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 10 September 2008, 28 (37) i
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Embedded Image Cellular/Molecular

Single Cocaine Treatment Induces LTP-Like Changes in VTA

Emanuela Argilli, David R. Sibley, Robert C. Malenka, Pamela M. England, and Antonello Bonci

(see pages 9092–9100)

A single systemic dose of cocaine is sufficient to produce long-term potentiation (LTP) of glutamatergic synapses onto the reward-responsive dopaminergic neurons in the ventral tegmental area (VTA) of rats. This week, Argilli et al. demonstrate that this LTP is produced locally in the VTA and develops within 3 h after cocaine is applied briefly to cultured midbrain slices. Cocaine treatment prevented the development of spike-timing-dependent LTP, suggesting that the two use similar mechanisms. Indeed, both significantly increase AMPA receptor/NMDA receptor ratio (measured by whole-cell recordings) by causing translocation of high-conductance GluR1 glutamate receptors into the synapse, both require initial activation of NMDA receptors, and both require protein synthesis. Cocaine blocks dopamine transporters, and the resulting increase in extracellular dopamine is likely to contribute to LTP by binding to D5 receptors, because LTP was prevented by specific D1/D5 antagonists (but not D2 antagonists), was induced by D1/D5 agonists, and was absent in D5-null mice.

Embedded Image Development/Plasticity/Repair

RhoA Increases Axonal Branching

Soichiro Ohnami, Mitsuharu Endo, Satoshi Hirai, Naofumi Uesaka, Yumiko Hatanaka, Toshihide Yamashita, and Nobuhiko Yamamoto

(see pages 9117–9121)

The Rho family of small GTPases regulates morphology and movement in many cell types by regulating the actin cytoskeleton. Ohnami et al. report that RhoA contributes to activity-induced branching of horizontally growing axons in the upper layers of the cortex in rats. In organotypic slice cultures, increasing RhoA activity pharmacologically or by introducing (via electroporation) a constitutively active form increased the number of short branches of horizontal axons without affecting the number of long branches. Conversely, an inhibitor of RhoA-kinase (a downstream effector of RhoA) reduced branching. Daily live imaging revealed that constitutively active RhoA altered branch dynamics by increasing both elongation and elimination of axons. These data suggest that RhoA increases branch formation without affecting stabilization. To link RhoA to neuronal activity, the authors blocked activity with sodium-channel and glutamate-receptor blockers. These decreased the amount of active RhoA. Furthermore, introducing constitutively active RhoA increased branching when activity was blocked.

Embedded Image Behavioral/Systems/Cognitive

Melanin Concentrating Hormone Regulates Hypocretin Neurons

Yan Rao, Min Lu, Fei Ge, Donald J. Marsh, Su Qian, Alex Hanxiang Wang, Marina R. Picciotto, and Xiao-Bing Gao

(see pages 9101–9110)

The neuropeptides hypocretin (aka orexin) and melanin concentrating hormone (MCH) are secreted by different neurons in the hypothalamus. In addition to projecting broadly throughout the brain, hypocretin- and MCH-expressing neurons innervate each other. They regulate body functions such as wakefulness, food intake, and reward. Hypocretin and dopamine increase spike frequency in hypocretin neurons by enhancing glutamate release from presynaptic terminals, and hypocretin also depolarizes MCH neurons. But the effect of MCH on hypocretin neurons is unknown. To address this question, Rao et al. used MCH receptor-1 knock-out mice. The basal firing rate of hypocretin neurons was similar in mutant and wild-type mice, but hypocretin- and dopamine-induced increases in firing were greater in mutants. In addition, miniature EPSCs in hypocretin neurons were larger in mutant mice than in controls. The results suggest that MCH exerts an inhibitory effect on hypocretin neurons, acting as negative feedback that counteracts positive feedback produced by hypocretin.

Embedded Image Neurobiology of Disease

Status Epilepticus Triggers Functional Changes in Microglia

Elena Avignone, Lauriane Ulmann, Françoise Levavasseur, François Rassendren, and Etienne Audinat

(see pages 9133–9144)

Injured neurons and glia release ATP, which activates microglia via purinergic receptors, thus triggering migration, phagocytosis, and release of inflammatory mediators. Because identifying microglia in situ is difficult, little is known about the activation process in vivo. Avignone et al. used mice in which GFP was expressed specifically in microglia (enabling identification) to elucidate changes that occur in these cells after kainate-induced status epilepticus, a model of epilepsy. Within 3 h after kainate injection, inflammatory mediators increased in the hippocampus, and expression of a purinergic receptor that regulates phagocytosis was upregulated. By 48 h, levels of all microglial purinergic receptors were elevated—including P2Y12, which is downregulated in other injury models. In addition, activated microglia proliferated, grew larger, and extended thicker processes that extend more quickly toward a source of purinergic agonist than controls. Finally, whole-cell recordings in hippocampal slices revealed a voltage-activated potassium current in activated microglia that was not present in controls.

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

Purinergic receptors, including P2Y12 receptors (red), are upregulated in activated microglia cells (green) 48 h after status epilepticus (right) compared to controls (left). See the article by Avignone et al. for details.

Back to top

In this issue

The Journal of Neuroscience: 28 (37)
Journal of Neuroscience
Vol. 28, Issue 37
10 Sep 2008
  • 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 10 September 2008, 28 (37) 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 10 September 2008, 28 (37) i
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
    • 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.