Hot off the presses! Aug 01 Nat Rev Neurosci

The Aug 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 10(8):541 (2009)
  
• Neurogenetics: Schizophrenia: missing heritability found?
  - Nat Rev Neurosci 10(8):543 (2009)
  
• Pain: A parting of ways
  - Nat Rev Neurosci 10(8):544 (2009)
  
• Ion channels: A regulatory sidekick
  - Nat Rev Neurosci 10(8):544 (2009)
  
• In brief: Peptides, Synaptic plasticity, Repair, Psychiatric disorders
  - Nat Rev Neurosci 10(8):545 (2009)
  
• Neuronal plasticity: Mossy fibres WNT more contact with CA3
  - Nat Rev Neurosci 10(8):546 (2009)
  
• Psychiatric disorders: Averting panic attacks
  - Nat Rev Neurosci 10(8):546 (2009)
  
• Sleep: Play it again
  - Nat Rev Neurosci 10(8):546 (2009)
  
• In brief: Neurodegenerative disease, Feeding behaviour, Learning and memory, Cognitive neuroscience
  - Nat Rev Neurosci 10(8):547 (2009)
  
• Neurodegenerative disease: Spreading the tau
  - Nat Rev Neurosci 10(8):548 (2009)
  
• Neuron–glia interactions: Kif1b motors mRNA
  - Nat Rev Neurosci 10(8):548 (2009)
  
• The genetic and molecular regulation of sleep: from fruit flies to humans
  - Nat Rev Neurosci 10(8):549-560 (2009)
  It has been known for a long time that genetic factors affect sleep quantity and quality. Genetic screens have identified several mutations that affect sleep across species, pointing to an evolutionary conserved regulation of sleep. Moreover, it has also been recognized that sleep affects gene expression. These findings have given valuable insights into the molecular underpinnings of sleep regulation and function that might lead the way to more efficient treatments for sleep disorders.
• The glutamate homeostasis hypothesis of addiction
  - Nat Rev Neurosci 10(8):561-572 (2009)
  Addiction is associated with neuroplasticity in the corticostriatal brain circuitry that is important for guiding adaptive behaviour. The hierarchy of corticostriatal information processing that normally permits the prefrontal cortex to regulate reinforcement-seeking behaviours is impaired by chronic drug use. A failure of the prefrontal cortex to control drug-seeking behaviours can be linked to an enduring imbalance between synaptic and non-synaptic glutamate, termed glutamate homeostasis. The imbalance in glutamate homeostasis engenders changes in neuroplasticity that impair communication between the prefrontal cortex and the nucleus accumbens. Some of these pathological changes are amenable to new glutamate- and neuroplasticity-based pharmacotherapies for treating addiction.
• New insights into symptoms and neurocircuit function of anorexia nervosa
  - Nat Rev Neurosci 10(8):573-584 (2009)
  Individuals with anorexia nervosa have a relentless preoccupation with dieting and weight loss that results in severe emaciation and sometimes death. It is controversial whether such symptoms are secondary to psychosocial influences, are a consequence of obsessions and anxiety or reflect a primary disturbance of brain appetitive circuits. New brain imaging technology provides insights into ventral and dorsal neural circuit dysfunction — perhaps related to altered serotonin and dopamine metabolism — that contributes to the puzzling symptoms found in people with eating disorders. For example, altered insula activity could explain interoceptive dysfunction, and altered striatal activity might shed light on altered reward modulation in people with anorexia nervosa.
• Inside the brain of an elite athlete: the neural processes that support high achievement in sports
  - Nat Rev Neurosci 10(8):585-596 (2009)
  Events like the World Championships in athletics and the Olympic Games raise the public profile of competitive sports. They may also leave us wondering what sets the competitors in these events apart from those of us who simply watch. Here we attempt to link neural and cognitive processes that have been found to be important for elite performance with computational and physiological theories inspired by much simpler laboratory tasks. In this way we hope to inspire neuroscientists to consider how their basic research might help to explain sporting skill at the highest levels of performance.
• Spinal muscular atrophy: why do low levels of survival motor neuron protein make motor neurons sick?
  - Nat Rev Neurosci 10(8):597-609 (2009)
  Many neurogenetic disorders are caused by the mutation of ubiquitously expressed genes. One such disorder, spinal muscular atrophy, is caused by loss or mutation of the survival motor neuron1 gene (SMN1), leading to reduced SMN protein levels and a selective dysfunction of motor neurons. SMN, together with partner proteins, functions in the assembly of small nuclear ribonucleoproteins (snRNPs), which are important for pre-mRNA splicing. It has also been suggested that SMN might function in the assembly of other ribonucleoprotein complexes. Two hypotheses have been proposed to explain the molecular dysfunction that gives rise to spinal muscular atrophy (SMA) and its specificity to a particular group of neurons. The first hypothesis states that the loss of SMN's well-known function in snRNP assembly causes an alteration in the splicing of a specific gene (or genes). The second hypothesis proposes that SMN is crucial for the transport of mRNA in neurons and that disruptio! n of this function results in SMA.
• How the olfactory bulb got its glomeruli: a just so story?
  - Nat Rev Neurosci 10(8):611-618 (2009)
  The nearly 2,000 glomeruli that cover the surface of the olfactory bulb are so distinctive that they were noted specifically in the earliest of Cajal's catalogues. They have variously been considered a functional unit, an organizational unit and a crucial component of the olfactory coding circuit. Despite their central position in olfactory processing, the development of the glomeruli has only recently begun to be investigated with new and powerful genetic tools. Some unexpected findings have been made that may lead to a new understanding of the processes involved in wiring sensory regions of the brain. It may no longer be sufficient to simply invoke genes, spikes and their interplay in the construction of brain circuits. The story of 'how the olfactory bulb got its glomeruli' may be more complex, and more revealing, than has been supposed.