Evidence map›Paper›PMID 15152034›Full record

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

Cholecystokinin modulates migration of gonadotropin-releasing hormone-1 neurons.

Paolo Giacobini, Alan S Kopin, Philip M Beart, Linda D Mercer, Aldo Fasolo, Susan Wray

Open access · bronzeAbstract read
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 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

46 citing papers in PubMed, 83 citations in OpenAlex.

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  8. Nasal Placode Development, GnRH Neuronal Migration and Kallmann Syndrome.Frontiers in cell and developmental biology · 2019
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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

6 authors at 5 institutions in 3 countries.

Paolo GiacobiniCellular and Developmental Neurobiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-4156, USA.
Alan S Kopin
Philip M Beart
Linda D Mercer
Aldo Fasolo
Susan Wray
Monash University · AUNational Institute of Neurological Disorders and Stroke · USTufts Medical Center · USUniversity of Melbourne · AUUniversity of Turin · IT

Funding

Development And Regulation Of The Luteinizing Hormone Releasing Hormone SystemZIANS002824 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI WRAY, SUSAN · 2009 to 2025
$41.2M
The Luteinizing Hormone Releasing Hormone SystemZ01NS002824 · NINDS · NEUROLOGICAL DISORDERS AND STROKE · PI WRAY, SUSAN · 1991 to 2008
$4.9M
STRUCTURE/FUNCTION RELATIONSHIPS OF THE CCK B RECEPTORR01DK046767 · NIDDK · TUFTS MEDICAL CENTER · PI KOPIN, ALAN S · 1992 to 2004
$1.3M
NIDDK NIH HHS DK46767NIDDK NIH HHS R01 DK046767
6 · The paper itself

Abstract

Expression of the brain-gut peptide cholecystokinin (CCK) in the developing olfactory-gonadotropin-releasing hormone-1 (GnRH-1) neuroendocrine systems was characterized, and the function of CCK in these systems was analyzed both in vivo and in vitro. We present novel data demonstrating that CCK transcript and protein are expressed in sensory cells in the developing olfactory epithelium and vomeronasal organ, with both ligand and receptors (CCK-1R and CCK-2R) found on olfactory axons throughout prenatal development. In addition, migrating GnRH-1 neurons in nasal regions express CCK-1R but not CCK-2R receptors. The role of CCK in olfactory-GnRH-1 system development was evaluated using nasal explants, after assessing that the in vivo expression of both CCK and CCK receptors was mimicked in this in vitro model. Exogenous application of CCK (10(-7) m) reduced both olfactory axon outgrowth and migration of GnRH-1 cells. This inhibition was mediated by CCK-1R receptors. Moreover, CCK-1R but not CCK-2R antagonism caused a shift in the location of GnRH-1 neurons, increasing the distance that the cells migrated. GnRH-1 neuronal migration in mice carrying a genetic deletion of either CCK-1R or CCK-2R receptor genes was also analyzed. At embryonic day 14.5, the total number of GnRH-1 cells was identical in wild-type and mutant mice; however, the number of GnRH-1 neurons within forebrain was significantly greater in CCK-1R-/- embryos, consistent with an accelerated migratory process. These results indicate that CCK provides an inhibitory influence on GnRH-1 neuronal migration, contributing to the appropriate entrance of these neuroendocrine cells into the brain, and thus represent the first report of a developmental role for CCK.

Indexed as

AnimalsAntigens, DifferentiationCell MovementCholecystokininGonadotropin-Releasing HormoneIn Situ HybridizationMiceMice, Inbred C57BLMice, KnockoutNeurons, AfferentOlfactory MucosaOlfactory PathwaysOrgan Culture TechniquesReceptor, Cholecystokinin AReceptor, Cholecystokinin BRNA, MessengerAntigens, DifferentiationCholecystokininGonadotropin-Releasing HormoneReceptor, Cholecystokinin AReceptor, Cholecystokinin BRNA, Messenger

Identifiers

PMID15152034
PMCPMC6729465
OpenAlexW2019168583

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.