Top 7 papers in neuroscience

#1 Neurons complete hippocampus loop There's a new, important function for a once-obscure cell population in the brain: CA2 pyramidal neurons, a subset of cells in the hippocampus, form a link between electrical inputs and outputs in the hippocampus. V. Chevaleye et al., "Strong CA2 pyramidal neuron synapses define a powerful disynaptic cortico-hippocampal loop," linkurl:Neuron,;http://www.ncbi.nlm.nih.gov/sites/entrez/20510860?dopt=Abstract&holding=f1000,f1000m,isrctn 66:560-72, 2010. linkurl:Eval by;http://f1000biology.com/article/z0w6412lm929myg/id/3514956/evaluation/sections Stephen Fitzjohn and Graham Collingridge, MRC Centre for Synaptic Plasticity, UK; Johannes Hell, University of California, Davis.

Neurons in the mouse brain
Image: linkurl:Wikimedia Commons, Neurollero;http://www.flickr.com/photos/neurollero/17873944/in/set-366106/

#2 Non-overlapping neurons The medial entorhinal cortex, a hub for memory and navigation in the brain, consists of two tangled but functionally separate networks that have different long-range axonal targets, and thus may be involved in different functions in the brain. The finding offers insights to how neural networks function, and -- in conditions like epilepsy -- dysfunction. C. Varga et al., "Target-selective GABAergic control of entorhinal cortex output," linkurl:Nat Neurosci,;http://www.ncbi.nlm.nih.gov/sites/entrez/20512133?dopt=Abstract&holding=f1000,f1000m,isrctn 13:822-4, 2010. linkurl:Eval by;http://f1000biology.com/article/mf8ms20zl7z9qt0/id/3507956/evaluation/sections Edvard Moser, Norwegian University of Science and Technology, Norway; Jeff Isaacson, University of California, San Diego. #3 "We're going to need a bigger model" In a detailed mathematical analysis, researchers analyze the capacity of computational models to model neuronal oscillations -- the repetitive rise and fall of membrane potentials. They find that current single-cell oscillation models are not adequate, and there is a need for additional computational models to assess this mechanism. M.W. Remme et al., "Democracy-independence trade-off in oscillating dendrites and its implications for grid cells," linkurl:Neuron,;http://www.ncbi.nlm.nih.gov/sites/entrez/20471355?dopt=Abstract&holding=f1000,f1000m,isrctn 66:560-72, 2010. linkurl:Eval by;http://f1000biology.com/article/pywfn2bz9pshgy8/id/3548974/evaluation/sections Lisa Giocomo and Edvard Moser, Norwegian University of Science and Technology, Norway; Neil Burgess, University College London. #4 Key step to making dendrites For the first time, researchers demonstrate that a protein that fuses membranes instructs the development of dendrites in C. elegans. The protein, EFF-1, causes overlapping branches to fuse together, a novel control mechanism for the poorly understood morphogenesis of dendrites. M. Oren-Suissa et al., "The fusogen EFF-1 controls sculpting of mechanosensory dendrites," linkurl:Science,;http://www.ncbi.nlm.nih.gov/sites/entrez/20448153?dopt=Abstract&holding=f1000,f1000m,isrctn 328:1285-8, 2010. linkurl:Eval by;http://f1000biology.com/article/5zcyjj2v5q1y4gd/id/3929957/evaluation/sections Tina Schwabe and Thomas Clandinin, Stanford University, California; Andrew Chisholm, University of California, San Diego. #5 How amyloid kills synapses New findings suggest an explanation for why amyloid causes synapses to fail in Alzheimer's and other diseases: The binding of amyloid beta oligomers causes glutamate receptors in synaptic membranes to form clusters, resulting in increased intracellular calcium and eventual deterioration of the synapse. M. Renner et al., "Deleterious effects of amyloid beta oligomers acting as an extracellular scaffold for mGluR5," linkurl:Neuron,;http://www.ncbi.nlm.nih.gov/sites/entrez/20547131?dopt=Abstract&holding=f1000,f1000m,isrctn 66:739-54, 2010. linkurl:Eval by;http://f1000biology.com/article/dtzwfjsgrfrv59p/id/3743957/evaluation/sections Joel Bockaert, Institute of Functional Genomics, France; Hui-Chen Lu and Kenneth Mackie, Indiana University. #6 New mechanism for synaptic plasticity Researchers have uncovered another key mechanism behind one of the most important processes in learning and memory, synaptic plasticity. Specifically, two signaling molecules, BRAG2 and Arf6, trigger endocytosis of AMPA receptors in the brain, inducing long-term depression (LTD), a long-lasting reduction in the sensitivity of neurons and a well-known form of synaptic plasticity. R. Scholz et al., "AMPA receptor signaling through BRAG2 and Arf6 critical for long-term synaptic depression," linkurl:Neuron,;http://www.ncbi.nlm.nih.gov/sites/entrez/20547133?dopt=Abstract&holding=f1000,f1000m,isrctn 66:768-80, 2010. linkurl:Eval by;http://f1000biology.com/article/fqxs35cc3srtcmh/id/3606964/evaluation/sections Stephen Fitzjohn and Graham Collingridge, MRC Centre for Synaptic Plasticity, UK; Johannes Hell, University of California, Davis. #7 Cell division affects cell fate Through live imaging of a zebrafish embryo, researchers show that asymmetrical cell division is important in establishing cell fate in the vertebrate central nervous system. P. Alexandre et al., "Neurons derive from the more apical daughter in asymmetric divisions in the zebrafish neural tube," linkurl:Nat Neurosci,;http://www.ncbi.nlm.nih.gov/sites/entrez/20453852?dopt=Abstract&holding=f1000,f1000m,isrctn 13:673-9, 2010. linkurl:Eval by;http://f1000biology.com/article/zpy3twwp0r1hh2k/id/3565956/evaluation/sections Judith Eisen, University of Oregon; Caren Norden and William Harris, University of Cambridge, UK. The F1000 Top 7 is a snapshot of the highest ranked articles from a 30-day period on Faculty of 1000 Neuroscience, as calculated on July 22, 2010. Faculty Members evaluate and rate the most important papers in their field. To see the latest rankings, search the database, and read daily evaluations, visit linkurl:http://f1000.com.;http://f1000.com
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[13th July 2010]