Evidence map›Paper›PMID 18667550›Full record

ArticleJournal of neurophysiology2008

Dual orexin actions on dorsal raphe and laterodorsal tegmentum neurons: noisy cation current activation and selective enhancement of Ca2+ transients mediated by L-type calcium channels.

K A Kohlmeier, S Watanabe, C J Tyler, S Burlet, C S Leonard

Open access · hybridAbstract read
In one paragraph

Article in Journal of neurophysiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

39 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Review
  3. A molecular network map of orexin-orexin receptor signaling system.Journal of cell communication and signaling · 2023
    Article
  4. Article
  5. Orexin Signaling: A Complex, Multifaceted Process.Frontiers in cellular neuroscience · 2022
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Acute suppressive and long-term phase modulation actions of orexin on the mammalian circadian clock.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  19. Review
  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

5 authors at 1 institution in 1 country.

K A KohlmeierDepartment of Physiology, New York Medical College, Valhalla, NY 10595, USA.
S Watanabe
C J Tyler
S Burlet
C S Leonard
New York Medical College · US

Funding

"Synaptic Modulation of Mesopontine Cholingergic Neurons"R01NS027881 · NINDS · NEW YORK UNIVERSITY · PI LEONARD, CHRISTOPHER S · 1992 to 2022
$7.1M
K+-CHANNELS REGULATING REM-RELATED CHOLINGERGIC NEURONSR01HL064150 · NHLBI · NEW YORK MEDICAL COLLEGE · PI LEONARD, CHRISTOPHER S · 1999 to 2011
$2.6M
SYNAPTIC MODULATION OF MESOPONTINE CHOLINERGIC NEURONSR55NS027881 · NINDS · NEW YORK UNIVERSITY · PI LEONARD, CHRISTOPHER S · 1991 to 1991
–
NHLBI NIH HHS HL-64150NHLBI NIH HHS R01 HL064150NINDS NIH HHS NS-27881
6 · The paper itself

Abstract

The hypocretin/orexins (Hcrt/Orxs) are hypothalamic neuropeptides that regulate stress, addiction, feeding, and arousal behaviors. They depolarize many types of central neurons and can increase [Ca2+]i in some, including those of the dorsal raphe (DR) and laterodorsal tegmental (LDT) nuclei-two structures likely to contribute to the behavioral actions of Hcrt/Orx. In this study, we used simultaneous whole cell and Ca2+-imaging methods in mouse brain slices to compare the Hcrt/Orx-activated current in DR and LDT neurons and to determine whether it contributes to the Ca2+ influx evoked by Hcrt/Orx. We found Hcrt/Orx activates a similar noisy cation current that reversed near 0 mV in both cell types. Contrary to our expectation, this current did not contribute to the somatic Ca2+ influx evoked by Hcrt/Orx. In contrast, Hcrt/Orx enhanced the Ca2+ transients produced by voltage steps (-60 to -30 mV) by approximately 30% even in neurons lacking an inward current. This effect was abolished by nifedipine, augmented by Bay-K and abolished by bisindolylmaleimide I. Thus Hcrt/Orx has two independent actions: activation of noisy cation channels that generate depolarization and activation of a protein kinase C (PKC)-dependent enhancement of Ca2+ transients mediated by L-type Ca2+ channels. Immunocytochemistry verified that both these actions occurred in serotonergic and cholinergic neurons, indicating that Hcrt/Orx can function as a neuromodulator in these key neurons of the reticular activating system. Because regulation of Ca2+ transients mediated by L-channels is often linked to the control of transcriptional signaling, our findings imply that Hcrt/Orxs may also function in the regulation of long-term homeostatic or trophic processes.

Indexed as

AnimalsCalcium Channels, L-TypeCalcium SignalingCationsElectrophysiologyImmunohistochemistryIntracellular Signaling Peptides and ProteinsIn Vitro TechniquesIon ChannelsMiceMice, Inbred C57BLNeuronsNeuropeptidesNeurotransmitter AgentsOrexinsParasympathetic Nervous SystemCalcium Channels, L-TypeCationsIntracellular Signaling Peptides and ProteinsIon ChannelsNeuropeptidesNeurotransmitter AgentsOrexinsProtein Kinase CSerotoninSodium Channels

Identifiers

PMID18667550
PMCPMC2576219
OpenAlexW2024400557

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.