Evidence map›Paper›PMID 18082230›Full record

ArticleNeuropharmacology2008

Brown adipose tissue sympathetic nerve activity is potentiated by activation of 5-hydroxytryptamine (5-HT)1A/5-HT7 receptors in the rat spinal cord.

C J Madden, S F Morrison

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuropharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

24 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  18. Central neural pathways for thermoregulation.Frontiers in bioscience (Landmark edition) · 2011
    Review
  19. Inhibition of brown adipose tissue thermogenesis by neurons in the ventrolateral medulla and in the nucleus tractus solitarius.American journal of physiology. Regulatory, integrative and comparative physiology · 2010
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

C J MaddenNeurological Sciences Institute, Oregon Health and Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA. maddench@ohsu.edu
S F Morrison
Oregon Health & Science University · US

Funding

Central Sympathetic Regulation of Thermogenesis in FeverR01NS040987 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI MORRISON, SHAUN F · 2001 to 2013
$3.7M
CENTRAL REGULATION OF SYMPATHETIC ACTIVITY TO BROWN FATR01DK057838 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI MORRISON, SHAUN F · 2001 to 2010
$2.1M
Central neural circuits involved in the febrile responseF32DK065401 · NIDDK · OREGON HEALTH & SCIENCE UNIVERSITY · PI MADDEN, CHRISTOPHER J · 2004 to 2006
$149k
NIDDK NIH HHS DK065401NIDDK NIH HHS DK57838NIDDK NIH HHS F32 DK065401NINDS NIH HHS NS40987NINDS NIH HHS R01 NS040987
6 · The paper itself

Abstract

In urethane-chloralose anesthetized, neuromuscularly blocked, ventilated rats, microinjection of NMDA (12 pmol) into the right fourth thoracic segment (T4) spinal intermediolateral nucleus (IML) immediately increased ipsilateral brown adipose tissue (BAT) sympathetic nerve activity (SNA; peak +492% of control), expired CO2 (+0.1%) heart rate (+48 beats min(-1)) and arterial pressure (+8 mmHg). The increase in BAT SNA evoked by T4 IML microinjection of NMDA was potentiated when it was administered immediately following a T4 IML microinjection of 5-hydroxytryptamine (5-HT, 100 pmol) or the 5-HT1A/5-HT7 receptor agonist, 8-OH-DPAT (600 pmol), (area under the curve: 184%, and 259% of the NMDA-only response, respectively). In contrast, T4 IML microinjection of the 5-HT2 receptor agonist, DOI (28 pmol) did not potentiate the NMDA-evoked increase in BAT SNA (101% of NMDA-only response). Microinjection into the T4 IML of the selective 5-HT1A antagonist, WAY-100635 (500 pmol), plus the 5-HT7 antagonist, SB-269970 (500 pmol), prevented the 5-HT-induced potentiation of the NMDA-evoked increase in BAT SNA. When administered separately, WAY-100635 (800 pmol) and SB-269970 (800 pmol) attenuated the 8-OH-DPAT-induced potentiation of the NMDA-evoked increase in BAT SNA through effects on the amplitude and duration of the response, respectively. The selective 5-HT2 receptor antagonist, ketanserin (100 pmol), did not attenuate the potentiations of the NMDA-evoked increase in BAT SNA induced by either 5-HT or 8-OH-DPAT. These results demonstrate that activation of 5-HT1A/5-HT7 receptors can act synergistically with NMDA receptor activation within the IML to markedly increase BAT SNA.

Indexed as

8-Hydroxy-2-(di-n-propylamino)tetralinAction PotentialsAdipose Tissue, BrownAnalysis of VarianceAnimalsBlood PressureDrug InteractionsExcitatory Amino Acid AgonistsHeart RateMaleN-MethylaspartateRatsRats, Sprague-DawleyReceptor, Serotonin, 5-HT1AReceptors, SerotoninSerotonin5-HT(7) receptor, rat8-Hydroxy-2-(di-n-propylamino)tetralinExcitatory Amino Acid AgonistsN-MethylaspartateReceptor, Serotonin, 5-HT1AReceptors, SerotoninSerotoninSerotonin AntagonistsSerotonin Receptor Agonists

Identifiers

PMID18082230
PMCPMC2322875
OpenAlexW2008626322

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.