Thursday, June 25, 2015

Nature Neuroscience Contents: July 2015 Volume 18 Number 7, pp 927 - 1057

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Nature Neuroscience

TABLE OF CONTENTS

July 2015 Volume 18, Issue 7

Editorial
News and Views
Reviews
Brief Communications
Articles
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Editorial

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Welcome aboard!   p927
doi:10.1038/nn.4059
Nature Neuroscience editors share useful tips on the initial submission process.

News and Views

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Genetic variation links creativity to psychiatric disorders   pp928 - 929
Matthew C Keller and Peter M Visscher
doi:10.1038/nn.4047
Epidemiological studies and anecdotal evidence show overlap between psychiatric disorders and creativity, but why? A new study uses genome-wide association data from schizophrenia and bipolar disorder to show that genetics are part of the explanation.

See also: Brief Communication by Power et al.

Go with your gut: microbiota meet microglia   pp930 - 931
Kira Irving Mosher and Tony Wyss-Coray
doi:10.1038/nn.4051
Discovering the environmental factors that control microglia is key to understanding and managing brain health. A new study finds that microbiota in the gut are essential to the regulation of microglial maturation and activation.

See also: Article by Erny et al.

MIR137: big impacts from small changes   pp931 - 933
Jinju Han, Anindita Sarkar and Fred H Gage
doi:10.1038/nn.4045
Schizophrenia-linked single nucleotide polymorphisms in MIR137 alter expression of miR-137 in neurons. Abnormal expression of miR-137 affects vesicle release at presynaptic terminals and in turn alters hippocampal functioning.

See also: Article by Siegert et al.

How amyloid, sleep and memory connect   pp933 - 934
Brendan P Lucey and David M Holtzman
doi:10.1038/nn.4048
In a bidirectional relationship, the sleep/wake cycle regulates amyloid-β (Aβ) levels and Aβ accumulation then disrupts sleep. A quantitative three-way model now suggests that Aβ impairs memory via its effect on sleep.

See also: Article by Mander et al.

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University of Iowa
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Reviews

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Molecular mechanisms governing Ca2+ regulation of evoked and spontaneous release   pp935 - 941
Ralf Schneggenburger and Christian Rosenmund
doi:10.1038/nn.4044
In this Review, Schneggenburger and Rosenmund discuss the molecular mechanisms that control the Ca2+ dependence of synaptic vesicle fusion during spontaneous and evoked modes of release at mammalian brain synapses. They argue that the same pool of vesicles is recruited during spontaneous and evoked release but at drastically different rates.

Diversity of astrocyte functions and phenotypes in neural circuits   pp942 - 952
Baljit S Khakh and Michael V Sofroniew
doi:10.1038/nn.4043
This Review article by Baljit Khakh and Michael Sofroniew discusses the latest progress in demonstration of molecular, cellular and functional heterogeneity of astrocytes in the central nervous system. The article highlights the way in which this diversity within and across astrocytes can affect normal function of the brain differently, and discusses pathological conditions where astrocyte heterogeneity is instrumental in manifesting various aspects of CNS dysfunction.

Brief Communications

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Polygenic risk scores for schizophrenia and bipolar disorder predict creativity   pp953 - 955
Robert A Power, Stacy Steinberg, Gyda Bjornsdottir, Cornelius A Rietveld, Abdel Abdellaoui et al.
doi:10.1038/nn.4040
Genetic risk scores derived from GWAS of psychotic disorders are greater in creative professionals unaffected by psychosis. This association cannot be explained by shared environment or education. Thus, a shared genetic architecture underlies the propensity for creativity and psychosis.

See also: News and Views by Keller & Visscher

Experience-dependent DNA methylation regulates plasticity in the developing visual cortex   pp956 - 958
Paola Tognini, Debora Napoli, Jonida Tola, Davide Silingardi, Floriana Della Ragione et al.
doi:10.1038/nn.4026
This study shows that ocular dominance plasticity (ODP) is accompanied by changes to DNA methylation at specific genes in the mouse visual cortex. The authors also show that pharmacological inhibition of the DNA methylation process can alter the functional consequence of ODP.

Activin receptor signaling regulates cocaine-primed behavioral and morphological plasticity   pp959 - 961
Amy M Gancarz, Zi-Jun Wang, Gabrielle L Schroeder, Diane Damez-Werno, Kevin M Braunscheidel et al.
doi:10.1038/nn.4036
Gancarz et al. identify Activin-receptor signaling—including the downstream transcription factor Smad3—as an intracellular signaling pathway that is regulated in the nucleus accumbens following abstinence from cocaine. The authors demonstrate that altering Activin-receptor signaling bi-directionally regulates relapse behavior and dendritic spine plasticity.

Excitatory transmission at thalamo-striatal synapses mediates susceptibility to social stress   pp962 - 964
Daniel J Christoffel, Sam A Golden, Jessica J Walsh, Kevin G Guise, Mitra Heshmati et al.
doi:10.1038/nn.4034
Chronic social stress has adverse behavioral consequences and can result in the development of depression in humans. Using a rodent social stress model, we report increased synaptic connectivity between the thalamus and striatum in susceptible mice that controls behavioral coping mechanisms relevant to depression.

Articles

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Host microbiota constantly control maturation and function of microglia in the CNS   pp965 - 977
Daniel Erny, Anna Lena Hrabe de Angelis, Diego Jaitin, Peter Wieghofer, Ori Staszewski et al.
doi:10.1038/nn.4030
In this study, the authors show that host microbiota play a key role in modulating microglia homeostasis. Germ-free mice or mice with only limited microbiota complexity displayed defects in microglial cell proportions and maturation, leading to impaired innate immune responses. The authors find that short-chain fatty acid signaling regulates these effects in vivo.

See also: News and Views by Mosher & Wyss-Coray

Central role for PICALM in amyloid-β blood-brain barrier transcytosis and clearance   pp978 - 987
Zhen Zhao, Abhay P Sagare, Qingyi Ma, Matthew R Halliday, Pan Kong et al.
doi:10.1038/nn.4025
Zhao et al. report that brain vessels have a major role in clearing Alzheimer's disease-related toxin Aβ from brain and show that PICALM gene product and its variant associated with an increased risk for Alzheimer's disease inactivate an Aβ clearance system in blood vessels, leading to Aβ brain accumulation and cognitive impairment.

The human epilepsy mutation GABRG2(Q390X) causes chronic subunit accumulation and neurodegeneration   pp988 - 996
Jing-Qiong Kang, Wangzhen Shen, Chengwen Zhou, Dong Xu and Robert L Macdonald
doi:10.1038/nn.4024
The Q390X mutation in the GABAA receptor GABRG2 has been associated with Dravet syndrome in humans. In this study, the authors generated a new genetic epileptic encephalopathy animal model, the Gabrg2+/Q390X knock-in mouse, and show that expression of this mutant protein leads to seizures, chronic accumulation and aggregation of mutant subunit protein and age-dependent neurodegeneration.

Distinct circuit-dependent functions of presynaptic neurexin-3 at GABAergic and glutamatergic synapses   pp997 - 1007
Jason Aoto, Csaba Földy, Silviana Maria Ciurea Ilcus, Katsuhiko Tabuchi and Thomas C Südhof
doi:10.1038/nn.4037
Neurexins are essential presynaptic cell-adhesion molecules whose biological significance is poorly understood. Here, the authors interrogate Nrxn3 function in two brain regions, using two types of preparations and in three mutant mouse lines, and find that Nrxn3 plays mechanistically distinct, brain region-specific functions to regulate either presynaptic release or AMPA receptor stability.

The schizophrenia risk gene product miR-137 alters presynaptic plasticity   pp1008 - 1016
Sandra Siegert, Jinsoo Seo, Ester J Kwon, Andrii Rudenko, Sukhee Cho et al.
doi:10.1038/nn.4023
Neurodevelopmental disorders are frequently associated with synaptic dysfunction. Recent genome-wide association studies associate the gene encoding microRNA-137 with an increased risk for schizophrenia. Using mouse and human models, the authors show that dysregulation of this miRNA leads to presynaptic defects and, consequently, to impaired synaptic plasticity and cognitive dysfunction.

See also: News and Views by Han et al.

mGluR5 in the nucleus accumbens is critical for promoting resilience to chronic stress   pp1017 - 1024
Sora Shin, Obin Kwon, Jee In Kang, Somin Kwon, Sora Oh et al.
doi:10.1038/nn.4028
The authors showed that mGluR5 can upregulate the expression of ΔFosB, a resilience molecule, in the nucleus accumbens. In stress-induced animal models of depression, mGluR5-induced upregulation of ΔFosB in the nucleus accumbens enhances resilience to stress.

A neural network that finds a naturalistic solution for the production of muscle activity   pp1025 - 1033
David Sussillo, Mark M Churchland, Matthew T Kaufman and Krishna V Shenoy
doi:10.1038/nn.4042
How motor cortical activity relates to muscle movement is still unclear. Here the authors trained neural networks to reproduce muscle activity of reaching monkeys. The optimal solutions produced by these networks resembled the single-neuron and population level neural activity seen in the motor cortex of the same monkeys.

Hand use predicts the structure of representations in sensorimotor cortex   pp1034 - 1040
Naveed Ejaz, Masashi Hamada and Jorn Diedrichsen
doi:10.1038/nn.4038
The cortical activity patterns associated with individual finger movements are highly variable across participants, with each person showing a distinct "cortical fingerprint". The idiosyncratic representations are subject to an invariant organization principle: the overlap between activation patterns is tightly shaped by how frequently fingers move together in everyday life.

Representation of retrieval confidence by single neurons in the human medial temporal lobe   pp1041 - 1050
Ueli Rutishauser, Shengxuan Ye, Matthieu Koroma, Oana Tudusciuc, Ian B Ross et al.
doi:10.1038/nn.4041
The authors show that memory-selective neurons in the human medial temporal lobe signal memory retrieval confidence. Using a balance-of-evidence model, the authors demonstrate that the signals provided by these neurons are sufficient to determine the choice certainty of declarative memory-based decision in single trials.

β-amyloid disrupts human NREM slow waves and related hippocampus-dependent memory consolidation   pp1051 - 1057
Bryce A Mander, Shawn M Marks, Jacob W Vogel, Vikram Rao, Brandon Lu et al.
doi:10.1038/nn.4035
The mechanisms through which β-amyloid impairs human memory remain unclear. This study shows that regional-specific β-amyloid load in cognitively normal older adults impairs NREM slow wave oscillations, thereby compromising overnight hippocampus-dependent memory consolidation. NREM sleep disruption therefore represents a novel mechanistic pathway through which β-amyloid contributes to hippocampus-dependent memory dysfunction in later life.

See also: News and Views by Lucey & Holtzman

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