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
Articles

Negative Feedback Neuroendocrine Control of Inflammatory Response in the Rat is Dependent on the Sympathetic Postganglionic Neuron

Paul G. Green, Wilfrid Jänig and Jon D. Levine
Journal of Neuroscience 1 May 1997, 17 (9) 3234-3238; DOI: https://doi.org/10.1523/JNEUROSCI.17-09-03234.1997
Paul G. Green
3Oral Surgery, and
4Division of Neurobiology, University of California, San Francisco, California 94143 and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Wilfrid Jänig
5Physiologisches Institut, Christian-Albrechts-Universität, 24098 Kiel, Germany
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
Jon D. Levine
1Departments of Anatomy,
2Medicine, and
3Oral Surgery, and
4Division of Neurobiology, University of California, San Francisco, California 94143 and
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF
Loading

Article Figures & Data

Figures

  • Fig. 1.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Fig. 1.

    A, Effect of electrical stimulation on BK-induced PE in the rat knee joint. In both groups of rats, baseline PE was established in the first three samples. In one group, BK (150 nm; ○, n = 8) was then added to the perfusion fluid (0.9% sodium chloride) and, for the remainder of the experiment, was the only substance in the perfusion fluid. In the second group (•, n = 6), BK was added after the first three baseline samples, and then 40 min after beginning knee perfusion, a noxious electrical stimulation of the hindpaw (ES, 25 mA, 0.5 msec. pulse duration, 1 Hz) was applied continuously for the remainder of the experiment. B, Effect of electrical stimulation on PAF-induced PE in the rat knee joint. In both groups of rats, baseline PE was established in the first three samples. In one group, PAF (35 nm; ○, n = 6) was then added to the perfusion fluid (0.9% sodium chloride) and, for the remainder of the experiment, was the only substance in the perfusion fluid. In the second group (•, n = 8), PAF was added after the first three baseline samples, and then 40 min after beginning knee perfusion, a noxious electrical stimulation (25 mA) was applied to the hindpaw continuously for the remainder of the experiment. In this and subsequent figures, data are presented as mean ± SEM ofn values, and ordinate is absorbance of light at 620 nm. After a drug is added to the perfusate, it is present throughout the experiment.

  • Fig. 2.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Fig. 2.

    Effect of sympathectomy on noxious stimulation-induced inhibition of BK-induced PE. For both groups in this figure, BK (150 nm) was added to the perfusion fluid after the first three baseline samples and remained in the perfusion fluid for the duration of the experiment. Both groups had undergone sympathectomy 1 week before the perfusion experiment. The first group (○, n = 15) received BK only, whereas the second group (•, n = 14) also received continuous noxious electrical stimulation of the hindpaw (ES, 25 mA, 0.5 msec, 1 Hz) 40 min after beginning knee perfusion.

  • Fig. 3.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Fig. 3.

    A, Effect of intravenous corticosterone on BK-induced PE in the rat knee joint. In both groups of rats, baseline PE was established in the first three samples. In one group, BK (150 nm; ○, n = 8) was then added to the perfusion fluid (0.9% sodium chloride) and, for the remainder of the experiment, was the only substance in the perfusion fluid. In the second group (•, n = 12), BK was added after the first three baseline samples, and then 40 min after knee perfusion corticosterone was infused intravenously at a rate of 5 μg/min for the remainder of the experiment. B, Effect of intravenous corticosterone on PAF-induced PE. For both groups in B, PAF (35 nm) was added to the perfusion fluid after the first three baseline samples and remained in the perfusion fluid for the duration of the experiment. The first group (○, n = 6) were normal animals, and the second group (•, n = 7) received corticosterone (5 μg/min, i.v.) 40 min after beginning knee perfusion.

  • Fig. 4.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Fig. 4.

    Effect of sympathectomy on corticosterone-induced inhibition of BK-induced PE. For both groups in this figure, BK (150 nm) was added to the perfusion fluid after the first three baseline samples and remained in the perfusion fluid for the duration of the experiment. Both groups had undergone sympathectomy 1 week before perfusion experiment. The first group (○, n = 15) received BK only, whereas the second group (•, n= 9) also received corticosterone (5 μg/min, i.v.) 40 min after beginning knee perfusion.

  • Fig. 5.
    • Download figure
    • Open in new tab
    • Download powerpoint
    Fig. 5.

    Effect of intra-articular phentolamine or ICI 118,551 on corticosterone-induced inhibition of BK-induced PE. For all groups in this figure, bradykinin (150 nm) was added to the perfusion fluid after the first three baseline samples and remained in the perfusion fluid for the duration of the experiment. The first group (○, n = 8) received BK only, whereas the second group (•, n = 5) also received phentolamine (1 μm) co-perfused with BK in the knee joint. The third group (▪, n = 5) received BK with ICI 118,551 (100 nm). Corticosterone infusion (5 μg/min, i.v.) was started 40 min after beginning knee perfusion.

Back to top

In this issue

The Journal of Neuroscience: 17 (9)
Journal of Neuroscience
Vol. 17, Issue 9
1 May 1997
  • Table of Contents
  • 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.
Negative Feedback Neuroendocrine Control of Inflammatory Response in the Rat is Dependent on the Sympathetic Postganglionic Neuron
(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
Negative Feedback Neuroendocrine Control of Inflammatory Response in the Rat is Dependent on the Sympathetic Postganglionic Neuron
Paul G. Green, Wilfrid Jänig, Jon D. Levine
Journal of Neuroscience 1 May 1997, 17 (9) 3234-3238; DOI: 10.1523/JNEUROSCI.17-09-03234.1997

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
Negative Feedback Neuroendocrine Control of Inflammatory Response in the Rat is Dependent on the Sympathetic Postganglionic Neuron
Paul G. Green, Wilfrid Jänig, Jon D. Levine
Journal of Neuroscience 1 May 1997, 17 (9) 3234-3238; DOI: 10.1523/JNEUROSCI.17-09-03234.1997
Reddit logo Twitter logo Facebook logo Mendeley logo
  • Tweet Widget
  • Facebook Like
  • Google Plus One

Jump to section

  • Article
    • Abstract
    • MATERIALS AND METHODS
    • RESULTS
    • DISCUSSION
    • Footnotes
    • REFERENCES
  • Figures & Data
  • Info & Metrics
  • eLetters
  • PDF

Keywords

  • neurogenic inflammation
  • sympathetic postganglionic neuron
  • sympathectomy
  • noxious electrical stimulation
  • hypothalamic-pituitary-adrenal axis
  • bradykinin
  • platelet activating factor
  • corticosterone
  • inflammation
  • negative feedback control

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

  • Choice Behavior Guided by Learned, But Not Innate, Taste Aversion Recruits the Orbitofrontal Cortex
  • Maturation of Spontaneous Firing Properties after Hearing Onset in Rat Auditory Nerve Fibers: Spontaneous Rates, Refractoriness, and Interfiber Correlations
  • Insulin Treatment Prevents Neuroinflammation and Neuronal Injury with Restored Neurobehavioral Function in Models of HIV/AIDS Neurodegeneration
Show more Articles
  • 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 © 2023 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.