Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice.

Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice. Research Abstract Details 

Research Abstract Table of Contents

Jump to the:

Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice. Abstract Text:

J R Fee,D R Sparta,M J Picker,T E Thiele,J R Fee,D R Sparta,M J Picker,T E Thiele,J R Fee,D R Sparta,M J Picker,T E Thiele,

RATIONALE: Manipulation of glucocorticoid receptor signaling has been shown to alter the acquisition and expression of ethanol-induced locomotor sensitization in mice. It is unknown if other components of the hypothalamic-pituitary-adrenal (HPA)-axis modulate locomotor sensitization resulting from repeated ethanol administration. In the present investigation, we determined if pretreatment with an i.p. injection of CP-154,526, a selective corticotropin releasing factor (CRF) type-1 receptor antagonist, would block the acquisition and/or expression of ethanol-induced locomotor sensitization in male DBA/2J mice. METHODS: To assess the role of the CRF(1) receptor in the acquisition of behavioral sensitization, mice were pretreated with an i.p. injection of CP-154,526 30 min before each of 10 sensitizing i.p. injections of ethanol. To determine the role of the CRF(1) receptor in modulating the expression of ethanol-induced sensitization, mice that had previously been sensitized to the locomotor stimulant effects of ethanol were pretreated with CP-154,526 30 min before an i.p. injection of ethanol on the test day. In a third study, ethanol-naïve mice were pretreated with CP-154,526 30 min before an initial i.p. injection of ethanol to determine the combined effects of the CRF(1) receptor antagonist and ethanol on locomotor activity. Blood ethanol concentrations were assessed at the termination of sensitization studies. RESULTS: Pretreatment with CP-154,526 blocked the expression of ethanol-induced locomotor sensitization in DBA/2J mice but did not prevent the acquisition of sensitization. The ability of CP-154,526 to block the expression of ethanol-induced locomotor sensitization was not attributable to alterations in blood ethanol levels or possible sedative effects produced by the combined administration of CP-154,526 and ethanol. CONCLUSIONS: These data provide novel evidence that CRF(1) receptor signaling modulates the expression of ethanol-induced locomotor sensitization, and add to a growing literature suggesting a role for neurochemicals and hormones associated with the HPA-axis in behavioral sensitization resulting from repeated exposure to drugs of abuse.

Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice. Publishing Authors By Initials

JR Fee,DR Sparta,MJ Picker,TE Thiele,JR Fee,DR Sparta,MJ Picker,TE Thiele,JR Fee,DR Sparta,MJ Picker,TE Thiele,

For similar abstracts research abstracts see: abstracts research

PUBMED ID PMID:

MEDLINE DATE:

Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Neuroscience

VOLUME: 150

Page Numbers: 14-21

Journal Abbreviation: Neuroscience

ISSN: 0306-4522

DAY: 8

MONTH: 09

YEAR: 2007

Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 7605074

Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice. Keywords Mesh Terms:

KEYWORDS:

MESH TERMS:

Chemical & Substance for Abstract: Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice. Information

Substance Name:

Registry Number:

Grant and Affiliation Information for Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice.

AFFILIATION: Department of Psychology, University of North Carolina, Davie Hall, CB# 3270, Chapel Hill, NC 27599-3270, USA.

Country: United States

AGENCY:

GRANT:

ACRONYM:

MEDLINETA: Neuroscience

REFSOURCE:

DATABASENAME:

ACCESSION NUMBER:

Number Hits: 0

Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice Related Publications

• A karate program for improving self-concept and quality of life in childhood epilepsy: Results of a pilot study.
• A simplified liquid culture medium for the growth of Hemophilus pertussis.
• Additional Flavonoids from the Leaves of Larrea tridentata.
• Controlling pattern formation in nanoparticle assemblies via directed solvent dewetting.
• Corticotropin releasing factor-1 receptor antagonist, CP-154,526, blocks the expression of ethanol-induced behavioral sensitization in DBA/2J mice.
• Decreased immunoreactivity of the melanocortin neuropeptide alpha-melanocyte-stimulating hormone (alpha-MSH) after chronic ethanol exposure in Sprague-Dawley rats.
• Doppler ultrasonography in rheumatology: adding color to the picture.
• Drosophila Ctr1A functions as a copper transporter essential for development.
• Efficacy of sirolimus in treating tuberous sclerosis and lymphangioleiomyomatosis.
• Elevated anxiety-like behavior following ethanol exposure in mutant mice lacking neuropeptide Y (NPY).
• Identification of a vacuole-associated metalloreductase and its role in Ctr2-mediated intracellular copper mobilization.
• Inactivation of glycogen synthase kinase-3 contributes to brain-derived neutrophic factor/TrkB-induced resistance to chemotherapy in neuroblastoma cells.
• Induction of translationally controlled tumor protein (TCTP) by transcriptional and post-transcriptional mechanisms.
• Intrafamilial phenotypic variability in tuberous sclerosis complex.
• Intrahepatic lymphocyte expression of dipeptidyl peptidase I-processed granzyme B and perforin induces hepatocyte expression of serine proteinase inhibitor 6 (Serpinb9/SPI-6).
• L(p) estimates for the bilinear Hilbert transform.
• On Calderon's conjecture for the bilinear hilbert transform.
• Oral supplementation with all-Rac- and RRR-alpha-tocopherol increases vitamin E levels in human sebum after a latency period of 14-21 days.
• Seizures in children: determining the variation.
• Seizures in children: laboratory diagnosis and management.
• Signals transduced via insulin-like growth factor I receptor (IGF(R)) mediate resistance to retinoic acid-induced cell growth arrest in a human neuroblastoma cell line.
• Structure of the Ctr1 copper trans'PORE'ter reveals novel architecture.
• Studies on the antigenicity of toxic extracts of Hemophilus pertussis.
• Targeting Akt to increase the sensitivity of neuroblastoma to chemotherapy: lessons learned from the brain-derived neurotrophic factor/TrkB signal transduction pathway.
• Transcatheter closure of postinfarction ventricular septal defects.
• Two novel human members of an emerging mammalian gene family related to mono-ADP-ribosylating bacterial toxins.
• Use of RNA interference to elucidate the effect of MYCN on cell cycle in neuroblastoma.
• [Not Available.]
• [Not Available.]
• [Not Available.]