Enhanced and delayed stress-induced alcohol drinking in mice lacking functional CRH1 receptors.

Abstract

There is a relation between stress and alcohol drinking. We show that the corticotropin-releasing hormone (CRH) system that mediates endocrine and behavioral responses to stress plays a role in the control of long-term alcohol drinking. In mice lacking a functional CRH1 receptor, stress leads to enhanced and progressively increasing alcohol intake. The effect of repeated stress on alcohol drinking behavior appeared with a delay and persisted throughout life. It was associated with an up-regulation of the N-methyl-d-aspartate receptor subunit NR2B. Alterations in the CRH1 receptor gene and adaptional changes in NR2B subunits may constitute a genetic risk factor for stress-induced alcohol drinking and alcoholism.

• Authors: Inge Sillaber, Gerhard Rammes, Stephan Zimmermann, Beatrice Mahal, Walter Zieglgänsberger, Wolfgang Wurst, Florian Holsboer, Rainer Spanagel
• Journal: Science (New York, N.Y.) (Science) Vol. 296 Issue 5569 Pg. 931-3 (May 03 2002) ISSN: 1095-9203 [Electronic] United States
• PMID: 11988580 (Publication Type: Journal Article)

Chemical References

• NR2B NMDA receptor
• Receptors, AMPA
• Receptors, Corticotropin-Releasing Hormone
• Receptors, Kainic Acid
• Receptors, N-Methyl-D-Aspartate
• Ethanol
• CRF receptor type 1
• Corticotropin-Releasing Hormone

Topics

• Action Potentials
• Alcohol Drinking
• Alcoholism (etiology, genetics)
• Animals
• Brain (metabolism)
• Corticotropin-Releasing Hormone (physiology)
• Ethanol (blood)
• Female
• Hippocampus (physiology)
• In Vitro Techniques
• Male
• Mice
• Mice, Knockout
• Models, Animal
• Mutation
• Receptors, AMPA (metabolism)
• Receptors, Corticotropin-Releasing Hormone (genetics, physiology)
• Receptors, Kainic Acid (metabolism)
• Receptors, N-Methyl-D-Aspartate (metabolism)
• Signal Transduction
• Stress, Physiological (physiopathology)
• Stress, Psychological (physiopathology)
• Up-Regulation