Evidence map›Paper›PMID 18567709›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2008

Plasticity of pre- and postsynaptic GABAB receptor function in the paraventricular nucleus in spontaneously hypertensive rats.

De-Pei Li, Qing Yang, Hao-Min Pan, Hui-Lin Pan

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Neuroadaptations of presynaptic and postsynaptic GABABritish journal of pharmacology · 2017
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. The lighter side of BDNF.American journal of physiology. Regulatory, integrative and comparative physiology · 2011
    Review
  18. Article
  19. 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

4 authors at 1 institution in 1 country.

De-Pei LiDept. of Critical Care, Unit 110, The Univ. of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030, USA. dpli@mdanderson.org
Qing Yang
Hao-Min Pan
Hui-Lin Pan
The University of Texas MD Anderson Cancer Center · US

Funding

Synaptic Mechanisms Regulating Sympathetic DriveR01HL077400 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PAN, HUI-LIN · 2005 to 2014
$3.8M
MECHANISMS OF ACTIVATION OF CARDIAC NOCICEPTORSR01HL060026 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI PAN, HUI-LIN · 1998 to 2005
$1.1M
NHLBI NIH HHS HL60026NHLBI NIH HHS HL77400
6 · The paper itself

Abstract

GABA(B) receptor function is upregulated in the paraventricular nucleus (PVN) of the hypothalamus in spontaneously hypertensive rats (SHR), but it is unclear whether this upregulation occurs pre- or postsynaptically. We therefore determined pre- and postsynaptic GABA(B) receptor function in retrogradely labeled spinally projecting PVN neurons using whole cell patch-clamp recording in brain slices in SHR and Wistar-Kyoto (WKY) rats. Bath application of the GABA(B) receptor agonist baclofen significantly decreased the spontaneous firing activity of labeled PVN neurons in both SHR and WKY rats. However, the magnitude of reduction in the firing rate was significantly greater in SHR than in WKY rats. Furthermore, baclofen produced larger membrane hyperpolarization and outward currents in labeled PVN neurons in SHR than in WKY rats. The baclofen-induced current was abolished by either including G protein inhibitor GDPbetaS in the pipette solution or bath application of the GABA(B) receptor antagonist in both SHR and WKY rats. Blocking N-methyl-d-aspartic acid receptors had no significant effect on baclofen-elicited outward currents in SHR. In addition, baclofen caused significantly greater inhibition of glutamatergic excitatory postsynaptic currents (EPSCs) in labeled PVN neurons in brain slices from SHR than WKY rats. By contrast, baclofen produced significantly less inhibition of GABAergic inhibitory postsynaptic currents (IPSCs) in labeled PVN neurons in SHR than in WKY rats. Although microinjection of the GABA(B) antagonist into the PVN increases sympathetic vasomotor tone in SHR, the GABA(B) antagonist did not affect EPSCs and IPSCs of the PVN neurons in vitro. These findings suggest that postsynaptic GABA(B) receptor function is upregulated in PVN presympathetic neurons in SHR. Whereas presynaptic GABA(B) receptor control of glutamatergic synaptic inputs is enhanced, presynaptic GABA(B) receptor control of GABAergic inputs in the PVN is attenuated in SHR. Changes in both pre- and postsynaptic GABA(B) receptors in the PVN may contribute to the control of sympathetic outflow in hypertension.

Indexed as

Neuronal PlasticitySynaptic TransmissionAnimalsBaclofenDisease Models, AnimalDose-Response Relationship, DrugExcitatory Postsynaptic PotentialsGABA AgonistsGABA AntagonistsGlutamineGTP-Binding ProteinsGuanosine DiphosphateHypertensionInhibitory Postsynaptic PotentialsIn Vitro TechniquesMaleBaclofenCGP 55845AGABA AgonistsGABA AntagonistsGlutamineGTP-Binding Proteinsguanosine 5'-O-(2-thiodiphosphate)Guanosine DiphosphatePhosphinic AcidsPropanolaminesReceptors, GABA-BThionucleotides

Identifiers

PMID18567709
PMCPMC2519208
OpenAlexW2109776154

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.