Evidence map›Paper›PMID 18617607›Full record

ArticleEndocrinology2008

Nonclassical mechanisms of progesterone action in the brain: II. Role of calmodulin-dependent protein kinase II in progesterone-mediated signaling in the hypothalamus of female rats.

Bhuvana Balasubramanian, Wendy Portillo, Andrea Reyna, Jian Zhong Chen, Anthony N Moore, Pramod K Dash, Shaila K Mani

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
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  5. Review
  6. Review
  7. Article
  8. Review
  9. Progesterone and neuroprotection.Hormones and behavior · 2013
    Review
  10. Article
  11. Article
  12. Convergence of multiple mechanisms of steroid hormone action.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2012
    Review
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Review
  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

7 authors at 2 institutions in 1 country.

Bhuvana BalasubramanianDepartment of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, USA.
Wendy Portillo
Andrea Reyna
Jian Zhong Chen
Anthony N Moore
Pramod K Dash
Shaila K Mani
The University of Texas at Austin · USBaylor College of Medicine · US

Funding

MECHANISMS OF MEMORY DEFICITS FOLLOWING BRAIN INJURYR01NS035457 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DASH, PRAMOD K · 1997 to 2006
$2.2M
Working memory deficits following brain traumaR01NS049160 · NINDS · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DASH, PRAMOD K · 2005 to 2009
$1.8M
Prefrontal cortex and memory storageR01MH072933 · NIMH · UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON · PI DASH, PRAMOD K · 2006 to 2010
$1.5M
Steroid Hormones Regulatory Mechanisms and BehaviorR01MH063954 · NIMH · BAYLOR COLLEGE OF MEDICINE · PI MANI, SHAILAJA K · 2002 to 2006
$1.5M
NIMH NIH HHS MH63954NIMH NIH HHS MH72933NIMH NIH HHS R01 MH063954NIMH NIH HHS R01 MH072933NINDS NIH HHS NS035457NINDS NIH HHS NS049160NINDS NIH HHS R01 NS035457NINDS NIH HHS R01 NS049160
6 · The paper itself

Abstract

In addition to the activation of classical progestin receptor-dependent genomic pathway, progesterone (P) can activate nonclassical, membrane-initiated signaling pathways in the brain. We recently demonstrated rapid P activation of second-messenger kinases, protein kinase A, and protein kinase C in the ventromedial nucleus (VMN) and preoptic area (POA) of rat brain. To determine whether P can activate yet another Ca+2 dependent kinase, we examined the rapid P modulation of calcium and calmodulin-dependent protein kinase II (CaMKII) in the VMN and POA in female rats. A rapid P-initiated activation of CaMKII basal activity was observed in the VMN but not the POA at 30 min. Estradiol benzoate (EB) priming enhanced this CaMKII basal activity in both the VMN and POA. CaMKII protein levels and phosphorylation of Thr-286 moiety on CaMKII, however, remained unchanged with EB and/or P treatments, suggesting that the changes in the CaMKII kinase activity are due to rapid P modulation of the kinase activity and not its synthesis or autoactivation. Furthermore, intracerebroventricular (icv) administration of a CaMKII-specific inhibitor, KN-93, 30 min prior to the P infusion, in EB-primed, ovariectomized female rats inhibited CaMKII activation but not protein kinase A and protein kinase C activities. Interestingly, icv administration of KN-93 30 min prior to P infusion (icv) resulted in a reduction but not total inhibition of P-facilitated lordosis response in EB-primed female rats. These observations suggest a redundancy or, alternately, a hierarchy in the P-regulated activation of kinase signaling cascades in female reproductive behavior.

Indexed as

AnimalsBenzenesulfonamidesBenzylaminesBrainCalcium-Calmodulin-Dependent Protein Kinase Type 2Cerebral CortexEnzyme ActivationEstradiolFemaleHypothalamusOvariectomyPhosphorylationPreoptic AreaProgesteroneProtein Kinase CProtein Kinase InhibitorsBenzenesulfonamidesBenzylaminesCalcium-Calmodulin-Dependent Protein Kinase Type 2Estradiolestradiol 3-benzoateKN 93ProgesteroneProtein Kinase CProtein Kinase InhibitorsSulfonamides

Identifiers

PMID18617607
PMCPMC2584600
OpenAlexW2002975562

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.