendritic branch tips of cortical layer 2/3 interneurons in an input-specific manner. Neighboring pyramidal cells show a corresponding loss of inhibitory inputs. This decreased inhibition seems to be permissive for the subsequent addition of new synapse-bearing branch tips.

Perceptual learning has been proposed to result from improvements either in early sensory processing or at the later stage of sensory decoding. Here the authors show that altering the feedforward connectivity in a recurrent neural network so as to improve probabilistic inference in early visual areas results in both modest changes in tuning curves and reduced noise correlations.

This study demonstrates that D-serine released from Bergmann glia can act as a ligand for Δ2 glutamate receptor to regulate long-term depression at parallel fiber–Purkinje cell synapses in immature cerebellum.

Previous work has shown that two members of the Mas-related GPCR family, MrgprA3 and MrgprC11, mediate histamine-independent itch signaling. Here, Wilson et al. demonstrate that TRPA1 is a downstream target of both of these receptors in sensory neurons and is required for Mrgpr-evoked itch.

Brief and synchronous inter-ictal events can occur between seizures. Using human tissue samples and electroencephalography, this study shows that the transition from pre-ictal discharge to ictal discharge involves distinct temporal and spatial characteristics as well as glutamatergic mechanisms.

Amyloid-β is known to inhibit hippocampal long-term potentiation (LTP), but the underlying molecular mechanisms are only partially understood. In this capacity, Jo and colleagues report the involvement of a signaling pathway comprised of caspase-3, Akt1 and glycogen synthase kinase-3β.

Homeostatic plasticity is mostly thought be a global event that affects all synapses of the same neuron. Here, Deeg and Aizenman finds sensory pathway–specific homeostatic plasticity in the Xenopus optic tectum.

People with nonsyndromic congenital retinal nonattachment (NCRNA) are blind from birth. The authors show that NCRNA is caused by a deletion spanning a remote cis regulatory element upstream from ATOH7 (Math5), a transcription factor gene required for retinal development. The deleted region is a conserved secondary transcriptional enhancer of ATOH7.

This study uses a combination of TMS, fMRI and EEG to provide causal evidence for the role of the prefrontal cortex in the modulation of selective attention. Participants with greater decrement in visual association cortex modulation when TMS was used to knock out the prefrontal contribution had greater working memory performance decline.

Previous work suggests that occipital pole areas corresponding to the central retina can be driven by retinal activity elsewhere when the central retina is lesioned. This fMRI study in individuals with macular degeneration with retinal lesions finds no evidence for such remapping of activity, suggesting that plasticity in adult visual cortex is limited.

Epileptic seizures are traditionally considered to reflect hypersynchronous neuronal activity arising from runaway excitation. Here the authors analyze spike train patterns of single neurons during seizures in human epilepsy patients, finding that spiking activity during seizure initiation was highly heterogeneous in small cortical patches and across the network.

Developing skeletal muscle fibers are intrinsically pre-patterned prior to motor neuron innervation. Chen and colleagues show that a functional skeletal muscle dihydropyridine receptor (DHPR) is required for muscle pre-patterning during neuromuscular junction development. DHPR is an L-type calcium channel and its regulation of muscle pre-patterning requires calcium influx.

This work shows that HDAC1 and HDAC2 control Schwann cell differentiation and peripheral myelination: HDAC1 maintains Schwann cell survival by downregulating active β-catenin and HDAC2 induces myelination transcription programming.

Using genetic approaches, this study shows that HDAC1 and HDAC2 acetylation of NF-κB is required for proper Schwann cell myelination in the peripheral nervous system and for Schwann cell differentiation.

The authors report that the protein Flotillin-1/Reggie-2 (Flot1) is required for PKC-regulated internalization of the dopamine transporter (DAT) and the glial glutamate transporter EAAT2. Flot1 was required to localize DAT within plasma membrane microdomains in stable cell lines, and for amphetamine-induced reverse transport of dopamine in neurons.

In this Technical Report, Kleinlogel and colleagues created and characterized a new channelrhodopsin-2 mutant with an enhanced permeability to calcium. Dubbed CatCh (calcium translocating channelrhodopsin), this new variant's enhanced calcium permeability mediates an accelerated response time and voltage response that is ~70-fold more light sensitive than that of wild-type channelrhodopsin-2.