Skip to main content

Main menu

  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
    • Special Collections
  • EDITORIAL BOARD
    • Editorial Board
    • ECR Advisory Board
    • Journal Staff
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
    • Accessibility
  • SUBSCRIBE

User menu

  • Log out
  • Log in
  • My Cart

Search

  • Advanced search
Journal of Neuroscience
  • Log out
  • Log in
  • My Cart
Journal of Neuroscience

Advanced Search

Submit a Manuscript
  • HOME
  • CONTENT
    • Early Release
    • Featured
    • Current Issue
    • Issue Archive
    • Collections
    • Podcast
  • ALERTS
  • FOR AUTHORS
    • Information for Authors
    • Fees
    • Journal Clubs
    • eLetters
    • Submit
    • Special Collections
  • EDITORIAL BOARD
    • Editorial Board
    • ECR Advisory Board
    • Journal Staff
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
    • Accessibility
  • SUBSCRIBE
PreviousNext
This Week in The Journal

This Week in The Journal

Journal of Neuroscience 3 March 2010, 30 (9) i
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Embedded Image Cellular/Molecular

Ubiquitination Regulates Synaptic Vesicle Release

Gina V. Rinetti and Felix E. Schweizer

(see pages 3157–3166)

Ubiquitination involves attaching the polypeptide ubiquitin to lysine residues of a target protein. The role of polyubiquitination in tagging proteins for degradation is widely recognized, but ubiquitination also has other functions, including triggering internalization and recycling of membrane proteins, assembling signaling complexes, and promoting DNA repair. In neurons, ubiquitination plays roles in axon guidance and synaptogenesis, and it regulates levels of synaptic vesicle proteins and neurotransmitter receptors. Rinetti and Schweizer found that blocking degradation in the proteasome rapidly increased the frequency of spontaneous and miniature EPSCs and IPSCs in cultured hippocampal neurons, probably by increasing synaptic vesicle release. This effect was not likely mediated by accumulation of protein that would normally be degraded, because it occurred even when protein synthesis was blocked. Blocking ubiquitination produced the same effect as blocking degradation, leading the authors to conclude that the effect of degradation results from sequestering of ubiquitin in undegraded proteins, thus preventing other ubiquitin-mediated functions.

Embedded Image Development/Plasticity/Repair

Handedness Shapes Brain Morphology

Stefan Klöppel, Jean-Francois Mangin, Anna Vongerichten, Richard S. J. Frackowiak, and Hartwig R. Siebner

(see pages 3271–3275)

More than 90% of humans are right handed, and evidence suggests that handedness is genetic and arises before birth. Handedness is reflected in brain asymmetries: in right-handers, the left central sulcus is deeper than the right and the cortical representation of the right hand is larger than that of the left. Whether these differences drive or result from handedness is not clear. To address this question, Klöppel et al. compared brain morphology in right-handers, consistent left-handers, and “converted” left-handers who were forced to write with their right hands as children. The area of the left central sulcus in converted left-handers resembled that in right-handers and was significantly greater than that in consistent left-handers, suggesting the difference results from hand use. Interestingly, the middle part of the putamen was smaller in converted individuals than in either consistent left-handers or right-handers, and it was smallest in those converted left-handers that retained the most left hand dexterity.

Embedded Image Behavioral/Systems/Cognitive

LIP Reflects Attention Shifts Before MT

Todd M. Herrington and John A. Assad

(see pages 3287–3296)

Detecting a subtle visual stimulus is easier if you know where to look and you attend to that spot. Directing attention is thought to increase the responsiveness of visual cortical neurons: neurons fire more when an animal is attending to the location where a stimulus is presented than if it is attending to a different location. To determine which neural pathways might drive this change in responsiveness, Herrington and Assad measured the relative timing of activity changes in two brain areas as monkeys' attention shifted. As expected, neuronal firing rate increased in both the middle temporal area (MT) and in the lateral intraparietal area (LIP)—a later stage of processing in visual cortex—when the monkey switched its attention to the recorded neuron's receptive field. The change in activity occurred sooner in LIP than in MT, however, indicating that signals related to attention may propagate from later stages to earlier ones.

Figure
  • Download figure
  • Open in new tab
  • Download powerpoint

Attentional modulation, measured as difference in spike rate when attention is directed in or out of a neuron's receptive field, arises sooner after attention shift (vertical line) in LIP neurons (green) than in MT neurons (blue). See the article by Herrington and Assad for details.

Embedded Image Neurobiology of Disease

Some α-Synuclein Oligomers From Asymptomatic Mice Are Toxic

Elpida Tsika, Maria Moysidou, Jing Guo, Mimi Cushman, Patrick Gannon, et al.

(see pages 3409–3418)

α-Synuclein is normally localized to synaptic terminals throughout the brain, but mutations cause it to polymerize first into oligomers and then in fibrils that aggregate in intracellular inclusions in specific classes of neurons, leading to degeneration. Whether α-synuclein oligomers are toxic at early stages of polymerization, before fibrils and inclusions form, is unclear. Tsika et al. purified α-synuclein from mice expressing a human mutant form of the protein that causes inclusions to form in spinal cord neurons. Unlike insoluble α-synuclein aggregates, which were detected only in extracts from spinal cord of symptomatic mice, soluble α-synuclein oligomers were extracted from spinal cord before symptom onset, as well as from brain regions where inclusions are never found. Although oligomers from different regions were similar in size and shared other biochemical properties, only fractions isolated from spinal cord accelerated aggregation of α-synuclein in neurons in vitro; fractions extracted from other regions delayed aggregation.

Back to top

In this issue

The Journal of Neuroscience: 30 (9)
Journal of Neuroscience
Vol. 30, Issue 9
3 Mar 2010
  • Table of Contents
  • Table of Contents (PDF)
  • About the Cover
  • Index by author
  • Advertising (PDF)
  • Ed Board (PDF)
Email

Thank you for sharing this Journal of Neuroscience article.

NOTE: We request your email address only to inform the recipient that it was you who recommended this article, and that it is not junk mail. We do not retain these email addresses.

Enter multiple addresses on separate lines or separate them with commas.
This Week in The Journal
(Your Name) has forwarded a page to you from Journal of Neuroscience
(Your Name) thought you would be interested in this article in Journal of Neuroscience.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Print
View Full Page PDF
Citation Tools
This Week in The Journal
Journal of Neuroscience 3 March 2010, 30 (9) i

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Respond to this article
Request Permissions
Share
This Week in The Journal
Journal of Neuroscience 3 March 2010, 30 (9) i
Twitter logo Facebook logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Cellular/Molecular
    • Development/Plasticity/Repair
    • Behavioral/Systems/Cognitive
    • Neurobiology of Disease
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF

Responses to this article

Respond to this article

Jump to comment:

No eLetters have been published for this article.

Related Articles

Cited By...

More in this TOC Section

  • This Week in The Journal
  • This Week in The Journal
  • This Week in The Journal
Show more This Week in The Journal
  • Home
  • Alerts
  • Follow SFN on BlueSky
  • Visit Society for Neuroscience on Facebook
  • Follow Society for Neuroscience on Twitter
  • Follow Society for Neuroscience on LinkedIn
  • Visit Society for Neuroscience on Youtube
  • Follow our RSS feeds

Content

  • Early Release
  • Current Issue
  • Issue Archive
  • Collections

Information

  • For Authors
  • For Advertisers
  • For the Media
  • For Subscribers

About

  • About the Journal
  • Editorial Board
  • Privacy Notice
  • Contact
  • Accessibility
(JNeurosci logo)
(SfN logo)

Copyright © 2025 by the Society for Neuroscience.
JNeurosci Online ISSN: 1529-2401

The ideas and opinions expressed in JNeurosci do not necessarily reflect those of SfN or the JNeurosci Editorial Board. Publication of an advertisement or other product mention in JNeurosci should not be construed as an endorsement of the manufacturer’s claims. SfN does not assume any responsibility for any injury and/or damage to persons or property arising from or related to any use of any material contained in JNeurosci.