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 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
  • EDITORIAL BOARD
  • ABOUT
    • Overview
    • Advertise
    • For the Media
    • Rights and Permissions
    • Privacy Policy
    • Feedback
  • SUBSCRIBE
PreviousNext
THIS WEEK IN THE JOURNAL

This Week in the Journal

Journal of Neuroscience 26 November 2003, 23 (34)
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Embedded Image Cellular/Molecular

Oxidative Stress in a Model of PD

Mechanism of Toxicity in Rotenone Models of Parkinson's Disease

Todd B. Sherer, Ranjita Betarbet, Claudia M. Testa, Byoung Boo Seo, Jason R. Richardson, Jin Ho Kim, Gary W. Miller, Takao Yagi, Akemi Matsuno-Yagi, and J. Timothy Greenamyre

(see pages 10756-10764)

The pathological hallmarks of Parkinson's disease (PD) include selective loss of nigrostriatal dopamine neurons and cytoplasmic inclusion bodies. Although the underlying mechanisms of cell death in PD are not fully resolved, several lines of evidence implicate mitochondrial dysfunction. Recently, rotenone, a pesticide that inhibits complex I of the mitochondrial electron transfer chain, has been shown to produce a PD-like syndrome in rats that includes death of dopamine neurons and motor deficits. Complex I inhibition could cause injury attributable to ATP depletion or to production of reactive oxygen species (ROS). Now, experiments by Sherer et al. indicate the latter as the probable cause of rotenone-induced toxicity. In neuroblastoma cells, rescue of complex I by transfection with the yeast protein NDI1 prevented toxicity. Depletion of ATP alone could not account for the action of rotenone in these cells. In contrast, rotenone-induced oxidative damage in brain slices was reduced by the antioxidants α-tocopherol (vitamin E) and coenzyme Q10. Oxidative damage and cell-specific neurodegeneration were also present in brains of rotenone-treated rats. The report adds credence to the possible role of environmental factors and mitochondrial dysfunction in PD, and may renew interest in a therapeutic role for antioxidants.

Embedded Image Development/Plasticity/Repair

De-Tuning and Re-Tuning Adult Auditory Cortex

Progressive Degradation and Subsequent Refinement of Acoustic Representations in the Adult Auditory Cortex

Shaowen Bao, Edward F. Chang, Jonathan D. Davis, Kevin T. Gobeske, and Michael M. Merzenich

(see pages 10765-10775)

During development and adulthood, the sensory cortex can be reorganized in response to correlated neuronal activity, but receptive field plasticity requires different circumstances in these two stages of life. During the early critical period, the sensory cortex is shaped by activity that lacks behavioral significance, whereas in adults, reinforcement or attention appears necessary for cortical reorganization. In this week's Journal, Bao et al. manipulated the organization of the adult primary auditory receptive field (AI) in rats. First, they paired pulsed noise stimulation to activate broadly correlated cortical activity with stimulation of the nucleus basalis (NB) to trigger cholinergic input. Noise pairing degraded the organization such that the AI resembled the nonprimary auditory cortex. In addition, spectral tuning broadened, and tonotopic maps were disrupted. However, by pairing NB stimulation with pulsed tone pips that triggered locally correlated activity, the AI regained its receptive field features over a 4 week trial period. It seems you can teach an old dog new tricks, provided they pay attention.

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

A, B, Degradation of primary auditory cortical tonotopic maps by pairing noise with nucleus basalis stimulation. C, Subsequent pairing of pure tones with nucleus basalis stimulation refined the map. Hatched regions had receptive field irregularity index scores of >2. See the article by Bao et al. for details.

Embedded Image Behavioral/Systems/Cognitive

Swimming with Serotonin

Spike Timing-Dependent Serotonergic Neuromodulation of Synaptic Strength Intrinsic to a Central Pattern Generator Circuit

Akira Sakurai and Paul S. Katz

(see pages 10745-10755)

Usually spike timing is thought of as a means to alter homosynaptic plasticity. However, this week Sakurai and Katz describe spike-timing dependence of a heterosynaptic pathway in the mollusk Tritonia diomedea. In these pink-colored beasts, a central pattern generator circuit includes dorsal and ventral swim interneurons (DSIs and VSIs, respectively) and a cerebral interneuron C2. This circuit initiates the escape swimming response in efferent flexion neurons and keeps Tritonia out of the way of hungry echinoderms. The serotonergic DSI neurons modulate both C2 and VSI neurons. The authors analyzed the synapse between VSI and ventral flexion neurons. When VSI neurons fired within 10 sec of the neuromodulatory DSI neurons, the VSI-evoked synaptic response on motor neurons was greatly enhanced, but with an interval of ≥20 sec, the response was dampened. This biphasic response was also observed with simulated escape swim activity. Although the underlying cellular mechanisms remain to be explored, the timing seems matched to the practical needs of the escape response with enhancing activity when it is needed most.

Back to top

In this issue

The Journal of Neuroscience: 23 (34)
Journal of Neuroscience
Vol. 23, Issue 34
26 Nov 2003
  • Table of Contents
  • About the Cover
  • 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
View Full Page PDF
Citation Tools
This Week in the Journal
Journal of Neuroscience 26 November 2003, 23 (34)

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 26 November 2003, 23 (34)
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Cellular/Molecular
    • Development/Plasticity/Repair
    • Behavioral/Systems/Cognitive
  • 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
  • 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 © 2022 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.