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Volume 20 Issue 12, December 2017

Cerebellar dysfunction has been implicated in the pathogenesis of autism spectrum disorders (ASD). Tsai, Stoodley and colleagues show that the cerebellum modulates cortical association areas and that the underlying circuits show atypical connectivity in an ASD mouse model and individuals with autism.

Image: Anila DʼMello. Cover Design: Erin Dewalt.

Volume 20 Issue 12

News & Views

  • Sommeijer et al. describe a previously unrecognized role of the thalamus: development of inhibition in the thalamus regulates ocular dominance plasticity, a form of critical-period plasticity regulation previously ascribed solely to the cortex.

    • Brian B. Jeon
    • Sandra J. Kuhlman
    News & Views

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  • A leaky blood–brain barrier may contribute to neuropsychiatric disease. Chronic stress is shown to alter blood–brain barrier permeability, allowing an inflammatory response to penetrate the brain. The deficit is mostly around the nucleus accumbens, an area central to motivation. The affected animals exhibit features of depression.

    • E. David Leonardo
    • Alex Dranovsky
    News & Views
  • To decide how much we would like to eat a food item, our brain automatically decomposes it into constituent nutrients. The quantities of the different nutrients are represented in distinct parts of the lateral orbitofrontal cortex and then integrated by the medial orbitofrontal cortex to provide a global value judgment.

    • Mathias Pessiglione
    • Antonius Wiehler
    News & Views
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Comment

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Review Articles

  • The authors propose a new framework for the thalamus in cognition. They review findings from rodents and primates, emphasizing thalamic control of functional cortical connectivity, its putative mechanisms and role in flexible construction of task-relevant cortical networks.

    • Michael M. Halassa
    • Sabine Kastner
    Review Article
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Brief Communications

  • The authors show that PKC-δ-expressing neurons in the central amygdala, are essential for synaptic plasticity underlying learning in the lateral amygdala, as they convey information about unconditioned stimulus to the lateral amygdala as a teaching signal.

    • Kai Yu
    • Sandra Ahrens
    • Bo Li
    Brief Communication
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Articles

  • 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 GABAA-receptor-positive allosteric modulator.

    • Eui-Man Jung
    • Jeffrey Jay Moffat
    • Woo-Yang Kim
    Article
  • 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.

    • Jean-Pierre Sommeijer
    • Mehran Ahmadlou
    • Christiaan N. Levelt
    Article
  • The authors show that unlike body sensory neurons, craniofacial nociceptive neurons directly synapse with noxious-stimulus-activated lateral parabrachial neurons (PBL), 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.

    • Erica Rodriguez
    • Katsuyasu Sakurai
    • Fan Wang
    Article
  • 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.

    • Catherine J. Stoodley
    • Anila M. D’Mello
    • Peter T. Tsai
    Article
  • 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.

    • Caroline Menard
    • Madeline L. Pfau
    • Scott J. Russo
    Article
  • 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.

    • Aaron T. Winder
    • Christina Echagarruga
    • Patrick J. Drew
    Article
  • 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.

    • Aishwarya Parthasarathy
    • Roger Herikstad
    • Shih-Cheng Yen
    Article
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Resources

  • Quantitative mass spectrometry was used to produce a proteomic survey of postnatal human brain regions. Compared to matched RNA-seq, protein levels showed more regional variation, especially for membrane-associated proteins in the neocortex.

    • Becky C. Carlyle
    • Robert R. Kitchen
    • Angus C. Nairn
    Resource
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Technical Reports

  • The authors develop a methods suite for millisecond-precise, single-cell-resolution control of neural activity through protein engineering of novel opsin/trafficking sequence combinations, as well as optimized holographic two-photon optics.

    • Or A. Shemesh
    • Dimitrii Tanese
    • Valentina Emiliani
    Technical Report
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