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 7 January 2009, 29 (1) i
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Embedded Image Cellular/Molecular

Exocytosis Can Form Stable Membrane Deposits in Neurons

Joris de Wit, Ruud F. Toonen, and Matthijs Verhage

(see pages 23–37)

Neurons secrete neuropeptides, neurotrophic factors, guidance molecules, and proteases via secretory dense-core vesicles. Although secretion of such molecules has been extensively studied in neuroendocrine cells, relatively little is known about release of these molecules by neurons. To remedy this, de Wit et al. labeled neuropeptide Y, brain-derived neurotrophic factor, semaphorin 3A, and the protease tPA (tissue plasminogen activator) with a pH-sensitive marker to track vesicle fusion in cultured mouse neurons. They found evidence that secretory vesicles in neurons sometimes exhibit partial fusion, in which only some of the cargo is released before the vesicle reforms and reacidifies. In addition, they discovered that neuronal exocytosis sometimes stably deposited vesicle cargo at the cell membrane. These stable deposits did not depend on the presence of extracellular matrix molecules, but instead appeared to result from interactions between basic residues of the cargo with the intravesicular matrix that persisted after incorporation of the vesicle into the plasma membrane.

Embedded Image Development/Plasticity/Repair

Cofilin Links Reelin Signaling to Cytoskeletal Dynamics

Xuejun Chai, Eckart Förster, Shanting Zhao, Hans H. Bock, and Michael Frotscher

(see pages 288–299)

During cerebral cortical development, layers are formed from the inside out, as newly generated neurons migrate past older neurons to form more superficial layers. Cajal-Retzius cells, which form the most superficial layer of the developing cortex, secrete the protein Reelin, which is required for proper layer formation. Although receptors, adaptor proteins, and several kinases involved in Reelin signaling have been identified, the downstream effectors of migratory control—which likely include cytoskeletal proteins—have remained elusive. Chai et al. report that one such effector is cofilin, an actin-depolymerizing protein that enables the formation of motile lamellipodia and is necessary for migration. They show that Reelin signaling increases phosphorylation of cofilin, which disrupts its ability to bind to actin and thereby increases neurite stability and hinders migration. They propose that the leading processes of migrating neurons become stabilized when they contact Reelin, and this allows proper migration of the neurons by nuclear translocation.

Figure1
  • Download figure
  • Open in new tab
  • Download powerpoint

Phosphorylated cofilin (green) is present in the leading processes (arrowheads) of late-generated cortical neurons and in the cell bodies (asterisks) of early-generated neurons. Reelin (red) labels the marginal zone (MZ). Scale, 40 μm. See the article by Chai et al. for details.

Embedded Image Behavioral/Systems/Cognitive

Oxytocin Improves Social Recognition in Humans

Ulrike Rimmele, Karin Hediger, Markus Heinrichs, and Peter Klaver

(see pages 38–42)

In humans, oxytocin is best known for its effects during labor and lactation. Less is known about oxytocin's effects on social interactions in humans, although its effects in other animals have been extensively documented. In rodents, oxytocin is necessary for recognition of conspecifics, and it appears to reduce anxiety in social interactions and thus facilitate approach behaviors. Such effects are also thought to be present in humans, and deficiencies in oxytocin-mediated signaling have been implicated in social disorders such as autism and borderline personality disorder. This week, Rimmele et al. demonstrate a modest effect of oxytocin in a socially relevant task: face recognition. Oxytocin, administered intranasally before presentation of photographs, increased subjects' recognition of faces the next day. In contrast, oxytocin had no effect on recognition of objects. The largest effect appeared to be on the identification of novel faces, which oxytocin-treated subjects were less likely than controls to report as familiar.

Embedded Image Neurobiology of Disease

Anti-Inflammatory Drug Mimics Effects of Omega-3 Fatty Acid

Cai Song, Xiang Yang Zhang, and Mehar Manku

(see pages 14–22)

Omega-3 fatty acids (OFAs) are essential for normal cognitive function. OFA deficits have been linked to several neurological disorders including dementia, schizophrenia, and depression, and the OFA ethyl-eicosapentaenoate (EPA) has been used successfully to treat depression in humans. To gain insight into the molecular underpinnings of depression and how they are affected by EPA, Song et al. examined levels of inflammatory mediators and nerve growth factor (NGF) in olfactory bulbectomized rats, which show many of the behavioral, neural, and immunological changes observed in depressed humans. Bulbectomy increased phospholipase A2 and corticotrophin-releasing hormone expression in hypothalamus, increased interleukin-1β, prostaglandin E2, and corticosterone in blood, decreased expression of NGF in hippocampus, and slowed spatial learning. All these effects were prevented by treatment with EPA or an anti-inflammatory drug. The results support models of depression based on inflammation and reduced neurotrophic factor expression, and suggest that OFAs ameliorate depression by acting on these pathways.

Back to top

In this issue

The Journal of Neuroscience: 29 (1)
Journal of Neuroscience
Vol. 29, Issue 1
7 Jan 2009
  • Table of Contents
  • Table of Contents (PDF)
  • 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 7 January 2009, 29 (1) 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 7 January 2009, 29 (1) 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.