Evidence map›Paper›PMID 15659593›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Chronic cocaine administration switches corticotropin-releasing factor2 receptor-mediated depression to facilitation of glutamatergic transmission in the lateral septum.

Jie Liu, Baojian Yu, Luis Orozco-Cabal, Dimitri E Grigoriadis, Jean Rivier, Wylie W Vale, Patricia Shinnick-Gallagher, Joel P Gallagher

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.5field-weighted citation impact, top 23% 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

37 citing papers in PubMed, 65 citations in OpenAlex.

  1. Change in brain molecular landscapes following electrical stimulation of the nucleus accumbens.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  5. Insidious Transmission of a Stress-Related Neuroadaptation.Frontiers in behavioral neuroscience · 2020
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  13. CRF-R2 and the heterosynaptic regulation of VTA glutamate during reinstatement of cocaine seeking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
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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

8 authors at 3 institutions in 1 country.

Jie LiuDepartment of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston, Texas 77555-1031, USA.
Baojian Yu
Luis Orozco-Cabal
Dimitri E Grigoriadis
Jean Rivier
Wylie W Vale
Patricia Shinnick-Gallagher
Joel P Gallagher
The University of Texas Medical Branch at Galveston · USSalk Institute for Biological Studies · USNeurocrine Biosciences (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Corticotropin-releasing factor (CRF) and urocortin (Ucn I) are endogenous members among a family of CRF-related peptides that activate two different and synaptically localized G-protein-coupled receptors, CRF1 and CRF2. These peptides and their receptors have been implicated in stress responses and stress with cocaine abuse. In this study, we observed significant alterations in excitatory transmission and CRF-related peptide regulation of excitatory transmission in the lateral septum mediolateral nucleus (LSMLN) after chronic cocaine administration. In brain slice recordings from the LSMLN of control (saline-treated) rats, glutamatergic synaptic transmission was facilitated by activation of CRF1 receptors with CRF but was depressed after activation of CRF2 receptors with Ucn I. After acute withdrawal from a chronic cocaine administration regimen, CRF1 activation remained facilitatory, but CRF2 activation facilitated rather than depressed LSMLN EPSCs. These alterations in CRF2 effects occurred through both presynaptic and postsynaptic mechanisms. In saline-treated rats, CRF1 and CRF2 coupled predominantly to protein kinase A signaling pathways, whereas after cocaine withdrawal, protein kinase C activity was more prominent and likely contributed to the CRF2-mediated presynaptic facilitation. Neither CRF nor Ucn I altered monosynaptic GABA(A)-mediated IPSCs before or after chronic cocaine administration, suggesting that loss of GABAA-mediated inhibition could not account for the facilitation. This switch in polarity of Ucn I-mediated neuromodulation, from a negative to positive regulation of excitatory glutamatergic transmission after chronic cocaine administration, could generate an imbalance in the brain reward circuitry associated with the LSMLN.

Indexed as

AnimalsCocaine-Related DisordersCorticotropin-Releasing HormoneCRF Receptor, Type 1Excitatory Postsynaptic PotentialsLong-Term PotentiationLong-Term Synaptic DepressionMaleNeural InhibitionNeuronal PlasticityPatch-Clamp TechniquesProtein KinasesRatsRats, Sprague-DawleyReceptors, Corticotropin-Releasing HormoneReceptors, GABA-ACorticotropin-Releasing HormoneCRF Receptor, Type 1CRF receptor type 2Protein KinasesReceptors, Corticotropin-Releasing HormoneReceptors, GABA-AReceptors, GlutamateUrocortins

Identifiers

PMID15659593
PMCPMC6725320
OpenAlexW1980342652

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.