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
PreviousNext
This Week in The Journal

This Week in The Journal

Journal of Neuroscience 16 May 2012, 32 (20) i
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Embedded Image Cellular/Molecular

NMDA Receptor Activation Increases Amacrine Cell Coupling

W. Wade Kothmann, E. Brady Trexler, Christopher M. Whitaker, Wei Li, Stephen C. Massey, et al.

(see pages 6747–6759)

AII amacrine cells, part of the rod photoreceptor pathway, can form extensive electrically coupled networks depending on ambient light levels. The cells are relatively uncoupled in total darkness, but coupling increases with light levels until illumination reaches photopic levels, when coupling strength returns to baseline. The increase in coupling parallels phosphorylation of the gap junction protein connexin 36 (Cx36), and dopamine-dependent dephosphorylation of Cx36 in bright light reduces coupling strength. What drives Cx36 phosphorylation in dim light was hitherto unknown, but Kothmann et al. answer this question as well as another: given that NMDA receptors (NMDARs) are not located near glutamatergic synapses in AII amacrines, what do the NMDARs do? It turns out that NMDARs and the calcium-dependent kinase CaMKII colocalize with Cx36 in AII amacrines. Stimulating NMDARs increased Cx36 phosphorylation in dark-adapted rabbit retinas, whereas inhibiting NMDARs or CaMKII in light-adapted retinas caused dephosphorylation, indicating that these proteins regulate amacrine coupling strength.

Embedded Image Development/Plasticity/Repair

Semaphorin and Plexin Confine Horizontal Cell Axons to OPL

Ryota L. Matsuoka, Zheng Jiang, Ivy S. Samuels, Kim T. Nguyen-Ba-Charvet, Lu O. Sun, et al.

(see pages 6859–6868)

In the retina's outer plexiform layer (OPL), photoreceptor terminals form ribbon synapses with bipolar and horizontal cells. Dendrites and axons of horizontal cells are confined to the OPL—the former contacting cones and the latter contacting rods—and they are thought to mediate lateral inhibition. Stratification of the OPL during development depends largely on glutamatergic signaling from photoreceptors: if release is prevented, neurites from rods, and bipolar and horizontal cells grow ectopically in the outer nuclear layer (ONL). Matsuoka et al. show that stratification of mouse horizontal cell neurites also depends on signaling by semaphorin 6A (Sema6a) and its receptor plexin A4 (PlexA4). Knocking out either protein allowed horizontal cell axons to grow through the ONL. As a result, many rod ribbon synapses contained only one horizontal cell axon, instead of the normal two. Although horizontal cell dendrites remained confined to the OPL in mutant mice, they did not exhibit self-avoidance like wild-type dendrites.

Embedded Image Behavioral/Systems/Cognitive

V4 Neurons Respond to Real and Illusory Contours

Yanxia Pan, Minggui Chen, Jiapeng Yin, Xu An, Xian Zhang, et al.

(see pages 6760–6770)

Neurons in visual cortical areas V1, V2, and V4 respond preferentially to lines of particular orientations. The brain represents object contours by combining the responses of many such neurons. Orientation-selective neurons also respond to illusory contours created by some stimuli (Figure). To identify the cortical level at which neurons respond to illusory contours as if they were real, Pan et al. detected responses to real and illusory gratings across V1, V2, and V4 using optical imaging, and then compared orientation maps for each stimulus type. The response profiles for real and illusory gratings precisely overlapped only in V4, remaining closely matched even when the inducing lines were orthogonal to the illusory contours and would thus be expected to preferentially activate a distinct set of orientation-selective neurons. Single-unit recordings confirmed that most cells that responded preferentially to a moving bar of a given orientation responded maximally to illusory contours of the same orientation.

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

Precise alignment of black lines creates illusory contours across which no actual luminance change exists. Illusory and real contours are detected by the same neurons in V4. See the article by Pan et al. for details.

Embedded Image Neurobiology of Disease

Reduction of PGC-1α Increases Extrasynaptic NMDA Currents

Clare Puddifoot, Marc-Andre Martel, Francesc X. Soriano, Alberto Camacho, Antonio Vidal-Puig, et al.

(see pages 6995–7000)

Mutant huntingtin protein (mHtt) promotes neuronal death in part by reducing expression of the transcriptional coactivator PGC-1α, which regulates transcriptional programs involved in mitochondrial biogenesis. In addition, expression of mHtt enhances extrasynaptic NMDA receptor (eNMDAR) currents, which also suppress PGC-1α. Furthermore, although activation of synaptic NMDARs limits the effects of mHtt by promoting its aggregation in cytoplasmic inclusions, activation of eNMDARs increases mHtt toxicity, partly by inducing disaggregation. Puddifoot et al. now report that suppression of PGC-1α activity further amplifies these effects by increasing eNMDAR current. Knocking down PGC-1α in cultured rat neurons increased eNMDAR currents and NMDA-induced excitotoxicity, whereas expression of exogenous PGC-1α reduced extrasynaptic currents and protected neurons from excitotoxicity. Overexpression of PGC-1α also prevented mHtt-induced increases in eNMDAR currents, suggesting mHtt increases the latter by suppressing the former. PGC-1α is suppressed in Alzheimer's and Parkinson's diseases, so its enhancement of eNMDAR currents might contribute to neurodegeneration in those diseases as well as Huntington's.

Back to top

In this issue

The Journal of Neuroscience: 32 (20)
Journal of Neuroscience
Vol. 32, Issue 20
16 May 2012
  • 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 16 May 2012, 32 (20) 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 16 May 2012, 32 (20) i
del.icio.us logo Digg logo Reddit logo Twitter 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
    • 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
  • 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.