Hot off the presses! Jul 01 Nat Rev Neurosci

The Jul 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(7):467 (2009)
  
• Cerebellum: An olive branch to two theories
  - Nat Rev Neurosci 10(7):468 (2009)
  
• MicroRNA: MicroRNAs have receptor subunits in a bind
  - Nat Rev Neurosci 10(7):469 (2009)
  
• Development: Terminal differentiation
  - Nat Rev Neurosci 10(7):469 (2009)
  
• Synaptic plasticity: The advantages of youth
  - Nat Rev Neurosci 10(7):470 (2009)
  
• Sleep: What goes up, must come down
  - Nat Rev Neurosci 10(7):470 (2009)
  
• In brief: Neuronal circuits, Neurological disorders, Reward, Neurogenesis
  - Nat Rev Neurosci 10(7):470 (2009)
  
• Learning and memory: HDAC2 is the one
  - Nat Rev Neurosci 10(7):471 (2009)
  
• Neuronal metabolism: A question of balance
  - Nat Rev Neurosci 10(7):472 (2009)
  
• Spine formation: Signalling growth
  - Nat Rev Neurosci 10(7):472 (2009)
  
• Addiction: Let me count the genes
  - Nat Rev Neurosci 10(7):472 (2009)
  
• In brief: Reward, Fear, Attention
  - Nat Rev Neurosci 10(7):473 (2009)
  
• New sites of action for GIRK and SK channels
  - Nat Rev Neurosci 10(7):475-480 (2009)
  It was recently discovered that two different types of voltage-insensitive K+ channels, G protein-coupled inwardly rectifying K+ (GIRK) and small-conductance Ca2+-activated K+ (SK) channels, are located on dendritic branches, spines and shafts in the postsynaptic densities of excitatory synapses in many central neurons. Together with increases in our knowledge of how these channels are regulated through stable protein–protein interactions in multi-protein complexes, this has added another layer of complexity to our understanding of synaptic transmission and plasticity.
• Mitochondrial membrane permeabilization in neuronal injury
  - Nat Rev Neurosci 10(7):481-494 (2009)
  Acute neurological conditions such as cerebrovascular diseases and trauma are associated with irreversible loss of neurons and glial cells. Severe or prolonged injury results in uncontrollable cell death within the core of lesions. Conversely, cells that are less severely damaged succumb in a relatively slow fashion, frequently via the intrinsic pathway of cell death, through the deterioration of mitochondrial functions. The permeabilization of mitochondrial membranes determines whether cells will succumb to or survive the injury, and represents a 'point of no return' in mitochondrial cell death. It is therefore an attractive target for the development of new neuroprotective interventions.
• The diverse functional roles and regulation of neuronal gap junctions in the retina
  - Nat Rev Neurosci 10(7):495-506 (2009)
  Electrical synaptic transmission through gap junctions underlies direct and rapid neuronal communication in the CNS. The diversity of functional roles that electrical synapses have is perhaps best exemplified in the vertebrate retina, in which gap junctions are formed by each of the five major neuron types. These junctions are dynamically regulated by ambient illumination and by circadian rhythms acting through light-activated neuromodulators such as dopamine and nitric oxide, which in turn activate intracellular signalling pathways in the retina.The networks formed by electrically coupled neurons are plastic and reconfigurable, and those in the retina are positioned to play key and diverse parts in the transmission and processing of visual information at every retinal level.
• Circuits controlling vertebrate locomotion: moving in a new direction
  - Nat Rev Neurosci 10(7):507-518 (2009)
  Neurobiologists have long sought to understand how circuits in the nervous system are organized to generate the precise neural outputs that underlie particular behaviours. The motor circuits in the spinal cord that control locomotion, commonly referred to as central pattern generator networks, provide an experimentally tractable model system for investigating how moderately complex ensembles of neurons generate select motor behaviours. The advent of novel molecular and genetic techniques coupled with recent advances in our knowledge of spinal cord development means that a comprehensive understanding of how the motor circuitry is organized and operates may be within our grasp.
• Tests to assess motor phenotype in mice: a user's guide
  - Nat Rev Neurosci 10(7):519-529 (2009)
  The characterization of mouse models of human disease is essential for understanding the underlying pathophysiology and developing new therapeutics. Many diseases are often associated with more than one model, and so there is a need to determine which model most closely represents the disease state or is most suited to the therapeutic approach under investigation. In the case of neurological disease, motor tests provide a good read-out of neurological function. This overview of available motor tasks aims to aid researchers in making the correct choice of test when attempting to tease out a transgenic phenotype or when assessing the recovery of motor function following therapeutic intervention.
• Principles of neural ensemble physiology underlying the operation of brain–machine interfaces
  - Nat Rev Neurosci 10(7):530-540 (2009)
  Research on brain–machine interfaces has been ongoing for at least a decade. During this period, simultaneous recordings of the extracellular electrical activity of hundreds of individual neurons have been used for direct, real-time control of various artificial devices. Brain–machine interfaces have also added greatly to our knowledge of the fundamental physiological principles governing the operation of large neural ensembles. Further understanding of these principles is likely to have a key role in the future development of neuroprosthetics for restoring mobility in severely paralysed patients.