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:

• Neurodegenerative disease: Preventing 'SIRTain' death by mutant huntingtin | PDF (407 KB)
  - Nat Rev Neurosci 13(2):71 (2012)
  Huntington's disease is an inherited neurodegenerative disease caused by a glutamine repeat expansion in huntingtin (HTT) protein that results in HTT accumulation. Studies have shown that calorie restriction ameliorates the pathogenesis of the disease in mice, but the role of the NAD-dependent protein deacetylase sirtuin 1 (SIRT1), which is one of the mediators of the beneficial roles of calorie restriction in Huntington's disease, was unclear.
• Neuronal circuits: The sound of fear | PDF (215 KB)
  - Nat Rev Neurosci 13(2):72 (2012)
  At the cellular level, the process of learning is associated with changes in synaptic strength, but much less is known about the neuronal circuits that underlie learning-induced changes in neuronal activity and ultimately in behavioural output. Reporting in Nature
• Synaptic plasticity: Ubiquitin activates synaptic plasticity | PDF (314 KB)
  - Nat Rev Neurosci 13(2):73 (2012)
  Ubiquitylation of synaptic proteins and their subsequent degradation by the proteasome is thought to be a key mechanism for the regulation of synaptic plasticity. Ubiquitylation can also alter protein function by modifying interactions between proteins or by modulating protein activity; however, less is known about the roles of these non-proteolytic functions of ubiquitin in synaptic plasticity.
• Psychiatric disorders: Why two is better than one | PDF (258 KB)
  - Nat Rev Neurosci 13(2):73 (2012)
  Many depression and anxiety disorders are most effectively treated with a combination of psychotherapy and antidepressant drugs. The biological basis for this observation is not well understood, but Castr and colleagues now show that the antidepressant fluoxetine increases synaptic plasticity in the amygdala and thereby facilitates long-lasting fear extinction.
• Sensory transduction: How TRPs discriminate between different stimuli | PDF (216 KB)
  - Nat Rev Neurosci 13(2):74 (2012)
  Transient receptor potential (TRP) channels transduce a wide variety of stimuli and are used by many different organisms to monitor changes in their environment. How these channels are able to discriminate between different stimuli is unknown, but a recent study in Drosophila melanogaster indicates that the existence of TRP channel isoforms might be key.
• Neuroimmunology: Interferon-γ tunes the rhythm | PDF (176 KB)
  - Nat Rev Neurosci 13(2):74 (2012)
  GABAergic inhibition has an important role in generating and regulating synchronized activity in neuronal networks, but how GABA activity is itself dynamically regulated is unknown. Zhu et al.
• Neural development: Clustering connections | PDF (265 KB)
  - Nat Rev Neurosci 13(2):74 (2012)
  Repetitive bursts of spontaneous neural activity occur in the developing mammalian brain before sensory systems become functional, and these bursts are thought to have a role in the formation of neural circuits. How such bursts of activity travel across networks and individual neurons has been well described, but little attention has been paid to spontaneous activity patterns at the level of synapses.
• Neural development: Epigenetic regulation of asymmetry | PDF (99 KB)
  - Nat Rev Neurosci 13(2):72 (2012)
  The brains of many species demonstrate structural and functional bilateral asymmetry, yet the underlying molecular mechanisms are mostly unknown. In the Caenorhabditis elegans nervous system, the lineages arising from the two daughter cells of a particular blastomere known as ABarap produce a different cell on each side of the body: a motor neuron on the right and an epithelial cell on the left.
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• Mitochondrial transport in neurons: impact on synaptic homeostasis and neurodegeneration
  - Nat Rev Neurosci 13(2):77 (2012)
  Mitochondria have a number of essential roles in neuronal function. Their complex mobility patterns within neurons are characterized by frequent changes in direction. Mobile mitochondria can become stationary or pause in regions that have a high metabolic demand and can move again rapidly in response to physiological changes. Defects in mitochondrial transport are implicated in the pathogenesis of several major neurological disorders. Research into the mechanisms that regulate mitochondrial transport is thus an important emerging frontier.
• Activity-dependent neurotransmitter respecification
  - Nat Rev Neurosci 13(2):94 (2012)
  For many years it has been assumed that the identity of the transmitters expressed by neurons is stable and unchanging. Recent work, however, shows that electrical activity can respecify neurotransmitter expression during development and in the mature nervous system, and an understanding is emerging of the molecular mechanisms underlying activity-dependent transmitter respecification. Changes in postsynaptic neurotransmitter receptor expression accompany and match changes in transmitter specification, thus enabling synaptic transmission. The functional roles of neurotransmitter respecification are beginning to be understood and appear to involve homeostatic synaptic regulation, which in turn influences behaviour. Activation of this novel form of plasticity by sensorimotor stimuli may provide clinical benefits.
• Interneuron dysfunction in psychiatric disorders
  - Nat Rev Neurosci 13(2):107 (2012)
  Schizophrenia, autism and intellectual disabilities are best understood as spectrums of diseases that have broad sets of causes. However, it is becoming evident that these conditions also have overlapping phenotypes and genetics, which is suggestive of common deficits. In this context, the idea that the disruption of inhibitory circuits might be responsible for some of the clinical features of these disorders is gaining support. Recent studies in animal models demonstrate that the molecular basis of such disruption is linked to specific defects in the development and function of interneurons — the cells that are responsible for establishing inhibitory circuits in the brain. These insights are leading to a better understanding of the causes of schizophrenia, autism and intellectual disabilities, and may contribute to the development of more-effective therapeutic interventions.
• Spectral fingerprints of large-scale neuronal interactions
  - Nat Rev Neurosci 13(2):121 (2012)
  Cognition results from interactions among functionally specialized but widely distributed brain regions; however, neuroscience has so far largely focused on characterizing the function of individual brain regions and neurons therein. Here we discuss recent studies that have instead investigated the interactions between brain regions during cognitive processes by assessing correlations between neuronal oscillations in different regions of the primate cerebral cortex. These studies have opened a new window onto the large-scale circuit mechanisms underlying sensorimotor decision-making and top-down attention. We propose that frequency-specific neuronal correlations in large-scale cortical networks may be 'fingerprints' of canonical neuronal computations underlying cognitive processes.
• Computational neuroanatomy of speech production
  - Nat Rev Neurosci 13(2):135 (2012)
  Speech production has been studied predominantly from within two traditions, psycholinguistics and motor control. These traditions have rarely interacted, and the resulting chasm between these approaches seems to reflect a level of analysis difference: whereas motor control is concerned with lower-level articulatory control, psycholinguistics focuses on higher-level linguistic processing. However, closer examination of both approaches reveals a substantial convergence of ideas. The goal of this article is to integrate psycholinguistic and motor control approaches to speech production. The result of this synthesis is a neuroanatomically grounded, hierarchical state feedback control model of speech production.