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

Teresa Esch [Ph.D.]
Journal of Neuroscience 2 March 2016, 36 (9) i
Teresa Esch
Ph.D.
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • ORCID record for Teresa Esch
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Interneurons from Medial Ganglionic Eminence Drive Hippocampal Giant Depolarizing Potentials

Jason C. Wester and Chris J. McBain

(see pages 2646–2662)

Spontaneous neural activity occurs during periods of peak synaptogenesis in many parts of the developing nervous system. In the rodent hippocampus, for example, spontaneous waves of locally synchronous activity, called giant depolarizing potentials (GDPs), occur during the first 2 postnatal weeks. These waves propagate across the hippocampus and are thought to shape emerging neural circuits.

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

Optically inhibiting (during time indicated by green shading) hippocampal interneurons born in the medial ganglionic eminence (top) greatly reduced the frequency of GDPs. In contrast, optically inhibiting neurons from the caudal ganglionic eminence (bottom) had little effect. See Wester and McBain for details.

GDP generation depends largely on GABA-mediated depolarization, and GDPs disappear as GABA becomes hyperpolarizing later in development. Cholecystokinin-expressing neurons are thought to be especially important for GDP generation, because inhibiting GABA release from these neurons suppresses GDPs. But the extent to which other classes of GABAergic interneurons contribute to GDP generation is unclear.

To address this question, Wester and McBain took advantage of the fact that the medial and caudal ganglionic eminences give rise to different classes of hippocampal interneurons. Using optogenetics, they inhibited interneurons derived from either the medial or caudal ganglionic eminence in mouse hippocampal slices and examined the effect on GDP generation. Unexpectedly, inhibiting caudally derived interneurons—which include cholecystokinin-expressing neurons—had a relatively small effect on GDP generation. Although GDP frequency sometimes decreased when neurons from the caudal ganglionic eminence were inhibited, the frequency sometimes increased or was unchanged. In contrast, inhibiting medially derived interneurons—which include parvalbumin- and somatostatin-expressing interneurons—consistently reduced GDP frequency.

While these results are surprising based on previous findings, they make sense given results from paired recordings. Specifically, medially derived interneurons were far more likely than caudally derived neurons to form synapses with pyramidal neurons. In addition, most interneurons from the medial ganglionic eminence appeared to innervate pyramidal cell bodies and have a high release probability, suggesting they provide strong recurrent excitation.

These results suggest that interneurons from the medial ganglionic eminence play a more prominent role in GDP generation than those from the caudal ganglionic eminence, including those that express cholecystokinin. The innervation pattern of the medially derived interneurons suggests that they are primarily fast-spiking, parvalbumin-expressing basket cells. Therefore, these neurons are likely to play an important role in shaping neural circuits in the developing hippocampus.

Upregulating Synaptotagmin 10 Protects Neurons

Anne M.H. Woitecki, Johannes Alexander Müller, Karen M.J. van Loo, Ramona F. Sowade, Albert J. Becker, et al.

(see pages 2561–2570)

Activation of synaptic NMDA receptors leads to calcium influx and downstream activation of various kinases, phosphatases, and transcription factors. These molecules not only drive synaptic plasticity, but also promote neuronal survival. In fact, several “activity-regulated inhibitor of death” (AID) genes are induced by activity-associated calcium influx. The proteins encoded by these genes increase survival of neurons exposed to various insults, including kainic-acid-induced excitotoxicity (Zhang et al., 2009, PLoS Genet 5:e1000604).

How AID proteins protect neurons from insults is largely unknown, but Woitecki, Müller, et al. report that one of the proteins, the transcription factor NPAS4, promotes survival at least in part by increasing expression of synaptotagmin 10 (Syt10), a vesicular calcium sensor. The Syt10 promoter has an NPAS4 binding sequence and NPAS4 drove expression of a luciferase reporter from that promoter. In addition, overexpressing Npas4 increased Syt10 expression in rat hippocampal cultures, whereas knocking down Npas4 decreased levels of Syt10 mRNA.

Like Npas4, Syt10 mRNA was upregulated in hippocampal cultures treated with kainic acid. Notably, kainic acid caused more neuronal death in hippocampal cultures from Syt10-null mice than in control cultures. Furthermore, Npas4 overexpression failed to protect neurons lacking Syt10 from excitotoxic death, although it protected wild-type neurons. Nevertheless, survival of Syt10-deficient neurons increased when they were co-cultured with wild-type neurons, suggesting that wild-type neurons secreted a factor that protected neurons lacking Syt-10.

These results strongly suggest that NPAS4 protects neurons from excitotoxic death at least in part by upregulating Syt10, which in turn promotes secretion of neuroprotective factors. Although the identity of these factors is unknown, one candidate is brain-derived neurotrophic factor, which has well known neuroprotective functions and is also regulated by NPAS4 (Lin et al., 2008, Nature 455:1198). Elucidating the role of Syt10 in neuroprotection may lead to new therapies for reducing excitotoxic neuronal death after stroke and seizures, as well as in neurodegenerative diseases.

Footnotes

  • This Week in The Journal is written by Teresa Esch, Ph.D.

Back to top

In this issue

The Journal of Neuroscience: 36 (9)
Journal of Neuroscience
Vol. 36, Issue 9
2 Mar 2016
  • 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 2 March 2016, 36 (9) 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 2 March 2016, 36 (9) i
Twitter logo Facebook logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Interneurons from Medial Ganglionic Eminence Drive Hippocampal Giant Depolarizing Potentials
    • Upregulating Synaptotagmin 10 Protects Neurons
    • Footnotes
  • 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.