GO:0045471 response to ethanol: Behavioral and Physiological Mechanisms, Genes, Functions and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0045471 (response to ethanol) describes any process that changes a cell or organism's state or activity in response to an ethanol stimulus, including movement, secretion, enzyme production, and gene expression [1,2,4].
• Ethanol responses span multiple physiological systems: ventilatory control, autonomic function, dopaminergic signaling, and neuroendocrine regulation [6,7].
• Genetic variation strongly influences ethanol response; Taok2 controls behavioral responses to ethanol in mice, and genetic ethanol preference modulates resistance to extinction of ethanol-seeking behavior.
• Developmental timing matters: adolescent and adult rats show different autonomic responses to ethanol, and prenatal ethanol exposure can enhance later ethanol-induced appetitive reinforcement.
• Chronic ethanol consumption alters endocrine responses, including erythropoietin production and parathyroid hormone response to hypocalcemia.
• CRISPR-based models (knockout, point mutation, knock-in, overexpression) enable causal testing of candidate genes in ethanol response pathways.
Description
Response to ethanol (GO:0045471) is a biological process defined as any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of an ethanol stimulus. This GO term captures the full spectrum of physiological, behavioral, and molecular reactions triggered by ethanol exposure, from acute ventilatory changes to long-term neuroadaptations [1,2,4]. Ethanol is one of the most widely consumed psychoactive substances, and understanding how organisms respond to it is central to addiction biology, toxicology, and neuropharmacology [2,5]. The term is deliberately broad, encompassing responses across diverse systems including respiratory control, autonomic regulation, dopaminergic neurotransmission, and endocrine function [6,7]. Researchers study GO:0045471 to identify genetic and environmental factors that shape ethanol sensitivity, tolerance, and dependence. Because ethanol responses are highly context-dependent, varying by dose, developmental stage, and genetic background, this GO term provides a unifying framework for comparing findings across model organisms and experimental paradigms [4,8]. The breadth of the term reflects the reality that ethanol affects virtually every organ system, making it a rich but challenging target for mechanistic dissection.
response to ethanol At A Glance
| GO ID | GO:0045471 |
|---|---|
| GO term | response to ethanol |
| Ontology | biological_process |
| Synonym | None |
| Definition | Any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of an ethanol stimulus. |
| Major function | Mediates physiological, behavioral, and molecular adaptations to ethanol exposure across multiple organ systems. |
| Related systems | Respiratory control, autonomic nervous system, dopaminergic signaling, neuroendocrine regulation. |
| Model organisms | Rats, mice, and other mammalian models used in ethanol research. |
| Key research areas | Addiction biology, developmental ethanol effects, ethanol tolerance and sensitization. |
What Is GO:0045471?
GO:0045471 (response to ethanol) is a biological process term in the Gene Ontology. It is defined as any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of an ethanol stimulus. In practical terms, this includes behavioral, physiological, cellular, and molecular changes triggered by ethanol exposure, such as altered breathing patterns, modified autonomic nervous system activity, changes in dopamine release, and shifts in hormone production [6,7]. The term has no synonyms in the current QuickGO annotation.
Why Is response to ethanol Important in Cell Biology?
GO:0045471 is important because ethanol is a ubiquitous environmental and pharmacological stimulus with profound effects on human health, and understanding the biological response to ethanol is essential for addressing alcohol use disorders, developmental ethanol toxicity, and ethanol-drug interactions. The term encompasses responses that range from acute physiological adjustments, such as ventilatory changes and autonomic activation, to long-lasting neuroadaptations that drive addiction-related behaviors. Genetic studies in model organisms have identified specific genes, such as Taok2, that control behavioral responses to ethanol, demonstrating that ethanol sensitivity is genetically tractable. Developmental stage critically modulates ethanol responses, with adolescent and adult animals showing distinct autonomic reactions and prenatal exposure producing lasting changes in ethanol reinforcement. Chronic ethanol also disrupts endocrine function, affecting erythropoietin and parathyroid hormone regulation. Thus, GO:0045471 provides a framework for integrating molecular, physiological, and behavioral data to understand how organisms cope with ethanol and why some individuals are more vulnerable to its effects.
• Ethanol response pathways are central to understanding alcohol use disorders and addiction liability [2,5].
• Genetic variation in ethanol response genes, such as Taok2, influences behavioral sensitivity to ethanol.
• Developmental ethanol exposure produces lasting changes in ethanol reinforcement and reward.
• Ethanol alters autonomic function in a dose- and age-dependent manner.
• Ethanol affects ventilatory control, including long-term facilitation and hypoxic responses.
• Dopaminergic responses to repeated ethanol exposure differ between developmental stages.
• Chronic ethanol consumption disrupts endocrine systems, including erythropoietin and parathyroid hormone regulation [6,7].
• Ethanol-related cues can induce long-lasting resistance to extinction of drug-seeking behavior.
• Model organisms provide tractable systems for dissecting conserved ethanol response mechanisms [1,2,4].
• CRISPR-based genetic models enable causal testing of candidate genes in ethanol response pathways.
What Happens During response to ethanol?
Acute Physiological and Autonomic Responses
In simple terms: When an organism encounters ethanol, its body immediately adjusts breathing, heart rate, and other automatic functions.
Acute ethanol exposure triggers rapid physiological adjustments across multiple systems. In female rats, ethanol abolishes ventilatory long-term facilitation and blunts the ventilatory response to hypoxia, indicating that ethanol disrupts respiratory plasticity mechanisms. Autonomic responses to ethanol are dose-dependent and differ between adolescent and adult rats, with age-specific patterns of heart rate and other autonomic measures. These acute responses represent the first line of organismal reaction to ethanol and are critical for understanding ethanol's immediate physiological impact.
Neurochemical and Dopaminergic Signaling Changes
In simple terms: Ethanol changes how brain cells communicate, especially in reward centers that use dopamine.
Ethanol exposure alters dopaminergic signaling in brain regions associated with reward and motivation. Developmental differences exist in the accumbal dopaminergic response to repeated ethanol exposure, with distinct patterns observed in adolescent versus adult animals. These neurochemical changes are thought to contribute to ethanol's reinforcing properties and may underlie developmental differences in susceptibility to ethanol-related behaviors [3,8].
Behavioral and Motivational Responses
In simple terms: Ethanol affects behavior, including how much an animal seeks ethanol and how persistent that seeking is.
Behavioral responses to ethanol include changes in locomotor activity, ethanol consumption, and drug-seeking behavior. Taok2 controls behavioral response to ethanol in mice, demonstrating a specific genetic contribution to ethanol-induced behavioral changes. Genetic ethanol preference influences the long-lasting resistance to extinction of response reinstatement induced by ethanol-related stimuli, meaning that animals with different genetic backgrounds show different persistence in ethanol-seeking behavior. Prenatal ethanol exposure leads to greater ethanol-induced appetitive reinforcement, suggesting that early-life ethanol exposure sensitizes later motivational responses to ethanol.
Endocrine and Metabolic Adaptations
In simple terms: Long-term ethanol use changes hormone levels and how the body handles stress and metabolism.
Chronic ethanol administration affects endocrine function across multiple axes. In mice, chronic ethanol administration alters both the production of and response to erythropoietin, a hormone critical for red blood cell production. In pregnant rats, chronic ethanol consumption affects the response of parathyroid hormone to hypocalcemia, indicating that ethanol disrupts calcium-regulating endocrine feedback loops. These endocrine adaptations represent systemic consequences of prolonged ethanol exposure that can have broad health implications.
Developmental and Age-Dependent Effects
In simple terms: The same amount of ethanol can affect young and old organisms differently.
Developmental stage is a critical modifier of ethanol responses. Adolescent and adult rats show different autonomic responses to ethanol across a range of doses, and the accumbal dopaminergic response to repeated ethanol exposure differs between developmental stages. Prenatal ethanol exposure produces lasting increases in ethanol-induced appetitive reinforcement, indicating that ethanol exposure during critical developmental windows can permanently alter motivational responses to ethanol later in life. These findings highlight the importance of considering age and developmental timing in studies of GO:0045471.
Key Genes Involved in GO:0045471 response to ethanol
The following genes and proteins have been experimentally implicated in response to ethanol (GO:0045471) based on the verified literature.
| Gene | Major Role | Research Relevance |
|---|---|---|
| Taok2 | Controls behavioral response to ethanol in mice | Demonstrates genetic control of ethanol sensitivity; knockout and point-mutation models can test kinase-dependent mechanisms |
| Dopamine receptor genes (e.g., Drd1, Drd2) | Mediate accumbal dopaminergic responses to repeated ethanol exposure | Targets for studying developmental differences in ethanol reward |
| Erythropoietin (Epo) | Hormone whose production and response are altered by chronic ethanol | Model for ethanol effects on hematopoietic and endocrine systems |
| Parathyroid hormone (Pth) | Regulates calcium homeostasis; response to hypocalcemia is altered by chronic ethanol | Model for ethanol effects on endocrine feedback loops during pregnancy |
| Genes underlying genetic ethanol preference | Modulate resistance to extinction of ethanol-seeking behavior | Candidate genes for addiction liability and relapse |
| Genes affecting ventilatory control | Mediate ethanol effects on respiratory plasticity and hypoxic response | Targets for studying ethanol effects on brainstem respiratory circuits |
| Genes affecting autonomic function | Determine age- and dose-dependent autonomic responses to ethanol | Relevant to cardiovascular effects of ethanol |
| Genes mediating prenatal ethanol effects | Underlie enhanced ethanol-induced appetitive reinforcement after prenatal exposure | Developmental ethanol sensitivity models |
| Ethanol-metabolizing enzymes (e.g., Adh, Aldh) | Metabolize ethanol and generate reactive metabolites | Modulate systemic ethanol exposure levels and downstream responses |
| Neurotransmitter receptors (e.g., GABA-A, NMDA) | Mediate acute ethanol effects on neuronal excitability | Primary targets of ethanol in the brain |
| Stress-response genes (e.g., Hspa family) | Protect cells from ethanol-induced protein damage | Cellular defense against ethanol toxicity |
| Inflammatory mediators (e.g., cytokines) | Mediate neuroimmune responses to ethanol | Link ethanol to neuroinflammation |
| Oxidative stress genes (e.g., Sod, Cat) | Counteract ethanol-induced reactive oxygen species | Modulate ethanol toxicity |
| Ion channel genes | Regulate neuronal excitability under ethanol | Determinants of acute ethanol sensitivity |
| Transcription factors (e.g., Creb) | Mediate long-term gene expression changes after ethanol | Substrates of ethanol-induced neuroadaptation |
| Synaptic plasticity genes | Underlie ethanol effects on learning and memory | Relevant to addiction-related plasticity |
| Neurotrophic factor genes (e.g., Bdnf) | Modulate neuronal survival and plasticity in response to ethanol | Candidate modifiers of ethanol sensitivity |
| Circadian genes | Influence ethanol sensitivity and consumption patterns | Link ethanol response to biological rhythms |
How Is response to ethanol Regulated?
Response to ethanol (GO:0045471) is regulated at multiple levels. Genetic factors strongly influence ethanol responses, as demonstrated by Taok2 control of behavioral ethanol sensitivity in mice and by genetic ethanol preference modulating resistance to extinction of ethanol-seeking behavior. Developmental stage regulates ethanol responses, with adolescent and adult animals showing distinct autonomic and dopaminergic reactions [3,4]. Prenatal ethanol exposure can reprogram later ethanol reinforcement, indicating developmental regulation of ethanol response systems. Chronic ethanol exposure regulates endocrine feedback loops, altering erythropoietin production and parathyroid hormone responses [6,7]. At the physiological level, ethanol modulates ventilatory control and autonomic function through mechanisms that are dose- and context-dependent [1,4]. These regulatory layers collectively determine the magnitude and duration of an organism's response to ethanol.
response to ethanol and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| Taok2 | Alcohol use disorder; behavioral ethanol sensitivity | Taok2 knockout and point-mutation mice for ethanol behavioral testing |
| Dopamine receptor genes | Addiction; developmental ethanol sensitivity | Developmental stage-specific knockout or knockdown in reward circuits |
| Epo | Anemia; ethanol-induced hematopoietic changes | Chronic ethanol administration in Epo reporter or knockout mice |
| Pth | Calcium homeostasis disorders; pregnancy-related ethanol effects | Pregnant rat models with Pth pathway manipulation |
| Genes underlying ethanol preference | Relapse; extinction resistance | Selectively bred lines or knockout models for ethanol preference genes |
Alcohol Use Disorders and Addiction
Response to ethanol (GO:0045471) is directly relevant to alcohol use disorders. Genetic factors that control behavioral responses to ethanol, such as Taok2, and genetic ethanol preference that modulates resistance to extinction of ethanol-seeking behavior, provide mechanistic insights into addiction liability. Prenatal ethanol exposure enhancing later ethanol-induced appetitive reinforcement suggests that early-life ethanol responses can predispose to increased ethanol seeking later in life. These findings support the view that individual differences in ethanol response pathways contribute to addiction risk.
Developmental and Fetal Alcohol Spectrum Disorders
Ethanol exposure during development produces lasting changes in ethanol response systems. Prenatal ethanol exposure leads to greater ethanol-induced appetitive reinforcement, and developmental differences exist in accumbal dopaminergic responses to repeated ethanol exposure. Adolescent and adult rats show distinct autonomic responses to ethanol, indicating that developmental timing shapes ethanol sensitivity. These observations are relevant to fetal alcohol spectrum disorders and adolescent ethanol vulnerability.
Endocrine and Metabolic Disorders
Chronic ethanol consumption disrupts endocrine function, as shown by altered erythropoietin production and response in mice and impaired parathyroid hormone response to hypocalcemia in pregnant rats. These endocrine disruptions may contribute to anemia, bone disease, and calcium dysregulation in individuals with chronic ethanol use. The response to ethanol (GO:0045471) thus intersects with metabolic and endocrine pathology.
Respiratory and Autonomic Dysfunction
Ethanol affects ventilatory control and autonomic function. Ethanol abolishes ventilatory long-term facilitation and blunts the ventilatory response to hypoxia in female rats, and autonomic responses to ethanol differ by age and dose. These effects may be relevant to respiratory and cardiovascular complications associated with ethanol use, particularly in vulnerable populations.
From response to ethanol-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does a candidate gene control behavioral ethanol sensitivity? | Knockout mouse with behavioral ethanol response assays |
| Does a specific kinase domain mediate ethanol response? | Point-mutation knock-in of kinase-dead allele |
| Does a human variant alter ethanol response? | Knock-in of human variant into orthologous mouse locus |
| Where is a candidate protein expressed during ethanol exposure? | Tagged knock-in with fluorescent or epitope tag |
| Does overexpression of a gene enhance ethanol response? | Transgenic overexpression or viral delivery in target brain region |
| Does a gene mediate developmental ethanol effects? | Conditional knockout with developmental stage-specific induction |
How to Study the response to ethanol Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Behavioral ethanol response assays | Locomotor activity, ethanol consumption, seeking behavior | Testing gene effects on ethanol sensitivity [2,5] |
| Plethysmography | Ventilatory parameters and plasticity | Assessing ethanol effects on breathing |
| Autonomic monitoring | Heart rate, blood pressure variability | Age- and dose-dependent ethanol responses |
| Microdialysis or voltammetry | Neurotransmitter release (e.g., dopamine) | Accumbal dopaminergic responses to ethanol |
| Immunoassays | Hormone levels (e.g., erythropoietin, PTH) | Endocrine responses to chronic ethanol [6,7] |
| Operant conditioning | Ethanol reinforcement and motivation | Prenatal ethanol effects on appetitive reinforcement |
| Genetic knockout/mutation | Causal gene function | Testing candidate genes in ethanol response |
| Transcriptomics | Gene expression changes after ethanol | Identifying ethanol-responsive pathways |
Behavioral Assays for Ethanol Response
Behavioral assays are essential for quantifying ethanol responses in model organisms. Locomotor activity, ethanol consumption, and ethanol-seeking behavior can be measured using established paradigms. Taok2 control of behavioral response to ethanol was demonstrated using behavioral tests in mice, and resistance to extinction of ethanol-seeking behavior has been assessed in genetic ethanol preference models. Prenatal ethanol effects on appetitive reinforcement can be tested using operant or place-conditioning paradigms.
Physiological and Autonomic Measurements
Physiological measurements capture autonomic and ventilatory responses to ethanol. Ventilatory long-term facilitation and hypoxic ventilatory responses can be measured using plethysmography in rats. Autonomic responses, including heart rate variability, can be assessed in adolescent and adult rats across ethanol doses. These methods provide quantitative readouts of ethanol's effects on cardiorespiratory control.
Neurochemical and Molecular Analyses
Neurochemical methods measure ethanol-induced changes in neurotransmitter release and gene expression. Accumbal dopaminergic responses to repeated ethanol exposure can be assessed using microdialysis or voltammetry. Endocrine responses, such as erythropoietin production and parathyroid hormone levels, can be quantified using immunoassays in chronic ethanol models [6,7]. These molecular readouts link cellular changes to organismal ethanol responses.
Genetic and Pharmacological Manipulation
Genetic manipulation is a powerful approach for dissecting ethanol response mechanisms. Knockout, point-mutation, and knock-in models allow causal testing of candidate genes. Taok2 knockout and mutation studies demonstrated gene-specific effects on ethanol behavior. Pharmacological tools can complement genetic approaches by acutely modulating ethanol response pathways. Combining genetic and pharmacological methods provides robust evidence for gene function in GO:0045471.
How CRISPR Can Be Used to Study GO:0045471 response to ethanol
Knockout
CRISPR knockout models enable complete loss-of-function studies for genes implicated in response to ethanol (GO:0045471). For example, knocking out Taok2 in mice can test whether this gene is required for normal behavioral ethanol responses. Knockout approaches are ideal for determining whether a candidate gene is necessary for ethanol-induced physiological or behavioral changes. Researchers can generate constitutive or conditional knockouts to study developmental versus adult roles in ethanol response.
Point Mutation
CRISPR point-mutation models introduce specific amino acid changes to dissect domain-specific functions in ethanol response pathways. For a kinase like Taok2, a kinase-dead point mutation can distinguish scaffolding functions from catalytic activity in controlling ethanol behavior. Point mutations can also model human variants associated with altered ethanol sensitivity. These models provide precise mechanistic insights that complement knockout studies.
Knock-in
CRISPR knock-in models allow introduction of reporter tags, human variants, or conditional alleles at endogenous loci. Tagged knock-in of genes involved in ethanol response enables visualization of protein expression and localization in relevant tissues. Knock-in of human ethanol-response variants into mouse orthologs can test their functional impact. These models are valuable for translational studies linking genetic variation to ethanol response phenotypes.
Overexpression
CRISPR overexpression models, including transgenic or viral-mediated approaches, can test whether increased gene dosage enhances or alters ethanol responses. Overexpressing candidate genes in specific brain regions or cell types can reveal gain-of-function effects on ethanol sensitivity, tolerance, or reinforcement. Overexpression complements knockout studies by providing bidirectional evidence for gene function in GO:0045471.
How EDITGENE Supports response to ethanol Research
Researchers studying response to ethanol-related genes often need to determine whether a candidate gene is causally involved in ethanol sensitivity, tolerance, or reinforcement. EDITGENE provides end-to-end CRISPR services to generate precisely engineered cell and animal models for mechanistic studies of GO:0045471.
Contact EDITGENE today to design your custom CRISPR model for response to ethanol research.
Frequently Asked Questions About response to ethanol
What is GO:0045471 response to ethanol?
GO:0045471 is a Gene Ontology biological process term defined as any process that results in a change in state or activity of a cell or an organism (in terms of movement, secretion, enzyme production, gene expression, etc.) as a result of an ethanol stimulus. It encompasses physiological, behavioral, and molecular responses to ethanol [1,2,4].
What genes are involved in response to ethanol?
Genes experimentally implicated in response to ethanol include Taok2, which controls behavioral ethanol sensitivity in mice, dopamine receptor genes involved in accumbal dopaminergic responses, and genes underlying genetic ethanol preference that modulate extinction resistance. Endocrine-related genes such as erythropoietin and parathyroid hormone are also affected by chronic ethanol [6,7].
How does ethanol affect the brain?
Ethanol alters dopaminergic signaling in reward-related brain regions, with developmental differences in accumbal dopaminergic responses to repeated exposure. Ethanol also affects behavioral responses through genes such as Taok2 and can enhance ethanol-induced appetitive reinforcement after prenatal exposure.
What are the physiological effects of ethanol?
Ethanol affects ventilatory control, abolishing long-term facilitation and blunting hypoxic responses in female rats. It also produces dose- and age-dependent autonomic responses and disrupts endocrine function, including erythropoietin and parathyroid hormone regulation [6,7].
How is response to ethanol studied in the lab?
Response to ethanol is studied using behavioral assays [2,5], physiological measurements such as plethysmography and autonomic monitoring [1,4], neurochemical analyses like microdialysis, and endocrine immunoassays [6,7]. Genetic models including knockout and knock-in mice are used to test causal gene function.
Does age affect ethanol response?
Yes. Adolescent and adult rats show different autonomic responses to ethanol, and developmental differences exist in accumbal dopaminergic responses to repeated ethanol exposure. Prenatal ethanol exposure can also lead to greater ethanol-induced appetitive reinforcement later in life.
What is the role of Taok2 in ethanol response?
Taok2 controls behavioral response to ethanol in mice, as demonstrated by genetic studies showing that Taok2 manipulation alters ethanol-induced behaviors. This makes Taok2 a key gene for understanding genetic contributions to ethanol sensitivity.
Can CRISPR be used to study ethanol response genes?
Yes. CRISPR knockout, point-mutation, knock-in, and overexpression models enable causal testing of candidate genes in ethanol response pathways. For example, Taok2 knockout and mutation models have been used to study behavioral ethanol sensitivity.
What endocrine systems are affected by chronic ethanol?
Chronic ethanol affects erythropoietin production and response in mice and alters parathyroid hormone response to hypocalcemia in pregnant rats. These effects demonstrate that ethanol disrupts multiple endocrine feedback loops.
Why is response to ethanol important for addiction research?
Response to ethanol pathways mediate behavioral sensitivity, reinforcement, and extinction resistance, all of which are relevant to addiction. Genetic ethanol preference modulates resistance to extinction of ethanol-seeking behavior, and prenatal ethanol exposure enhances later ethanol reinforcement, highlighting developmental and genetic contributions to addiction risk.
Conclusion
GO:0045471 (response to ethanol) is a broad but essential biological process term that captures the diverse physiological, behavioral, and molecular changes triggered by ethanol. Research using model organisms has identified specific genes, such as Taok2, that control ethanol responses, and has revealed developmental, endocrine, and neurochemical mechanisms underlying ethanol sensitivity [1,3,4,6,7,8]. Understanding these pathways is critical for addressing alcohol use disorders and ethanol-related pathologies. CRISPR-based models provide powerful tools for causally testing candidate genes and accelerating discovery in this field.
References
- 1. Silverstein AL et al.. 2025. Ethanol abolishes ventilatory long-term facilitation and blunts the ventilatory response to hypoxia in female rats.. Respir Physiol Neurobiol 332:104373 PMID: 39603312
- 2. Kapfhamer D et al.. 2013. Taok2 controls behavioral response to ethanol in mice.. Genes Brain Behav 12(1):87-97 PMID: 22883308
- 3. Philpot R et al.. 2004. Developmental differences in the accumbal dopaminergic response to repeated ethanol exposure.. Ann N Y Acad Sci 1021:422-6 PMID: 15251921
- 4. Ristuccia RC et al.. 2008. Autonomic responses to ethanol in adolescent and adult rats: a dose-response analysis.. Alcohol 42(8):623-9 PMID: 18952397
- 5. Ciccocioppo R et al.. 2001. Long-lasting resistance to extinction of response reinstatement induced by ethanol-related stimuli: role of genetic ethanol preference.. Alcohol Clin Exp Res 25(10):1414-9 PMID: 11696659
- 6. Giglio MJ et al.. 1984. Effect of chronic ethanol administration on production of and response to erythropoietin in the mouse.. Alcohol Clin Exp Res 8(3):323-5 PMID: 6377952
- 7. Duggal S et al.. 2007. Effect of chronic ethanol consumption on the response of parathyroid hormone to hypocalcemia in the pregnant rat.. Alcohol Clin Exp Res 31(1):104-12 PMID: 17207108
- 8. Pautassi RM et al.. 2012. Prenatal ethanol exposure leads to greater ethanol-induced appetitive reinforcement.. Alcohol 46(6):585-93 PMID: 22698870
