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The Journal of Neuroscience, November 9, 2005, 25(45)
This Week in The Journal
Cellular/Molecular
Snapin-Less Mice and Chromaffin Cell Exocytosis
Jin-Hua Tian, Zheng-Xing Wu, Michael Unzicker, Li Lu, Qian Cai, Cuiling Li, Claudia Schirra, Ulf Matti, David Stevens, Chuxia Deng, Jens Rettig, and Zu-Hang Sheng
(see pages 10546-10555)
The calcium-dependent exocytosis of synaptic vesicles requires assembly of the soluble N-ethyl maleimide sensitive factor adaptor protein receptor (SNARE) complex, consisting of the vesicular membrane-associated protein synaptobrevin, the plasma membrane-associated protein syntaxin, and synaptosomal-associated protein 25 kDa (SNAP-25). Before release, the calcium-sensing protein synaptotagmin also must bind SNAP-25. Snapin, first identified as a SNAP-25-binding protein, enhances the association of synaptotagmin with SNAP-25. This week, Tian et al. examine the role of snapin in the release of dense-core vesicles in chromaffin cells using snapin-deficient mice. Heterozygous animals appeared normal, but homozygotes did not survive past birth. Although the loss of snapin did not affect formation of the SNARE complex, it did reduce the association between SNAP-25 and synaptotagmin. In chromaffin cells lacking snapin, the fast exocytotic burst of release was reduced by nearly one-half and was rescued by over-expression of snapin. Snapin appears to stabilize the readily releasable pool of primed vesicles.
Development/Plasticity/Repair
Two Axon Branches, Two Targets, Two Guidance Molecules
Yan Liu and Mary C. Halloran
(see pages 10556-10563)
Axons and dendrites often respond differentially to guidance factors in developing their characteristic patterns and orientations, but what about cells that send two axons along distinct paths? This week, Liu and Halloran address that question in Rohon-Beard (RB) sensory neurons in zebrafish embryos. Using live imaging, the authors report that central axons chugged along straight paths at a steady 20 µm/h. Peripheral axons emerged from the central axon and exited the spinal cord, scattering and branching often to form an epidermal network covering the trunk. The authors injected antisense morpholinos to knock down, or cDNAs to misexpress, putative guidance molecules. Semaphorin3D, normally expressed in the spinal cord roof plate, repelled peripheral but not central axons, suggesting it may guide peripheral axons out of the spinal cord. The RB-expressed Ig superfamily molecule transient axonal glycoprotein-1, however, was required for forward growth of central axons but had no effect on peripheral axons.
Behavioral/Systems/Cognitive
The Rubber-Hand Illusion Revisited
H. Henrik Ehrsson, Nicholas P. Holmes, and Richard E. Passingham
(see pages 10564-10572)
In this week's Journal, Ehrsson et al. tested the feeling of body ownership using the somewhat creepy sensation associated with the rubber-hand illusion. In the authors' version of the illusion, blindfolded participants were guided to touch a rubber hand with their left index finger. Simultaneously, the experimenter touched subjects on their right hand, creating, after some seconds, the feeling in most subjects that they were touching their own hand. The rubber hand, experimenter, and subjects all wore gloves to minimize tactile differences. Temporal synchrony of the sensory signals was key to the illusion. As opposed to previous uses of the illusion, these experiments did not include a visual component, showing that tactile and proprioceptive sensations are sufficient to fool the subject into ownership of the hand. Functional magnetic resonance imaging revealed that the ventral premotor and intraparietal cortices and cerebellum were activated during the illusion to a degree that correlated with the strength of the illusion.
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Want to test your sense of body ownership? Try the somatic rubber hand illusion. See the article by Ehrsson et al. for details.
Neurobiology of Disease
A2A, mGlu5, and Parkinsonism
Anil Kachroo, Lianna R. Orlando, David K. Grandy, Jiang-Fan Chen, Anne B. Young, and Michael A. Schwarzschild
(see pages 10414-10419)
Antagonists for the metabotropic glutamate receptor mGlu5 and the adenosine receptor A2A have shown anti-parkinsonian effects in preclinical studies. These receptors also assemble in heteromeric complexes in the striatum, suggesting they might work in concert. This week, Kachroo et al. treated mice with reserpine, which depletes striatal dopamine, and examined interactions between mGlu5 and A2A receptors. In normal and dopamine-depleted mice, the mGlu5 antagonist 2-methyl-6-(phenylethynyl)-pyridine (MPEP) induced locomotor activity that was augmented by the A2A antagonist KW-6002. The MPEP action was absent in mice lacking mGlu5 receptors and, interestingly, also in mice lacking A2A receptors, D2 dopamine receptors, or both. The behavior was similarly missing from mice in which A2A receptors were conditionally knocked out in postnatal forebrain, thus excluding a developmental effect. The D1 dopamine receptor agonist SKF 38393, however, increased motor behavior in all genotypes.
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