Hot off the presses! Dec 01 Nat Rev Neurosci

The Dec 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 11(12):783 (2010)
  
• Brain–machine interfaces: See what you want to see | PDF (180 KB)
  - Nat Rev Neurosci 11(12):785 (2010)
  Visual images that we associate with a familiar concept activate neurons in the medial temporal lobe (MTL) that encode that concept. Now, Cerf, Koch, Fried and colleagues show that when multiple images are viewed simultaneously, humans can use conscious thought to regulate the activity of MTL neurons encoding different concepts, indicating that internal, cognitive processes can override neuronal activation induced by sensory input.
• Depression: In pursuit of happiness | PDF (190 KB)
  - Nat Rev Neurosci 11(12):786 (2010)
  Major depressive disorder (MDD) is associated with structural alterations to the hippocampus that are thought to underlie some symptoms of the disease, such as impaired cognition and depressed mood. However, the molecular changes that cause the pathophysiology are largely unknown.
• Addiction: The ups and downs of cocaine in the NAc | PDF (194 KB)
  - Nat Rev Neurosci 11(12):786 (2010)
  The nucleus accumbens (NAc) is known to be important for the rewarding effects of cocaine, but little is known about how the subtypes of projection neurons in this region contribute to the effect. Now, Nestler and colleagues show that signalling through the brain-derived neurotrophic factor (BDNF) pathway has opposing effects on cocaine reward in the two main populations of neurons of the NAc.
• Neurodegenerative disease: Pieces of the Parkinson's puzzle | PDF (227 KB)
  - Nat Rev Neurosci 11(12):787 (2010)
  Many pathogenic molecules underlying rare, mostly autosomal-dominant forms of Parkinson's disease have been identified. However, less is known about pathogenic pathways that lead to the common, 'sporadic' form.
• Neuroimmunology: The origins of microglial cells | PDF (152 KB)
  - Nat Rev Neurosci 11(12):787 (2010)
  There is much debate as to the origin of microglial cells — the resident macrophages of the CNS — and it has been proposed that haematopoietic progenitor cells are recruited from the blood and differentiate in the CNS in waves during the embryonic and perinatal stages of development (a process termed definitive haematopoiesis). Ginhoux et al.
• Endocannabinoids: Dual effects at different sites | PDF (190 KB)
  - Nat Rev Neurosci 11(12):788 (2010)
  Endocannabinoids are released by neurons and are generally thought to inhibit synaptic transmission in many brain regions, including the hippocampus. Recent studies showed that in this region, both neurons and astrocytes express endocannabinoid 1 receptors (CB1Rs), but the role of astrocytic CB1Rs on synaptic transmission has remained unknown.
• Circadian rhythms: In the heat of the night | PDF (221 KB)
  - Nat Rev Neurosci 11(12):788 (2010)
  Mammalian cells contain cell-autonomous 'clocks', or sets of genes of which the cyclical expression controls processes governed by circadian rhythms. The task of ensuring that these millions of clocks are entrained (or reset) every 24 hours falls to the 'master clock' in the suprachiasmatic nucleus (SCN) of the hypothalamus, and a team led by Joseph Takahashi recently demonstrated how it might be achieved.
• Blood–brain barrier: Plugging the leak | PDF (188 KB)
  - Nat Rev Neurosci 11(12):789 (2010)
  Endothelial cells in the CNS are endowed with properties — such as tight junctions, low rates of transcytosis and the expression of various transporters — that allow them to regulate the movement of molecules, ions and cells between the blood and the brain, thus contributing to the blood–brain barrier (BBB). Pericytes, which surround capillaries, are also a component of the BBB, but their role in barrier function has remained unclear.
• Neuroimmunology: Keeping HSV-1 dormant | PDF (180 KB)
  - Nat Rev Neurosci 11(12):790 (2010)
  Following host infection, herpes simplex virus 1 (HSV-1) remains latent in peripheral neurons. β-nerve growth factor (NGF) was known to have a role in maintaining HSV-1 latency, but the molecular details had not been described.
• Cognitive neuroscience | Ion channels | Metabolism | Cancer | PDF (161 KB)
  - Nat Rev Neurosci 11(12):790 (2010)
  Modulating neuronal activity produces specific and long-lasting changes in numerical competence Cohen Kadosh, R.et al. Curr. Biol. 20, 1–5 (2010)
• The role of leucine-rich repeat kinase 2 (LRRK2) in Parkinson's disease
  - Nat Rev Neurosci 11(12):791 (2010)
  Parkinson's disease, like many common age-related conditions, is now recognized to have a substantial genetic component. Here, I discuss how mutations in a large complex gene — leucine-rich repeat kinase 2 (LRRK2) — affect protein function, and I review recent evidence that LRRK2 mutations affect pathways that involve other proteins that have been implicated in Parkinson's disease, specifically α-synuclein and tau. These concepts can be used to understand disease processes and to develop therapeutic opportunities for the treatment of Parkinson's disease.
• Functions of Nogo proteins and their receptors in the nervous system
  - Nat Rev Neurosci 11(12):799 (2010)
  The membrane protein Nogo-A was initially characterized as a CNS-specific inhibitor of axonal regeneration. Recent studies have uncovered regulatory roles of Nogo proteins and their receptors — in precursor migration, neurite growth and branching in the developing nervous system — as well as a growth-restricting function during CNS maturation. The function of Nogo in the adult CNS is now understood to be that of a negative regulator of neuronal growth, leading to stabilization of the CNS wiring at the expense of extensive plastic rearrangements and regeneration after injury. In addition, Nogo proteins interact with various intracellular components and may have roles in the regulation of endoplasmic reticulum (ER) structure, processing of amyloid precursor protein and cell survival.
• The diverse roles of ribbon synapses in sensory neurotransmission
  - Nat Rev Neurosci 11(12):812 (2010)
  Sensory synapses of the visual and auditory systems must faithfully encode a wide dynamic range of graded signals, and must be capable of sustained transmitter release over long periods of time. Functionally and morphologically, these sensory synapses are unique: their active zones are specialized in several ways for sustained, rapid vesicle exocytosis, but their most striking feature is an organelle called the synaptic ribbon, which is a proteinaceous structure that extends into the cytoplasm at the active zone and tethers a large pool of releasable vesicles. But precisely how does the ribbon function to support tonic release at these synapses? Recent genetic and biophysical advances have begun to open the 'black box' of the synaptic ribbon with some surprising findings and promise to resolve its function in vision and hearing.
• Neuronal circuitry for pain processing in the dorsal horn
  - Nat Rev Neurosci 11(12):823 (2010)
  Neurons in the spinal dorsal horn process sensory information, which is then transmitted to several brain regions, including those responsible for pain perception. The dorsal horn provides numerous potential targets for the development of novel analgesics and is thought to undergo changes that contribute to the exaggerated pain felt after nerve injury and inflammation. Despite its obvious importance, we still know little about the neuronal circuits that process sensory information, mainly because of the heterogeneity of the various neuronal components that make up these circuits. Recent studies have begun to shed light on the neuronal organization and circuitry of this complex region.
• The memory paradox
  - Nat Rev Neurosci 11(12):837 (2010)
  Declarative and emotional memories are key to quality of life and day-to-day functioning. The absence of memory or the inability to recall memories properly in an emotional context leads to dysfunction but, paradoxically, memories that generate too much emotion can be equally disabling.