Evidence map›Paper›PMID 15190106›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Hypocretinergic control of spinal cord motoneurons.

Jack Yamuy, Simon J Fung, Mingchu Xi, Michael H Chase

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

42 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Hypothalamic Control of Forelimb Motor Adaptation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  6. Sleep, Narcolepsy, and Sodium Oxybate.Current neuropharmacology · 2022
    Article
  7. [Orexin-A inhibits γ-aminobutyric acid current of neonatal rat spinal cord ventral horn neurons by activating OXNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
    Article
  8. Review
  9. Article
  10. Article
  11. Reduced plasma orexin-A levels in patients with bipolar disorder.Neuropsychiatric disease and treatment · 2019
    Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. The hypocretin system and psychiatric disorders.Current psychiatry reports · 2014
    Review
  20. Etiopathogenesis and neurobiology of narcolepsy: a review.Journal of clinical and diagnostic research : JCDR · 2014
    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

4 authors.

Jack YamuyDepartment of Physiology, University of California Los Angeles School of Medicine, Los Angeles, California 90095, USA. jyamuy@ucla.edu
Simon J Fung
Mingchu Xi
Michael H Chase

Funding

TRANSMITTER RELEASE ONTO AIRWAY MOTONEURONS DURING SLEEPP50HL060296 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHASE, MICHAEL H · 1998 to 2007
$12.5M
PHARMACOLOGICAL MODEL OF THE ATONIA OF ACTIVE/(REM)SLEEPR01MH043362 · NIMH · WEBSCIENCES INTERNATIONAL · PI CHASE, MICHAEL H · 1988 to 2007
$2.0M
STATE-DEPENDENT SOMATOMOTOR PROCESSESR01AG004307 · NIA · WEBSCIENCES INTERNATIONAL · PI CHASE, MICHAEL H · 1985 to 2003
$1.7M
STATE-DEPENDENT CONTROL OF SOMATIC REFLEX ACTIVITYR01NS009999 · NINDS · WEBSCIENCES INTERNATIONAL · PI CHASE, MICHAEL H · 1985 to 2004
$1.5M
TRANSMITTER SYSTEMS AND MOTOR CONTROL DURING SLEEPR01NS023426 · NINDS · WEBSCIENCES INTERNATIONAL · PI CHASE, MICHAEL H · 1986 to 2005
$1.5M
PHARMACOLOGICAL MODEL OF ATONIA OF ACTIVE SLEEPR37MH043362 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHASE, MICHAEL H · 1992 to 2001
$496k
STATE-DEPENDENT SOMATOMOTOR PROCESSES IN THE OLD CATR37AG004307 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI CHASE, MICHAEL H · 1988 to 1997
–
SYNTHESIS OF CONSTITUTIVELY ACTIVE SEROTONIN RECEPTORSF32NS009999 · NINDS · CALIFORNIA INSTITUTE OF TECHNOLOGY · PI ENGLAND, PAMELA MICHAEL · 1996 to 1998
–
NHLBI NIH HHS HL 60296NHLBI NIH HHS P50 HL060296NIA NIH HHS AG 04307NIA NIH HHS R01 AG004307NIMH NIH HHS MH 43362NIMH NIH HHS R01 MH043362NIMH NIH HHS R37 MH043362NINDS NIH HHS F32 NS009999NINDS NIH HHS NS 09999NINDS NIH HHS NS 23426NINDS NIH HHS R01 NS009999NINDS NIH HHS R01 NS023426
6 · The paper itself

Abstract

Hypocretinergic (orexinergic) neurons in the lateral hypothalamus project to motor columns in the lumbar spinal cord. Consequently, we sought to determine whether the hypocretinergic system modulates the electrical activity of motoneurons. Using in vivo intracellular recording techniques, we examined the response of spinal motoneurons in the cat to electrical stimulation of the lateral hypothalamus. In addition, we examined the membrane potential response to orthodromic stimulation and intracellular current injection before and after both hypothalamic stimulation and the juxtacellular application of hypocretin-1. It was found that (1) hypothalamic stimulation produced a complex sequence of depolarizing- hyperpolarizing potentials in spinal motoneurons; (2) the depolarizing potentials decreased in amplitude after the application of SB-334867, a hypocretin type 1 receptor antagonist; (3) the EPSP induced by dorsal root stimulation was not affected by the application of SB-334867; (4) subthreshold stimulation of dorsal roots and intracellular depolarizing current steps produced spike potentials when applied in concert to stimulation of the hypothalamus or after the local application of hypocretin-1; (5) the juxtacellular application of hypocretin-1 induced motoneuron depolarization and, frequently, high-frequency discharge; (6) hypocretin-1 produced a significant decrease in rheobase (36%), membrane time constant (16.4%), and the equalizing time constant (23.3%); (7) in a small number of motoneurons, hypocretin-1 produced an increase in the synaptic noise; and (8) the input resistance was not affected after hypocretin-1. The juxtacellular application of vehicle (saline) and denatured hypocretin-1 did not produce changes in the preceding electrophysiological properties. We conclude that hypothalamic hypocretinergic neurons are capable of modulating the activity of lumbar motoneurons through presynaptic and postsynaptic mechanisms. The lack of hypocretin-induced facilitation of motoneurons may be a critical component of the pathophysiology of cataplexy.

Indexed as

Intracellular Signaling Peptides and ProteinsAnimalsBenzoxazolesCarrier ProteinsCataplexyCatsElectric StimulationHypothalamusMembrane PotentialsMotor NeuronsNaphthyridinesNeuropeptidesOrexin ReceptorsOrexinsReceptors, G-Protein-CoupledReceptors, Neuropeptide1-(2-methylbenzoxazol-6-yl)-3-(1,5)naphthyridin-4-yl ureaBenzoxazolesCarrier ProteinsIntracellular Signaling Peptides and ProteinsNaphthyridinesNeuropeptidesOrexin ReceptorsOrexinsReceptors, G-Protein-CoupledReceptors, NeuropeptideSympathomimeticsUrea

Identifiers

PMID15190106
PMCPMC6729307

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.