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The Journal of Neuroscience, November 16, 2005, 25(46)
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This Week in The Journal
Cellular/Molecular
Mice and Men and Pittsburgh B
William E. Klunk, Brian J. Lopresti, Milos D. Ikonomovic, Iliya M. Lefterov, Radosveta P. Koldamova, Eric E. Abrahamson, Manik L. Debnath, Daniel P. Holt, Guo-feng Huang, Li Shao, Steven T. DeKosky, Julie C. Price, and Chester A. Mathis
(see pages 10598-10606)
This week, Klunk et al. continue efforts to image amyloid deposition in the brain. They used the positron emission tomography (PET) tracer Pittsburgh Compound-B (PIB), a derivative of the amyloid-binding dye thioflavin-T. PIB is retained in amyloid deposits in patients with Alzheimer's disease (AD). As in a recent Journal of Neuroscience article (http://www.jneurosci.org/cgi/content/full/25/43/10041), the authors imaged transgenic mice expressing mutant presenilin-1 (PS1)/amyloid precursor protein (APP). However, unlike the previous magnetic resonance imaging study, here plaques were undetectable with micro-PET despite extensive amyloid deposition. The in vitro binding affinity of PIB to PS1/APP brain was similar to synthetic A
, but there were 1000-fold fewer high-affinity sites (per molecule of A
Development/Plasticity/Repair
Gap Junctions and Retinal Progenitors
Rachael A. Pearson, Nanna L. Lüneborg, David L. Becker, and Peter Mobbs
(see pages 10803-10814)
During development of the chick retina, progenitor cells undergo multiple rounds of cell division at the ventricular zone, producing 200 million cells during the first week of development. In the process, the cell nuclei of progenitors make interkinetic movements in which they travel from the ventricular zone to the vitreal surface and back again, before completing mitosis. This week, Pearson et al. show that gap junctions and calcium transients facilitate these movements. In progenitor cells, spontaneous calcium transients usually preceded saltatory nuclear movements, whereas calcium chelators slowed movement. Pharmacological blockers of gap junctions also slowed movement, as did a dominant-negative form of the gap-junction protein connexin 43. Gap26, a connexin mimetic peptide that blocks hemichannels, also impaired movement, albeit to a lesser extent. The authors conclude that cell coupling by gap junctions as well as hemichannels may serve to enhance calcium signaling and facilitate interkinetic nuclear movement.
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Images of a retinal progenitor cell at time 0, 20, 40, and 60 minas it retracts a vitreal process (arrowhead) and migrates toward the ventricular zone (VZ). See the article by Pearson et al. for details.
Behavioral/Systems/Cognitive
Discriminating Depth in the Inferior Temporal Lobe
Takanori Uka, Seiji Tanabe, Masayuki Watanabe, and Ichiro Fujita
(see pages 10796-10802)
Depth perception arises from disparities created by binocular vision. In monkeys, neurons in several regions in the visual pathways are activated by disparity. In this week's Journal, Uka et al. examined how well activity of neurons in the inferior temporal cortex (IT), or ventral visual pathway, correlated with fine discrimination. Monkeys were trained to perform a stereoacuity task in which they reported the perceived depth of a shape by making a saccade to a horizontally displaced target. Extracellular recordings during a fixation task were used to construct a disparity-tuning curve. IT neurons were more strongly activated by stimuli in front of the fixation point ("near") than those behind the fixation point ("far"). During the depth discrimination task, no disparity cue was provided, forcing the monkeys to guess the depth. The monkeys reported the shape as "near" when neuronal activity was above average and "far" when activity was below average, suggesting a functional link between IT neurons and depth perception.
Neurobiology of Disease
-Synuclein, Astrocytes, and Multiple System Atrophy
Clifford W. Shults, Edward Rockenstein, Leslie Crews, Anthony Adame, Michael Mante, Gabriel Larrea, Makoto Hashimoto, David Song, Takeshi Iwatsubo, Kyoko Tsuboi, and Eliezer Masliah
(see pages 10689-10699)
In man, parkinsonian symptoms can be accompanied in some patients by autonomic and/or cerebellar dysfunction, an entity called multiple system atrophy (MSA). In this disorder,
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