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
  • EDITORIAL BOARD
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
  • SUBSCRIBE

User menu

  • Log in
  • My Cart

Search

  • Advanced search
Journal of Neuroscience
  • 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
  • EDITORIAL BOARD
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
  • SUBSCRIBE
Next
THIS WEEK IN THE JOURNAL

This Week in The Journal

Journal of Neuroscience 1 May 2003, 23 (9) 1
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
Loading

●  Cellular/Molecular

Antideath Transcription Factors

Sp1 and Sp3 Are Oxidative Stress-Inducible, Antideath Transcription Factors in Cortical Neurons

Hoon Ryu, Junghee Lee, Khalequz Zaman, James Kubilis, Robert J. Ferrante, Brian D. Ross, Rachael Neve, and Rajiv R. Ratan (see pages 3597–3606)

Cells react to oxidative stress with a complex tapestry of adaptive responses. “Antideath” molecules can counteract this cellular stress by reducing reactive oxygen species and repairing DNA damage. Because oxidative stress can alter the expression of antideath genes, the role of transcription factors in regulating this process has come under increasing scrutiny. A report this week from Ryu et al. shows that the zinc finger transcription factors Sp1 and Sp3 are redox-regulated in neurons. In cultured cortical neurons, oxidative stress dramatically increased the low basal DNA-binding activity of Sp1 and Sp3, an early response that was prevented by antioxidants and appeared to follow cellular increases in Sp1 and Sp3 protein. Furthermore, overexpression of the zinc finger DNA-binding proteins prevented oxidative stress- or DNA damage-induced neuronal death. To investigate the activity of Sp1 proteins in vivo, the authors used a transgenic and a chemical mouse model of Huntington's disease; Sp1 and Sp3 levels were increased in both model systems. Together, these results suggest that the Sp1 and Sp3 transcription factors form one thread of a compensatory neuronal response to oxidative stress.

▴  Development/Plasticity/Repair

Dendritic Patterns in Drosophila

Distinct Developmental Modes and Lesion-Induced Reactions of Dendrites of Two Classes of DrosophilaSensory Neurons

Kaoru Sugimura, Misato Yamamoto, Ryusuke Niwa, Daisuke Satoh, Satoshi Goto, Misako Taniguchi, Shigeo Hayashi, and Tadashi Uemura (see pages 3752–3760)

Many neurons, such as Purkinje cells, can be instantly recognized by their distinct dendritic arbors, yet the mechanisms underlying the extent of dendritic fields and branching patterns is far from clear. Advances in imaging technology are helping to answer such questions. Sugimura et al. generated cell-specific markers and then used time-lapse videomicroscopy to watch dendritic development in class I and class IV sensory neurons in the peripheral nervous system of theDrosophila embryo. They followed dendrite maturation in larva and the response to branch severing. They saw distinct branching behaviors in the dendritic arborization of class I and class IV neurons, which differ in their arbor complexity and morphology. Their analysis was aided by the fact that these neurons form largely two-dimensional dendritic arbors. One interesting property of class IV sensory neurons is the complete but minimal-overlapping innervation of their receptive fields, called “tiling.” Several signaling molecules have been identified recently as important to dendritic arbor formation. The current work, through laser ablation of dendritic branches, seems to confirm that a class-specific intercellular inhibitory communication between class IV neurons is necessary and sufficient for tiling. This system should be a useful model to investigate the underlying molecular mechanisms.

▪  Behavioral/Systems/Cognitive

Neural Correlates of Remembering

Functional Dissociation among Components of Remembering: Control, Perceived Oldness, and Content

Mark E. Wheeler and Randy L. Buckner (see pages3869–3880)

In an investigation of human brain function, Wheeler and Buckner used functional magnetic resonance imaging to examine specific components of that treasured cortical function, memory, and to define the cortical areas that mediate it. The very nature of remembering (the ability to recall events experienced at some time in one's past) requires multiple interdependent elements. Here, Wheeler and Buckner examined three such elements: control, the intentional retrieval of information; perceived oldness, the realization that information is in fact not new; and content, the actual “stuff” of the memory, which can be given context by the modality in which it was experienced. They separated the three components by manipulating the study content, the presentation, and the conditions of the retrieval tasks. They found distinct areas associated with each component. The control element correlated with activity in the left prefrontal cortex, whereas activity in parietal and frontal regions accompanied perceived oldness and activity in inferior temporal regions was content-related.

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

Word cues paired with pictures or sounds were used to test components of remembering. This image is taken from Figure 1 of this article.

Back to top

In this issue

The Journal of Neuroscience: 23 (9)
Journal of Neuroscience
Vol. 23, Issue 9
1 May 2003
  • Table of Contents
  • Index by author
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
Citation Tools
This Week in The Journal
Journal of Neuroscience 1 May 2003, 23 (9) 1

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 1 May 2003, 23 (9) 1
Reddit logo Twitter logo Facebook logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters

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
  • 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 Policy
  • Contact
(JNeurosci logo)
(SfN logo)

Copyright © 2023 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.