Ethanol concentration-dependent effects and the role of stress on ethanol drinking in corticotropin-releasing factor type 1 and double type 1 and 2 receptor knockout mice

Raúl Pastor, Cheryl Reed, Sue Burkhart-Kasch, Na Li, Amanda L. Sharpe, Sarah C. Coste, Mary Stenzel-Poore, Tamara Phillips

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Rationale Exposure to stressors promotes ethanol (EtOH) consumption and enhances drug craving during abstinence. Corticotropin-releasing factor (CRF), and in particular, CRF actions via type 1 CRF receptors (CRF 1) are critical in behavioral responses to stressors. CRF 1 play a role in EtOH-induced behavioral neuroadaptation, in binge-like EtOH consumption, and in heightened EtOH consumption in dependent animals. Objectives We investigated the involvement of CRF 1 in swim-stress-induced changes in EtOH consumption and in baseline consumption as a function of EtOH concentration. The role of CRF 2 in adapting to effects of the stressor was also examined. Methods Wild-type mice and knockout mice lacking CRF 1 were tested for two-bottle choice EtOH consumption at concentrations of 3-20%. Also, intake of 10% EtOH was examined in wild-type mice and knockout mice lacking CRF 1, or lacking both CRF 1 and CRF 2, before and after acute or repeated swim stress exposures. Results EtOH intake was reduced in CRF 1 compared with wild-type mice when presented at a concentration of 20% but not when presented at lower concentrations. No genotype-dependent effects were found for saccharin or quinine drinking. Acute swim stress had no effect, but repeated swim stress resulted in higher levels of EtOH consumption in wild-type mice, compared with both types of knockout mice. Stress effects on EtOH drinking were longer lasting in double knockout mice. Conclusions These data suggest a prominent role of CRF 1 in stressor-induced changes in EtOH consumption, with involvement of CRF 2 in recovery from stressor effects.

Original languageEnglish (US)
Pages (from-to)169-177
Number of pages9
JournalPsychopharmacology
Volume218
Issue number1
DOIs
StatePublished - Nov 2011

Fingerprint

Corticotropin-Releasing Hormone
Knockout Mice
Drinking
Ethanol
Saccharin
Quinine
Genotype

Keywords

  • Alcohol
  • CRF
  • Drinking
  • Knockout
  • Stress
  • Swim stress

ASJC Scopus subject areas

  • Pharmacology

Cite this

Ethanol concentration-dependent effects and the role of stress on ethanol drinking in corticotropin-releasing factor type 1 and double type 1 and 2 receptor knockout mice. / Pastor, Raúl; Reed, Cheryl; Burkhart-Kasch, Sue; Li, Na; Sharpe, Amanda L.; Coste, Sarah C.; Stenzel-Poore, Mary; Phillips, Tamara.

In: Psychopharmacology, Vol. 218, No. 1, 11.2011, p. 169-177.

Research output: Contribution to journalArticle

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title = "Ethanol concentration-dependent effects and the role of stress on ethanol drinking in corticotropin-releasing factor type 1 and double type 1 and 2 receptor knockout mice",
abstract = "Rationale Exposure to stressors promotes ethanol (EtOH) consumption and enhances drug craving during abstinence. Corticotropin-releasing factor (CRF), and in particular, CRF actions via type 1 CRF receptors (CRF 1) are critical in behavioral responses to stressors. CRF 1 play a role in EtOH-induced behavioral neuroadaptation, in binge-like EtOH consumption, and in heightened EtOH consumption in dependent animals. Objectives We investigated the involvement of CRF 1 in swim-stress-induced changes in EtOH consumption and in baseline consumption as a function of EtOH concentration. The role of CRF 2 in adapting to effects of the stressor was also examined. Methods Wild-type mice and knockout mice lacking CRF 1 were tested for two-bottle choice EtOH consumption at concentrations of 3-20{\%}. Also, intake of 10{\%} EtOH was examined in wild-type mice and knockout mice lacking CRF 1, or lacking both CRF 1 and CRF 2, before and after acute or repeated swim stress exposures. Results EtOH intake was reduced in CRF 1 compared with wild-type mice when presented at a concentration of 20{\%} but not when presented at lower concentrations. No genotype-dependent effects were found for saccharin or quinine drinking. Acute swim stress had no effect, but repeated swim stress resulted in higher levels of EtOH consumption in wild-type mice, compared with both types of knockout mice. Stress effects on EtOH drinking were longer lasting in double knockout mice. Conclusions These data suggest a prominent role of CRF 1 in stressor-induced changes in EtOH consumption, with involvement of CRF 2 in recovery from stressor effects.",
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AU - Pastor, Raúl

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AU - Burkhart-Kasch, Sue

AU - Li, Na

AU - Sharpe, Amanda L.

AU - Coste, Sarah C.

AU - Stenzel-Poore, Mary

AU - Phillips, Tamara

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N2 - Rationale Exposure to stressors promotes ethanol (EtOH) consumption and enhances drug craving during abstinence. Corticotropin-releasing factor (CRF), and in particular, CRF actions via type 1 CRF receptors (CRF 1) are critical in behavioral responses to stressors. CRF 1 play a role in EtOH-induced behavioral neuroadaptation, in binge-like EtOH consumption, and in heightened EtOH consumption in dependent animals. Objectives We investigated the involvement of CRF 1 in swim-stress-induced changes in EtOH consumption and in baseline consumption as a function of EtOH concentration. The role of CRF 2 in adapting to effects of the stressor was also examined. Methods Wild-type mice and knockout mice lacking CRF 1 were tested for two-bottle choice EtOH consumption at concentrations of 3-20%. Also, intake of 10% EtOH was examined in wild-type mice and knockout mice lacking CRF 1, or lacking both CRF 1 and CRF 2, before and after acute or repeated swim stress exposures. Results EtOH intake was reduced in CRF 1 compared with wild-type mice when presented at a concentration of 20% but not when presented at lower concentrations. No genotype-dependent effects were found for saccharin or quinine drinking. Acute swim stress had no effect, but repeated swim stress resulted in higher levels of EtOH consumption in wild-type mice, compared with both types of knockout mice. Stress effects on EtOH drinking were longer lasting in double knockout mice. Conclusions These data suggest a prominent role of CRF 1 in stressor-induced changes in EtOH consumption, with involvement of CRF 2 in recovery from stressor effects.

AB - Rationale Exposure to stressors promotes ethanol (EtOH) consumption and enhances drug craving during abstinence. Corticotropin-releasing factor (CRF), and in particular, CRF actions via type 1 CRF receptors (CRF 1) are critical in behavioral responses to stressors. CRF 1 play a role in EtOH-induced behavioral neuroadaptation, in binge-like EtOH consumption, and in heightened EtOH consumption in dependent animals. Objectives We investigated the involvement of CRF 1 in swim-stress-induced changes in EtOH consumption and in baseline consumption as a function of EtOH concentration. The role of CRF 2 in adapting to effects of the stressor was also examined. Methods Wild-type mice and knockout mice lacking CRF 1 were tested for two-bottle choice EtOH consumption at concentrations of 3-20%. Also, intake of 10% EtOH was examined in wild-type mice and knockout mice lacking CRF 1, or lacking both CRF 1 and CRF 2, before and after acute or repeated swim stress exposures. Results EtOH intake was reduced in CRF 1 compared with wild-type mice when presented at a concentration of 20% but not when presented at lower concentrations. No genotype-dependent effects were found for saccharin or quinine drinking. Acute swim stress had no effect, but repeated swim stress resulted in higher levels of EtOH consumption in wild-type mice, compared with both types of knockout mice. Stress effects on EtOH drinking were longer lasting in double knockout mice. Conclusions These data suggest a prominent role of CRF 1 in stressor-induced changes in EtOH consumption, with involvement of CRF 2 in recovery from stressor effects.

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