Evidence map›Paper›PMID 24835172›Full record

ArticleThe Journal of physiology2014

A functional coupling between extrasynaptic NMDA receptors and A-type K+ channels under astrocyte control regulates hypothalamic neurosecretory neuronal activity.

Krishna Naskar, Javier E Stern

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2014. 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
1.5field-weighted citation impact, top 22% 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, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. 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
  4. Article
  5. Angiotensin II inhibits the A-type KAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2022
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Control of Long-Term Plasticity by Glutamate Transporters.Frontiers in synaptic neuroscience · 2019
    Review
  13. Review
  14. Article
  15. Hypothalamic Ion Channels in Hypertension.Current hypertension reports · 2018
    Review
  16. Altered NMDA receptor-evoked intracellular CaThe Journal of physiology · 2017
    Article
  17. A-type KAmerican journal of physiology. Heart and circulatory physiology · 2017
    Article
  18. Article
  19. Article
  20. Dendritic Release of Neurotransmitters.Comprehensive Physiology · 2016
    Review
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.

Krishna NaskarDepartment of Physiology, Medical College of Georgia, Georgia Regents University, Augusta, GA, 30912, USA.
Javier E SternDepartment of Physiology, Medical College of Georgia, Georgia Regents University, Augusta, GA, 30912, USA jstern@gru.edu.
Augusta University · US

Funding

CENTRAL NEURONAL-GLIAL MECHANISMS AND NEUROHUMORAL ACTIVATION IN HYPERTENSIONR01HL112225 · NHLBI · GEORGIA STATE UNIVERSITY · PI STERN, JAVIER E · 2012 to 2015
$1.5M
NHLBI NIH HHS HL112225NHLBI NIH HHS R01 HL112225
6 · The paper itself

Abstract

Neuronal activity is controlled by a fine-tuned balance between intrinsic properties and extrinsic synaptic inputs. Moreover, neighbouring astrocytes are now recognized to influence a wide spectrum of neuronal functions. Yet, how these three key factors act in concert to modulate and fine-tune neuronal output is not well understood. Here, we show that in rat hypothalamic magnocellular neurosecretory cells (MNCs), glutamate NMDA receptors (NMDARs) are negatively coupled to the transient, voltage-gated A-type K(+) current (IA). We found that activation of NMDARs by extracellular glutamate levels influenced by astrocyte glutamate transporters resulted in a significant inhibition of IA. The NMDAR-IA functional coupling resulted from activation of extrasynaptic NMDARs, was calcium- and protein kinase C-dependent, and involved enhanced steady-state, voltage-dependent inactivation of IA. The NMDAR-IA coupling diminished the latency to the first evoked spike in response to membrane depolarization and increased the total number of evoked action potentials, thus strengthening the neuronal input/output function. Finally, we found a blunted NMDA-mediated inhibition of IA in dehydrated rats. Together, our findings support a novel signalling mechanism that involves a functional coupling between extrasynaptic NMDARs and A-type K(+) channels, which is influenced by local astrocytes. We show this signalling complex to play an important role in modulating hypothalamic neuronal excitability, which may contribute to adaptive responses during a sustained osmotic challenge such as dehydration.

Indexed as

Action PotentialsAnimalsAstrocytesCalciumGlutamic AcidHypothalamusMaleNeuronsNeurosecretory SystemsOsmotic PressurePotassium Channels, Voltage-GatedProtein Kinase CRatsRats, WistarReaction TimeReceptors, N-Methyl-D-AspartateCalciumGlutamic AcidPotassium Channels, Voltage-GatedProtein Kinase CReceptors, N-Methyl-D-Aspartate

Identifiers

PMID24835172
PMCPMC4221822
OpenAlexW1578846620

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.