Hot off the presses! Jun 01 Nat Rev Neurosci

The Jun 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:

• From the editors
  - Nat Rev Neurosci 11(6):371 (2010)
  Articles in this issue range from the epigenetic control of neuronal precursor fate, the molecular basis of nicotine addiction and the role of the somatosensory system in social perception, to the use of yeast in studying mechanisms of neurodegenerative diseases.Epigenetic control of developmental genes determines cell fate.
• Neuronal activation: The symphony of transcription
  - Nat Rev Neurosci 11(6):372 (2010)
  Part of the neuronal response to stimulation involves temporally and spatially controlled changes in gene expression. Most studies have elucidated the regulation of transcription through the activation of promoters, but mechanisms by which enhancers contribute to gene expression are poorly characterized.
• Sensory systems: Olfaction goes digital
  - Nat Rev Neurosci 11(6):373 (2010)
  Neural circuits that encode sensory inputs must be sensitive to small changes in the quality of a stimulus but must also be able to identify certain stimuli as identical despite minor variations caused by background 'noise'. A neural network could achieve this by classifying sensory inputs into discrete patterns of output activity.
• Neurogenesis: Is it mine?
  - Nat Rev Neurosci 11(6):373 (2010)
  In mammals, the ability to recognize close relatives, including offspring, is thought to involve the recognition of their unique, genetically programmed body odour. In contrast to maternal recognition behaviour, paternal recognition behaviour and associated changes in brain plasticity are largely unknown.
• Pain: Moreish analgesics dealt a blow
  - Nat Rev Neurosci 11(6):374 (2010)
  Administration of opioids to a treatment-naive subject induces powerful analgesic effects through activation of classical μ-opioid receptors (MORs). However, the clinical use of opioids is limited by aversive effects such as analgesic tolerance and addiction.
• Neurotransmitter receptors: Another trick up GABABR's sleeve
  - Nat Rev Neurosci 11(6):374 (2010)
  Metabotropic GABA (γ-aminobutyric acid) type B receptors (GABABRs) play an important part in the regulation of synaptic transmission as they inhibit presynaptic release and activate postsynaptic K+ channels. Now, Chalifoux and Carter show that GABABRs also suppress postsynaptic Ca2+ signals mediated by NMDARs (N-methyl-D-aspartate receptors) and inhibit multivesicular release at individual spines.
• Mirror neurons: Mirrors, mirrors, everywhere?
  - Nat Rev Neurosci 11(6):374 (2010)
  The discussion about a possible role of mirror neurons in learning and social cognition has been hampered by the lack of direct evidence that such neurons exist in humans. Fried and colleagues have now recorded single-cell activity from neurons in several brain areas in humans and report that some of these neurons show mirror-like activity.
• In brief: Psychiatric disorders, Neuronal migration, Neuroimaging, Neurological disorders
  - Nat Rev Neurosci 11(6):375 (2010)
  Reversal of hippocampal neuronal maturation by serotonergic antidepressants Kobayashi, K.et al. Proc. Natl Acad. Sci. USA 107, 8434–8439 (2010)
• Psychiatric disorders: Fear factors
  - Nat Rev Neurosci 11(6):376 (2010)
  The molecular events that underlie depression and anxiety are poorly understood but probably involve many factors. Corticotrophin-releasing factor (CRF) and serotonin (5-hydroxytryptamine (5-HT)) have been independently implicated in these disorders through their activation of CRF receptor 1 (CRFR1) and several 5-HT receptors, respectively.
• In brief: Endocannabinoids, Cognitive neuroscience, Cognitive neuroscience, Learning and memory
  - Nat Rev Neurosci 11(6):376 (2010)
  Endogenous cannabinoid signaling is essential for stress adaptation Hill, M. N.et al. Proc. Natl Acad. Sci. USA3 May 2010 (doi: 10.1073/pnas.0914661107)
• Epigenetic control of neural precursor cell fate during development
  - Nat Rev Neurosci 11(6):377 (2010)
  The temporally and spatially restricted nature of the differentiation capacity of cells in the neural lineage has been studied extensively in recent years. Epigenetic control of developmental genes, which is heritable through cell divisions, has emerged as a key mechanism defining the differentiation potential of cells. Short-term or reversible repression of developmental genes puts them in a 'poised state', ready to be activated in response to differentiation-inducing cues, whereas long-term or permanent repression of developmental genes restricts the cell fates they regulate. Here, we review the molecular mechanisms that underlie the establishment and regulation of differentiation potential along the neural lineage during development.
• Nicotine addiction and nicotinic receptors: lessons from genetically modified mice
  - Nat Rev Neurosci 11(6):389 (2010)
  The past decades have seen a revolution in our understanding of brain diseases and in particular of drug addiction. This has been largely due to the identification of neurotransmitter receptors and the development of animal models, which together have enabled the investigation of brain functions from the molecular to the cognitive level. Tobacco smoking, the principal — yet avoidable — cause of lung cancer is associated with nicotine addiction. Recent studies in mice involving deletion and replacement of nicotinic acetylcholine receptor subunits have begun to identify the molecular mechanisms underlying nicotine addiction and might offer new therapeutic strategies to treat this addiction.
• 22q11.2 microdeletions: linking DNA structural variation to brain dysfunction and schizophrenia
  - Nat Rev Neurosci 11(6):402 (2010)
  Recent studies are beginning to paint a clear and consistent picture of the impairments in psychological and cognitive competencies that are associated with microdeletions in chromosome 22q11.2. These studies have highlighted a strong link between this genetic lesion and schizophrenia. Parallel studies in humans and animal models are starting to uncover the complex genetic and neural substrates altered by the microdeletion. In addition to offering a deeper understanding of the effects of this genetic lesion, these findings may guide analysis of other copy-number variants associated with cognitive dysfunction and psychiatric disorders.
• Somatosensation in social perception
  Keysers C Kaas JH Gazzola V - Nat Rev Neurosci 11(6):417 (2010)
  The discovery of mirror neurons in motor areas of the brain has led many to assume that our ability to understand other people's behaviour partially relies on vicarious activations of motor cortices. This Review focuses the limelight of social neuroscience on a different set of brain regions: the somatosensory cortices. These have anatomical connections that enable them to have a role in visual and auditory social perception. Studies that measure brain activity while participants witness the sensations, actions and somatic pain of others consistently show vicarious activation in the somatosensory cortices. Neuroscientists are starting to understand how the brain adds a somatosensory dimension to our perception of other people.
• Insights into the life and work of Sir Charles Sherrington
  Molnár Z Brown RE - Nat Rev Neurosci 11(6):429 (2010)
  Much of the original historical data behind the greatest discoveries in neuroscience are now lost. However, a recently rediscovered box of histological slides belonging to Sir Charles Sherrington, a pioneer in spinal cord and motor control research, has survived at the University of Oxford since 1936. Sherrington coined the term 'synapse', developed the concept of inhibition in neuronal function, demonstrated the integration of sensory and motor actions of the nervous system, and examined the synaptic activity of single neurons and their integration into neuronal circuits. Here, we explore Sherrington's lifetime of discoveries, with reference to histological specimens from his box of slides.
• Modelling neurodegeneration in Saccharomyces cerevisiae: why cook with baker's yeast?
  Khurana V Lindquist S - Nat Rev Neurosci 11(6):436 (2010)
  In ageing populations, neurodegenerative diseases increase in prevalence, exacting an enormous toll on individuals and their communities. Multiple complementary experimental approaches are needed to elucidate the mechanisms underlying these complex diseases and to develop novel therapeutics. Here, we describe why the budding yeast Saccharomyces cerevisiae has a unique role in the neurodegeneration armamentarium. As the best-understood and most readily analysed eukaryotic organism, S. cerevisiae is delivering mechanistic insights into cell-autonomous mechanisms of neurodegeneration at an interactome-wide scale.
• Correspondence: A second-person approach to other minds
  - Nat Rev Neurosci 11(6):449 (2010)
  In a recent Review (The functional role of the parieto-frontal mirror circuit: interpretations and misinterpretations. Nature Rev. Neurosci. 11, 264–274 (2010)
• Correspondence: Mirroring and making sense of others
  - Nat Rev Neurosci 11(6):449 (2010)
  In a recent Review (The functional role of the parieto-frontal mirror circuit: interpretations and misinterpretations. Nature Rev. Neurosci. 11, 264–274 (2010)
• Corrigendum: Roles of small regulatory RNAs in determining neuronal identity
  - Nat Rev Neurosci 11(6):449 (2010)
  On page 331 of the above article, we wrote that: "Surprisingly, these defects could be partially rescued by a single miRNA, miR-340 (Ref. 17)." This should have read: "Surprisingly, these defects could be partially rescued by a single miRNA, miR-430 (Ref. 17)." This was corrected online on 30 April 2010. The authors apologize for this error.
• Corrigendum: Branching out: mechanisms of dendritic arborization
  - Nat Rev Neurosci 11(6):449 (2010)
  On page 317 in box 1 of the above article, we wrote that: "For example, the ubiquitin ligase anaphase-promoting complex specifically regulates axon or dendrite morphogenesis in murine cerebellar granule cells depending on whether it recruits the co-activator cadherin 1 or CDC20 to the complex152,153." This should have read: "For example, the ubiquitin ligase anaphase-promoting complex specifically regulates axon or dendrite morphogenesis in murine cerebellar granule cells depending on whether it recruits the co-activator fizzy-related protein homologue or CDC20 to the complex152,153." This was corrected online on 30 April 2010. The authors apologize for this error.