Hot off the presses! Feb 01 Nat Rev Neurosci

The Feb 01 issue of the Nat Rev Neurosci is now up on Pubget (About Nat Rev Neurosci): if you're at a subscribing institution, just click the link in the latest link at the home page. (Note you'll only be able to get all the PDFs in the issue if your institution subscribes to Pubget.)

Latest Articles Include:

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  - Nat Rev Neurosci 12(2):59 (2011)
  
• Plasticity: A total makeover | PDF (221 KB)
  - Nat Rev Neurosci 12(2):60 (2011)
  The ability to generate neurons from other, easily accessible cell types from patients with a neurological or psychiatric disease is something of a holy grail for neuroscience, as such neurons would enable researchers to model the disease in vitro or to develop cell replacement therapies. Now, Tursun et al.in vivo.
• Neuroimmunology: MicroRNAs keep microglia quiet | PDF (201 KB)
  - Nat Rev Neurosci 12(2):61 (2011)
  MicroRNAs (miRNAs) regulate gene expression in many biological processes, and a new study shows that a brain-specific miRNA is a key regulator of microglial cell quiescence in the CNS, thereby helping to prevent CNS inflammation.Microglial cells are CNS-resident macrophages that, under normal conditions, have a resting phenotype that is characterized by low-level expression of CD45 and major histocompatibility complex (MHC) class II molecules.
• Why women cry | PDF (104 KB)
  - Nat Rev Neurosci 12(2):61 (2011)
  What is the function of tears? A paper published in Science by a group from the Weissmann Institute of Science, Rehovot, Israel, describes that sniffing tears from women reduced sexual arousal in men (6 Jan 2011; doi:10.1126/science.1198331
• Synaptic plasticity: Breaking the learning barrier with ACh | PDF (121 KB)
  - Nat Rev Neurosci 12(2):62 (2011)
  The neurotransmitter acetylcholine is known to facilitate long-term potentiation (LTP) in the hippocampus, thereby promoting learning and memory. However, the molecular mechanisms that mediate this effect are not clear.
• Neurogenesis: Food signals wake sleeping stem cells | PDF (199 KB)
  - Nat Rev Neurosci 12(2):62 (2011)
  Stem cells in neurogenic areas of the adult mammalian brain are able to switch between quiescence and proliferation, but what are the factors that trigger their reactivation? Chell and Brand show that in Drosophila, neural stem cell reactivation is induced by glial cells, which secrete insulin-like peptides (ILPs) in response to a nutritional stimulus.
• Psychiatric disorders | Developmental neuroscience | Place cells | Neurodegenerative disease | PDF (127 KB)
  - Nat Rev Neurosci 12(2):63 (2011)
  Antidepressant effect of optogenetic stimulation of the medial prefrontal cortex Covington, H. E. , IIIet al. J. Neurosci. 31, 16082–16090 (2011)
• Reward: A dopaminergic dichotomy | PDF (181 KB)
  - Nat Rev Neurosci 12(2):64 (2011)
  When an animal learns to associate a specific cue with a reward, the cue not only has predictive properties but may itself become desirable. Dopamine is known to play a key part in such reward-related processes, but its precise role is unclear.
• Developmental neuroscience: Asymmetric inhibition | PDF (186 KB)
  - Nat Rev Neurosci 12(2):64 (2011)
  Direction-selective ganglion cells (DS cells) in the retina respond to stimuli that move in a particular direction and not to stimuli that move in the opposite (null) direction. This direction sensitivity requires asymmetric inhibitory input from starburst amacrine cells, but how and when this asymmetric wiring is established has remained elusive.
• Systems neuroscience: The stress of dieting | PDF (130 KB)
  - Nat Rev Neurosci 12(2):65 (2011)
  Many readers will have experienced that it is all too easy to regain the weight lost after a diet, and that experiencing stress somehow makes high-calorie foods particularly tempting. Bale and colleagues now provide a link between yo-yo dieting and stress by showing that in mice, food restriction alters stress and feeding pathways in the brain, and promotes binge eating of high-fat foods upon subsequent exposure to stress.
• Neurodegenerative disease: Meet the mediator, but not as you know it | PDF (158 KB)
  - Nat Rev Neurosci 12(2):66 (2011)
  Amyloid-β plays an important part in the pathophysiology of Alzheimer's disease, but the mechanisms by which it causes synaptic changes remain a topic of intense investigation. D'Amelio et al.
• Glia: Aquaporin: not so swell? | PDF (188 KB)
  - Nat Rev Neurosci 12(2):66 (2011)
  Fluid accumulation — or oedema — in the brain is a potentially life-threatening condition. It increases intracranial pressure, which can damage brain tissue and restrict blood supply.
• Amyloid-β and tau — a toxic pas de deux in Alzheimer's disease
  - Nat Rev Neurosci 12(2):65 (2011)
  Amyloid-β and tau are the two hallmark proteins in Alzheimer's disease. Although both amyloid-β and tau have been extensively studied individually with regard to their separate modes of toxicity, more recently new light has been shed on their possible interactions and synergistic effects in Alzheimer's disease. Here, we review novel findings that have shifted our understanding of the role of tau in the pathogenesis of Alzheimer's disease towards being a crucial partner of amyloid-β. As we gain a deeper understanding of the different cellular functions of tau, the focus shifts from the axon, where tau has a principal role as a microtubule-associated protein, to the dendrite, where it mediates amyloid-β toxicity.
• The role of G protein-coupled receptors in the pathology of Alzheimer's disease
  - Nat Rev Neurosci 12(2):73 (2011)
  G protein-coupled receptors (GPCRs) are involved in numerous key neurotransmitter systems in the brain that are disrupted in Alzheimer's disease (AD). GPCRs also directly influence the amyloid cascade through modulation of the α-, β- and γ-secretases, proteolysis of the amyloid precursor protein (APP), and regulation of amyloid-β degradation. Additionally, amyloid-β has been shown to perturb GPCR function. Emerging insights into the mechanistic link between GPCRs and AD highlight the potential of this class of receptors as a therapeutic target for AD.
• The stem cell potential of glia: lessons from reactive gliosis
  - Nat Rev Neurosci 12(2):88 (2011)
  Astrocyte-like cells, which act as stem cells in the adult brain, reside in a few restricted stem cell niches. However, following brain injury, glia outside these niches acquire or reactivate stem cell potential as part of reactive gliosis. Recent studies have begun to uncover the molecular pathways involved in this process. A comparison of molecular pathways activated after injury with those involved in the normal neural stem cell niches highlights strategies that could overcome the inhibition of neurogenesis outside the stem cell niche and instruct parenchymal glia towards a neurogenic fate. This new view on reactive glia therefore suggests a widespread endogenous source of cells with stem cell potential, which might potentially be harnessed for local repair strategies.
• The role of phase synchronization in memory processes
  - Nat Rev Neurosci 12(2):105 (2011)
  In recent years, studies ranging from single-unit recordings in animals to electroencephalography and magnetoencephalography studies in humans have demonstrated the pivotal role of phase synchronization in memory processes. Phase synchronization — here referring to the synchronization of oscillatory phases between different brain regions — supports both working memory and long-term memory and acts by facilitating neural communication and by promoting neural plasticity. There is evidence that processes underlying working and long-term memory might interact in the medial temporal lobe. We propose that this is accomplished by neural operations involving phase–phase and phase–amplitude synchronization. A deeper understanding of how phase synchronization supports the flexibility of and interaction between memory systems may yield new insights into the functions of phase synchronization in general.
• Correspondence: Naive realism in public perceptions of neuroimages
  - Nat Rev Neurosci 12(2):118 (2011)
  The Perspectives article by Illes et al. (Neurotalk: improving the communication of neuroscience research, Nature Reviews Neuroscience11, 61–69 (2010))1 discussed the thorny but important issue of communicating neuroscience research. The authors identified a number of challenges for neuroscientists seeking to present their often complex findings in an accessible way.
• Hereditary spastic paraplegias: membrane traffic and the motor pathway
  - Nat Rev Neurosci 12(2):118 (2011)
  Nature Reviews Neuroscience12, 31–41 (2011) On page 37 of the above article, in figure 3a, the protein structure labelled VPS35C was incorrectly labelled VPS39C. This has been corrected in the online version