Evidence map›Paper›PMID 28972129›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

CaMKII Regulates Synaptic NMDA Receptor Activity of Hypothalamic Presympathetic Neurons and Sympathetic Outflow in Hypertension.

De-Pei Li, Jing-Jing Zhou, Jixiang Zhang, Hui-Lin Pan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

33 citing papers in PubMed, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Hypothalamic Corticotropin-Releasing Hormone Contributes to Hypertension in Spontaneously Hypertensive Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  14. Article
  15. Article
  16. Review
  17. 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 LiCenter for Neuroscience and Pain Research, Division of Anesthesiology and Critical Care, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030 dpli@mdanderson.org huilinpan@mdanderson.org.
Jing-Jing ZhouCenter for Neuroscience and Pain Research, Division of Anesthesiology and Critical Care, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030.
Jixiang ZhangCenter for Neuroscience and Pain Research, Division of Anesthesiology and Critical Care, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030.ORCID 0000-0002-1641-8650
Hui-Lin PanCenter for Neuroscience and Pain Research, Division of Anesthesiology and Critical Care, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030 dpli@mdanderson.org huilinpan@mdanderson.org.
The University of Texas MD Anderson Cancer Center · US

Funding

Signaling Mechanisms of CNS Neuronal Plasticity in HypertensionR01HL131161 · NHLBI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI PAN, HUI-LIN · 2016 to 2019
$2.1M
Hypothalamic Neuronal Plasticity in Chronic StressR01MH096086 · NIMH · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI LI, DE-PEI · 2013 to 2017
$1.8M
NHLBI NIH HHS R01 HL131161NIMH NIH HHS R01 MH096086
6 · The paper itself

Abstract

NMDAR activity in the hypothalamic paraventricular nucleus (PVN) is increased and critically involved in heightened sympathetic vasomotor tone in hypertension. Calcium/calmodulin-dependent protein kinase II (CaMKII) binds to and modulates NMDAR activity. In this study, we determined the role of CaMKII in regulating NMDAR activity of PVN presympathetic neurons in male spontaneously hypertensive rats (SHRs). NMDAR-mediated EPSCs and puff NMDA-elicited currents were recorded in spinally projecting PVN neurons in SHRs and male Wistar-Kyoto (WKY) rats. The basal amplitude of evoked NMDAR-EPSCs and puff NMDA currents in retrogradely labeled PVN neurons were significantly higher in SHRs than in WKY rats. The CaMKII inhibitor autocamtide-2-related inhibitory peptide (AIP) normalized the increased amplitude of NMDAR-EPSCs and puff NMDA currents in labeled PVN neurons in SHRs but had no effect in WKY rats. Treatment with AIP also normalized the higher frequency of NMDAR-mediated miniature EPSCs of PVN neurons in SHRs. CaMKII-mediated phosphorylation level of GluN2B serine 1303 (S1303) in the PVN, but not in the hippocampus and frontal cortex, was significantly higher in SHRs than in WKY rats. Lowering blood pressure with celiac ganglionectomy in SHRs did not alter the increased level of phosphorylated GluN2B S1303 in the PVN. In addition, microinjection of AIP into the PVN significantly reduced arterial blood pressure and lumbar sympathetic nerve discharges in SHRs. Our findings suggest that CaMKII activity is increased in the PVN and contributes to potentiated presynaptic and postsynaptic NMDAR activity to elevate sympathetic vasomotor tone in hypertension.

Indexed as

Adrenergic FibersAnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2Excitatory Postsynaptic PotentialsHypertensionHypothalamusMaleNeuronsOrgan Culture TechniquesRatsRats, Inbred SHRRats, Inbred WKYReceptors, N-Methyl-D-AspartateSynapsesCalcium-Calmodulin-Dependent Protein Kinase Type 2Receptors, N-Methyl-D-Aspartateautonomic nervous systemhypertensionhypothalamussympathetic nerve activitysynaptic transmission

Identifiers

PMID28972129
PMCPMC5666588
OpenAlexW2761859218

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.