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Article ; Online: Reproducibility of Experiments with Laboratory Animals: What Should We Do Now?

Crabbe, John C

Alcoholism, clinical and experimental research

2016 Volume 40, Issue 11, Page(s) 2305–2308

MeSH term(s)	Animals ; Animals, Laboratory ; Reproducibility of Results ; Research Design
Language	English
Publishing date	2016
Publishing country	England
Document type	Journal Article ; Comment
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1111/acer.13228
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Article ; Online: Progress With Nonhuman Animal Models of Addiction.

Crabbe, John C

Journal of studies on alcohol and drugs

2016 Volume 77, Issue 5, Page(s) 696–699

Abstract: Nonhuman animals have been major contributors to the science of the genetics of addiction. Given the explosion of interest in genetics, it is fair to ask, are we making reasonable progress toward our goals with animal models? I will argue that our goals ... ...

Abstract	Nonhuman animals have been major contributors to the science of the genetics of addiction. Given the explosion of interest in genetics, it is fair to ask, are we making reasonable progress toward our goals with animal models? I will argue that our goals are changing and that overall progress has been steady and seems likely to continue apace. Genetics tools have developed almost incredibly rapidly, enabling both more reductionist and more synthetic or integrative approaches. I believe that these approaches to making progress have been unbalanced in biomedical science, favoring reductionism, particularly in animal genetics. I argue that substantial, novel progress is also likely to come in the other direction, toward synthesis and abstraction. Another area in which future progress with genetic animal models seems poised to contribute more is the reconciliation of human and animal phenotypes, or consilience. The inherent power of the genetic animal models could be more profitably exploited. In the end, animal research has continued to provide novel insights about how genes influence individual differences in addiction risk and consequences. The rules of the genetics game are changing so fast that it is hard to remember how comparatively little we knew even a generation ago. Rather than worry about whether we have been wasting time and resources asking the questions we have been, we should look to the future and see if we can come up with some new ones. The valuable findings from the past will endure, and the sidetracks will be forgotten.
MeSH term(s)	Animals ; Behavior, Addictive/diagnosis ; Behavior, Addictive/genetics ; Behavior, Addictive/therapy ; CRISPR-Cas Systems/genetics ; Disease Models, Animal ; Gene Editing/trends ; Humans ; Models, Animal ; Substance-Related Disorders/diagnosis ; Substance-Related Disorders/genetics ; Substance-Related Disorders/therapy
Language	English
Publishing date	2016-09-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2266450-6
ISSN	1938-4114 ; 1934-2683 ; 1937-1888 ; 0096-882X
ISSN (online)	1938-4114 ; 1934-2683
ISSN	1937-1888 ; 0096-882X
DOI	10.15288/jsad.2016.77.696
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Article: Quantitative Trait Loci Mapping.

Grisel, Judith E / Crabbe, John C

Alcohol health and research world

2019 Volume 19, Issue 3, Page(s) 220–227

Abstract: Researchers interested in the physical locations of genes that influence a person's alcohol-related behaviors can use a method known as quantitative trait loci (QTL) mapping to identify the approximate locations of genes in the genome. QTL mapping can ... ...

Abstract	Researchers interested in the physical locations of genes that influence a person's alcohol-related behaviors can use a method known as quantitative trait loci (QTL) mapping to identify the approximate locations of genes in the genome. QTL mapping can use recombinant inbred mouse strains, which are sets of inbred strains derived from cross-breeding the offspring of two genetically distinct parent strains. The inbred strains exhibit different patterns of the parent strains' genes. QTL mapping involves comparing alcohol-related behaviors in these strains and identifying patterns of known genetic markers shared by strains with the same behaviors. The markers allow the identification of probable locations of genes that influence alcohol-related behaviors. These locations can then be verified using other tests, and specific genes can be sought there.
Language	English
Publishing date	2019-12-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	427760-0
ISSN	0090-838X
ISSN	0090-838X
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Article: Use of animal models of alcohol-related behavior.

Crabbe, John C

Handbook of clinical neurology

2014 Volume 125, Page(s) 71–86

Abstract: Alcoholism (alcohol dependence and alcohol use disorder, AUD) is quintessentially behavioral in nature. AUD is behaviorally and genetically complex. This review discusses behavioral assessment of alcohol sensitivity, tolerance, dependence, withdrawal, ... ...

Abstract	Alcoholism (alcohol dependence and alcohol use disorder, AUD) is quintessentially behavioral in nature. AUD is behaviorally and genetically complex. This review discusses behavioral assessment of alcohol sensitivity, tolerance, dependence, withdrawal, and reinforcement. The focus is on using laboratory animal models to explore genetic contributions to individual differences in alcohol responses. Rodent genetic animal models based on selective breeding for high vs low alcohol response, and those based on the use of inbred strains, are reviewed. Genetic strategies have revealed the complexity of alcohol responses where genetic influences on multiple alcohol-related behaviors are mostly discrete. They have also identified areas where genetic influences are consistent across behavioral assays and have been used to model genetic differences among humans at different risk for AUD.
MeSH term(s)	Alcohol-Related Disorders/diagnosis ; Alcohol-Related Disorders/genetics ; Alcohol-Related Disorders/psychology ; Alcoholism/diagnosis ; Alcoholism/genetics ; Alcoholism/psychology ; Animals ; Humans ; Mice ; Models, Animal ; Rats ; Reinforcement (Psychology) ; Species Specificity
Language	English
Publishing date	2014
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ISSN	0072-9752
ISSN	0072-9752
DOI	10.1016/B978-0-444-62619-6.00005-7
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Article: Rodent models of genetic contributions to motivation to abuse alcohol.

Crabbe, John C

Nebraska Symposium on Motivation. Nebraska Symposium on Motivation

2014 Volume 61, Page(s) 5–29

Abstract: In summary, there are remarkably few studies focused on the genetic contributions to alcohol's reinforcing values. Almost all such studies examine the two-bottle preference test. Despite the deficiencies I have raised in its interpretation, a rodent ... ...

Abstract	In summary, there are remarkably few studies focused on the genetic contributions to alcohol's reinforcing values. Almost all such studies examine the two-bottle preference test. Despite the deficiencies I have raised in its interpretation, a rodent genotype's willingness to drink ethanol when water is freely available offers a reasonable aggregate estimate of alcohol's reinforcing value relative to other genotypes (Green and Grahame 2008). As indicated above, however, preference drinking studies will likely never avoid the confounding role of taste preferences and most often yield intake levels not sufficient to yield a pharmacologically significant BAL. Thus, the quest for improved measures of reinforcing value continues. Of the potential motivational factors considered by McClearn in his seminal review in this series, we can safely conclude that rodent alcohol drinking is not primarily directed at obtaining calories. The role of taste (and odor) remains a challenge. McClearn appears to have been correct that especially those genotypes that avoid alcohol are probably doing so based on preingestive sensory cues; however, postingestive consequences are also important. Cunningham's intragastric model shows the role of both preingestional and postingestional modulating factors for the best known examples, the usually nearly absolutely alcohol-avoiding DBA/2J and HAP-2 mice. Much subsequent data reinforce McClearn's earlier conclusion that C57BL/6J mice, at least, do not regulate their intake around a given self-administered dose of alcohol by adjusting their intake. This leaves us with the puzzle of why nearly all genotypes, even those directionally selectively bred for high voluntary intake for many generations, fail to self-administer intoxicating amounts of alcohol. Since McClearn's review, many ingenious assays to index alcohol's motivational effects have been used extensively, and new methods for inducing dependence have supplanted the older ones prevalent in 1968. I have tried to identify promising areas where the power of genetics could be fruitfully harvested and generally feel that we have a much more clear idea now about some important experiments remaining to be performed.
MeSH term(s)	Alcoholism/genetics ; Animals ; Behavior, Animal ; Disease Models, Animal ; Genetic Predisposition to Disease/genetics ; Mice ; Motivation/genetics ; Rats
Language	English
Publishing date	2014-10-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ISSN	0146-7875
ISSN	0146-7875
DOI	10.1007/978-1-4939-0653-6_2
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Book: The genetic basis of alcohol and drug actions

Crabbe, John C.

1991

Author's details	ed. by John C. Crabbe
Keywords	Alcoholism / genetics ; Pharmacogenetics ; Substance-Related Disorders / genetics ; Alkohol ; Pharmakogenetik ; Halluzinogen ; Physiologie ; Tierversuch
Subject	Humanphysiologie ; Mensch ; Körperfunktion ; Halluzinogene Droge ; Bewusstseinserweiternde Droge ; Bewusstseinsverändernde Droge ; Psychodysleptikum ; Psychedelische Droge ; Eidetikum ; Psychomimetikum ; Psychotrope Substanz ; Experiment ; Tierexperiment
Size	XVI, 383 S. : graph. Darst.
Publisher	Plenum Pr
Publishing place	New York u.a.
Publishing country	United States
Document type	Book
HBZ-ID	HT004016895
ISBN	0-306-43868-2 ; 978-0-306-43868-4
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Article ; Online: The impact of Drinking in the Dark (DID) procedural manipulations on ethanol intake in High Drinking in the Dark (HDID) mice.

Savarese, Antonia M / Ozburn, Angela R / Barkley-Levenson, Amanda M / Metten, Pamela / Crabbe, John C

Alcohol (Fayetteville, N.Y.)

2021 Volume 93, Page(s) 45–56

Abstract: The High Drinking in the Dark mouse lines (HDID-1 and HDID-2) were selectively bred to achieve high blood ethanol concentrations (BECs) in the Drinking in the Dark (DID) task, a widely used model of binge-like intake of 20% ethanol. There are several ... ...

Abstract	The High Drinking in the Dark mouse lines (HDID-1 and HDID-2) were selectively bred to achieve high blood ethanol concentrations (BECs) in the Drinking in the Dark (DID) task, a widely used model of binge-like intake of 20% ethanol. There are several components that differentiate DID from other animal models of ethanol intake: time of day of testing, length of ethanol access, single-bottle access, and individual housing. Here, we sought to determine how some of these individual factors contribute to the high ethanol intake observed in HDID mice. HDID-1, HDID-2, and non-selected HS/NPT mice were tested in a series of DID experiments where one of the following factors was manipulated: length of ethanol access, fluid choice, number of ethanol bottles, and housing condition. We observed that 1) HDID mice achieve intoxicating BECs in DID, even when they are group-housed; 2) HDID mice continue to show elevated ethanol intake relative to HS/NPT mice during an extended access session, but this is most apparent during the first 4 h of access; and 3) offering a water choice during DID prevents elevated intake in the HDID-1 mice, but not necessarily in HDID-2 mice. Together, these results suggest that the lack of choice in the DID paradigm, together with the length of ethanol access, are important factors contributing to elevated ethanol intake in the HDID mice. These results further suggest important differences between the HDID lines in response to procedural manipulations of housing condition and ethanol bottle number in the DID paradigm, highlighting the distinct characteristics that each of these lines possess, despite being selectively bred for the same phenotype.
MeSH term(s)	Alcohol Drinking ; Animals ; Ethanol ; Female ; Male ; Mice ; Mice, Inbred C57BL
Chemical Substances	Ethanol (3K9958V90M)
Language	English
Publishing date	2021-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	605912-0
ISSN	1873-6823 ; 0741-8329
ISSN (online)	1873-6823
ISSN	0741-8329
DOI	10.1016/j.alcohol.2021.02.001
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Article ; Online: Long-term alcohol drinking in High Drinking in the Dark mice is stable for many months and does not show alcohol deprivation effects.

Crabbe, John C / Hack, Wyatt R / Ozburn, Angela R / Savarese, Antonia M / Metten, Pamela

Addiction biology

2021 Volume 27, Issue 1, Page(s) e13074

Abstract: We have modelled genetic risk for binge-like drinking by selectively breeding High Drinking in the Dark-1 and -2 (HDID-1 and HDID-2) mice for their propensity to reach intoxicating blood alcohol levels (BALs) after binge-like drinking in a single bottle, ...

Abstract	We have modelled genetic risk for binge-like drinking by selectively breeding High Drinking in the Dark-1 and -2 (HDID-1 and HDID-2) mice for their propensity to reach intoxicating blood alcohol levels (BALs) after binge-like drinking in a single bottle, limited access paradigm. Interestingly, in standard two-bottle choice (2BC) tests for continuously available alcohol versus water, HDID mice show modest levels of preference. This indicates some degree of independence of the genetic contributions to risk for binge-like and sustained, continuous access drinking. We had few data where the drinking in the dark (DID) tests of binge-like drinking had been repeatedly performed, so we serially offered multiple DID tests to see whether binge-like drinking escalated. It did not. We also asked whether HDID mice would escalate their voluntary intake with prolonged exposure to alcohol 2BC. They did not. Lastly, we assessed whether an alcohol deprivation effect (ADE) developed. ADE is a temporary elevation in drinking typically observed after a period of abstinence from sustained access to alcohol choice. With repetition, these periods of ADE sometimes have led to more sustained elevations in drinking. We therefore asked whether repeated ADE episodes would elevate choice drinking in HDID mice. They did not. After nearly 500 days of alcohol access, the intake of HDID mice remained stable. We conclude that a genetically-enhanced high risk for binge-like drinking is not sufficient to yield alterations in long-term alcohol intake.
MeSH term(s)	Alcohol Drinking/genetics ; Animals ; Binge Drinking/genetics ; Darkness ; Ethanol/blood ; Male ; Mice ; Models, Animal
Chemical Substances	Ethanol (3K9958V90M)
Language	English
Publishing date	2021-07-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	1324314-7
ISSN	1369-1600 ; 1355-6215
ISSN (online)	1369-1600
ISSN	1355-6215
DOI	10.1111/adb.13074
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Article: Corticosterone Levels and Glucocorticoid Receptor Gene Expression in High Drinking in the Dark Mice and Their Heterogeneous Stock (HS/NPT) Founder Line.

Savarese, Antonia M / Grigsby, Kolter B / Jensen, Bryan E / Borrego, Marissa B / Finn, Deborah A / Crabbe, John C / Ozburn, Angela R

Frontiers in behavioral neuroscience

2022 Volume 16, Page(s) 821859

Abstract: The High Drinking in the Dark (HDID-1) line of mice has been selectively bred for achieving high blood alcohol levels (BALs) in the Drinking in the Dark task, a model of binge-like drinking. Recently, we determined that glucocorticoid receptor (GR) ... ...

Abstract	The High Drinking in the Dark (HDID-1) line of mice has been selectively bred for achieving high blood alcohol levels (BALs) in the Drinking in the Dark task, a model of binge-like drinking. Recently, we determined that glucocorticoid receptor (GR) antagonism with either mifepristone or CORT113176 (a selective GR antagonist) reduced binge-like ethanol intake in the HDID-1 mice, but not in their founder line, HS/NPT. Here, we examined whether the selection process may have altered glucocorticoid functioning by measuring (1) plasma corticosterone levels and (2) expression of the genes encoding GR (
Language	English
Publishing date	2022-05-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452960-6
ISSN	1662-5153
ISSN	1662-5153
DOI	10.3389/fnbeh.2022.821859
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Article ; Online: Genetic and genomic signatures in ethanol withdrawal seizure-prone and seizure-resistant mice implicate genes involved in epilepsy and neuronal excitability.

Zhou, Zhifeng / Metten, Pamela / Yuan, Qiaoping / Sun, Hui / Hodgkinson, Colin A / Shen, Pei-Hong / Marietta, Cheryl / Crabbe, John C / Goldman, David

Molecular psychiatry

2022 Volume 27, Issue 11, Page(s) 4611–4623

Abstract: Alcohol withdrawal is a clinically important consequence and potential driver of Alcohol Use Disorder. However, susceptibility to withdrawal symptoms, ranging from craving and anxiety to seizures and delirium, varies greatly. Selectively bred Withdrawal ... ...

Abstract	Alcohol withdrawal is a clinically important consequence and potential driver of Alcohol Use Disorder. However, susceptibility to withdrawal symptoms, ranging from craving and anxiety to seizures and delirium, varies greatly. Selectively bred Withdrawal Seizure-Prone (WSP) and Seizure-Resistant (WSR) mice are an animal model of differential susceptibility to withdrawal and phenotypes with which withdrawal severity correlates. To identify innate drivers of alcohol withdrawal severity, we performed a multi-omic study of the WSP and WSR lines and F2 mice derived from them, using genomic, genetic, and transcriptomic analyses. Genes implicated in seizures and epilepsy were over-represented among those that segregated between WSP and WSR mice and that displayed differential expression in F2 mice high and low in withdrawal. Quantitative trait locus (QTL) analysis of ethanol withdrawal convulsions identified several genome-wide significant loci and pointed to genes that modulate potassium channel function and neural excitability. Perturbations of expression of genes involved in synaptic transmission, including GABAergic and glutamatergic genes, were prominent in prefrontal cortex transcriptome. Expression QTL (eQTL) analysis fine mapped genes within the peak ethanol withdrawal QTL regions. Genetic association analysis in human subjects provided converging evidence for the involvement of those genes in severity of alcohol withdrawal and dependence. Our results reveal a polygenic network and neural signaling pathways contributing to ethanol withdrawal seizures and related phenotypes that overlap with genes modulating epilepsy and neuronal excitability.
MeSH term(s)	Mice ; Humans ; Animals ; Substance Withdrawal Syndrome/genetics ; Alcoholism/genetics ; Seizures/genetics ; Ethanol ; Epilepsy
Chemical Substances	Ethanol (3K9958V90M)
Language	English
Publishing date	2022-10-05
Publishing country	England
Document type	Journal Article
ZDB-ID	1330655-8
ISSN	1476-5578 ; 1359-4184
ISSN (online)	1476-5578
ISSN	1359-4184
DOI	10.1038/s41380-022-01799-x
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