Thursday, August 20, 2015

Nature Reviews Neuroscience contents September 2015 Volume 16 Number 9 pp 507-574

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Nature Reviews Neuroscience


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TABLE OF CONTENTS
 
September 2015 Volume 16 Number 9
Nature Reviews Neuroscience cover
Impact Factor 31.427 *
In this issue
Research Highlights
Progress
Reviews
Perspectives

Also this month
 Featured article:
Auditory dysfunction in schizophrenia: integrating clinical and basic features
Daniel C. Javitt & Robert A. Sweet


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RESEARCH HIGHLIGHTS
Top

Neural coding: Speed awareness
p507 | doi:10.1038/nrn4008
A new study identifies a population of 'speed cells' in the rat medial entorhinal cortex that is likely to contribute to path integration.

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Neuropharmacology: Pain relief without pairing up
p508 | doi:10.1038/nrn4007
The formation of a heteromer between cannabinoid 1 receptor and 5-hydroxytryptamine (serotonin) receptor 2A in the brain is required for cannabinoid-induced cognitive impairment, but not analgesia, in mice.

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Neurotransmission: Sticking the brakes on
p508 | doi:10.1038/nrn4013
Presynaptic β-neurexins regulate synaptic strength at excitatory synapses by modulating endocannabinoid signalling.

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Neurodegeneration: Reelin' from loss
p509 | doi:10.1038/nrn4006
In the adult mouse CNS, reelin protects against amyloid-β-induced synaptic and behavioural deficits.

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Neurodegenerative disease: A neutrophil invasion
p510 | doi:10.1038/nrn4014
Neutrophil infiltration of the brain drives cognitive decline in mouse models of Alzheimer disease and is regulated by the integrin LFA-1.

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IN BRIEF

Genes and disease: Organoids assist in ASD research | Sensory processing: Itchy astrocytes | Neuronal circuits: Peckish flies are less picky | Glia: Gasping for breath | Cerebral Cortex: Cortical reconstruction | Learning and memory: Demethylated learning | Circadian rhythms: The rhythm regulator | Neurotransmitter receptors: Recoding the pathways
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PROGRESS
Top
NaV1.9: a sodium channel linked to human pain
Sulayman D. Dib-Hajj, Joel A. Black & Stephen G. Waxman
p511 | doi:10.1038/nrn3977
Emerging evidence suggests a role for the voltage-gated sodium channel NaV1.9 in pain. In this Progress article, Dib-Hajj, Black and Waxman analyse the findings from three studies that report mutations in the gene encoding NaV1.9 in pain disorders, and suggest that NaV1.9 may be a potential therapeutic target for pain.

Abstract | Full Text | PDF
 
REVIEWS
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Finding the engram
Sheena A. Josselyn, Stefan Köhler & Paul W. Frankland
p521 | doi:10.1038/nrn4000
Memory storage is thought to be mediated by lasting physical changes, or engrams, in the brain. In this Review, Josselyn and colleagues discuss characteristics of the engram and describe the recent progress that has been made in identifying neurons involved in specific engrams.
Abstract | Full Text | PDF

Auditory dysfunction in schizophrenia: integrating clinical and basic features
Daniel C. Javitt & Robert A. Sweet
p535 | doi:10.1038/nrn4002
Schizophrenia is characterized by various neurocognitive deficits, including impairments in auditory function. In this Review, Javitt and Sweet examine the behavioural, neurophysiological and structural evidence for auditory cortical dysfunction in this disorder and explore some of the possible underlying mechanisms.
Abstract | Full Text | PDF

From the genetic architecture to synaptic plasticity in autism spectrum disorder
Thomas Bourgeron
p551 | doi:10.1038/nrn3992
Recent years have seen considerable interest in the genetics of autism spectrum disorder (ASD). In this Review, Thomas Bourgeron examines the genetic architecture of this disorder and how ASD-linked mutations might affect synaptic plasticity, before exploring the synaptic homeostasis hypothesis of ASD.
Abstract | Full Text | PDF | Supplementary information

 
PERSPECTIVES
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OPINION
A genetic cause of Alzheimer disease: mechanistic insights from Down syndrome
Frances K. Wiseman et al.
p564 | doi:10.1038/nrn3983
Individuals with Down syndrome have an enhanced risk of developing early onset Alzheimer disease. Here, the authors describe the features of Alzheimer disease in Down syndrome and show how understanding the genetic and pathogenic mechanisms of this form of Alzheimer disease may shed light on more general mechanisms of neurodegeneration.
Abstract | Full Text | PDF | Supplementary information

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