Articles in 2017

The authors investigate grid cell dynamics after removal of a border between two environments. Near the transition between environments, grid fields changed location, resulting in local spatial periodicity and continuity between the original maps.

Grid cell activity may subserve path integration, but a direct link is lacking. The authors selectively disrupt retro-hippocampal region grid cell activity and show that disrupted grid cell firing impairs performance in a path integration task.

Long-lasting synaptic plasticity is regarded as a mechanism for learning and memory. Using genetically engineered mice in which the C-terminal domains of AMPA receptor subtypes are switched, the authors reveal that GluA1 and GluA2 differentially regulate synaptic plasticity and contribute to different forms of learning.

The authors show that Munc13-1 molecules form multiple supramolecular self-assemblies that serve as vesicular release sites. Having multiple Munc13-1 assemblies affords a stable synaptic weight, which confers robustness of synaptic computation.

Synaptotagmin-1 (Syt1) controls synaptic vesicle–membrane attachment activities via its C2B domain. These correlate with release synchronization and synaptic short-term facilitation, revealing a mechanism for Syt1-mediated synchronous release.

The mosquito-borne ZIKA virus triggers microcephaly in human newborns. The authors report that the microcephaly results from induction of endoplasmic stress that interferes with generation and survival of projection neurons in the cerebral cortex.

Humans can deliberately control the timing of their actions but the neural mechanisms underlying such control are largely unknown. In this article, Wang, Narain and their colleagues report that such flexibility emerges in rhesus monkeys from the ability of their brain to flexibly control the speed at which cortical responses unfold in time.

Like all terrestrial mammals, humans emit body odors that subtly communicate emotions. This study suggests that adults with autism may be misreading these chemical signals and that this may explain a portion of their social difficulties.

Apicco and colleagues show that reducing TIA1 inhibits tau-mediated neurodegeneration and improves survival in a mouse model of tauopathy. This rescue occurs with a transition in tau aggregation from oligomeric to fibrillar forms of tau. These findings suggest a key role for RNA binding proteins in the pathophysiology of tau.

Experience-dependent plasticity in the visual system has widely been considered to be exclusively cortical. Using chronic two-photon Ca²⁺imaging of individual thalamic boutons, Jaepel et al. now report that dLGN cells projecting to mouse visual cortex show pronounced ocular dominance plasticity after monocular deprivation.

The authors show that oxytocin-receptor-expressing neurons in the parabrachial nucleus are key regulators of fluid homeostasis that suppress fluid intake when activated, but do not decrease food intake after fasting or salt intake after salt depletion.

The authors show that unlike body sensory neurons, craniofacial nociceptive neurons directly synapse with noxious-stimulus-activated lateral parabrachial neurons (PB_L), which in turn project to multiple limbic centers processing emotions and affects. This monosynaptic pathway is both sufficient and necessary for craniofacial-pain-activated aversive behaviors.

Chronic social defeat stress induces loss of protein claudin-5, leading to abnormalities in blood vessel morphology, increased blood brain barrier permeability, infiltration of immune signals and depression-like behaviors.

The relationship of resting-state hemodynamics signals to ongoing neural activity is poorly understood. Using optical imaging, electrophysiology, and local pharmacological infusions, Winder et al. found that resting hemodynamic signals were weakly correlated with neural activity and that these hemodynamic fluctuations persisted when neural activity was silenced.

Arid1b haploinsufficiency causes autism and intellectual disability, yet the neurobiological basis of this is unknown. The authors demonstrate that Arid1b-heterozygous mice have impaired cortical interneuron development and epigenetic signatures. These mice also have cognitive and social deficits, which are reversed by treatment with a GABA^A-receptor-positive allosteric modulator.

Cerebellar right Crus I (RCrusI) has been implicated in autism spectrum disorder (ASD). RCrusI modulation altered RCrusI–inferior parietal lobule connectivity, and this connectivity was atypical in children with ASD and in a TscI mouse model of ASD. Inhibition of RCrusI in mice led to autism-related behaviors, and RCrusI activation rescued social impairments in TscI mice.

Suzuki et al. found that food valuation is related to beliefs about nutritive attributes. Functional MRI revealed these attribute codes in lateral orbitofrontal cortex, suggesting a mechanism by which value signals are constructed from constituent attributes.

The critical period of ocular dominance (OD) plasticity in the visual cortex is initiated by maturation of inhibition. The authors show that thalamic relay neurons in mouse dorsolateral geniculate nucleus also undergo OD plasticity. This process depends on thalamic inhibition and is required for consolidating the OD shift in visual cortex.

Animals must detect noxious stimuli to initiate protective behavior, but the evolutionary origin of nociceptive systems is poorly understood. The authors reveal a core function for TRPA1 in noxious heat transduction based on sensing H₂O₂ and ROS and demonstrate its conservation from planarians to humans.

Neurons in the lateral prefrontal cortex (but not the frontal eye fields) appear to maintain working memory information when disrupted by a transient distractor, not by using an immutable persistent code but by morphing from one persistent code to another. This code-morphing may provide the lateral prefrontal cortex with cognitive flexibility.