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Psikiyatrik Araştırmalarda Kullanılan Hayvan Deneyi Modelleri

Year 2025, Volume: 14 Issue: 1, 37 - 51, 30.04.2025

Onur Koçhan

https://doi.org/10.47493/abantmedj.1610414

Abstract

Hayvan modelleri, psikiyatrik bozuklukların oluşumunu anlamada ve tedavi denemeleri yapmada önemli rol oynamaktadır. Ancak psikiyatrik hastalıkların tüm klinik özelliklerini hayvanlarda sergileyen kapsamlı modeller oluşturmak mümkün değildir. Bunun yerine, araştırmalarda depresyon, anksiyete, şizofreni ve bağımlılık gibi bozuklukların belirli semptom kümelerine odaklanan kısmi modeller kullanılmaktadır.
Depresyon araştırmalarında hayvan deneyleri kronik hafif stres paradigmasıyla modellenir. Modelde depresyonun bağımlı değişkenleri ise intrakraniyal öz uyarım (ICSS), sakkaroz tercihi ve progresif oranlı pekiştireç tepkisi ölçümleridir. Her değişken güvenilirlik ve yapı geçerliliği açısından farklılık gösterse de, anhedoni ve motivasyonel eksiklikler hakkında geçerli ölçümler sunar. Anksiyete modellerinde; yükseltilmiş artı labirent, operant çatışma testi ve sosyal etkileşim değerlendirmeleri gibi testler bağımlı değişkenlerdir, ilaçların anksiyolitik etkilerini belirlemeye yardımcı olur, bu ölçümler ancak genellikle panik bozukluk veya PTSD gibi belirli alt tipler yerine yalnızca genelleştirilmiş anksiyeteyi yansıtır.
Şizofreniyi modellemek, pozitif, negatif ve bilişsel semptomların karmaşıklığı nedeniyle güçtür. Bu alanda farmakolojik manipülasyonlar (örn.; dopaminerjik veya glutamaterjik ajanlar), beyin lezyonu modelleri ve genetik yaklaşımlar geliştirilmiştir. Prepulse inhibisyon (PPI), latent inhibisyon ve çalışma belleği testleri, tam yüz geçerliliği sunmamakla birlikte insanlardaki bulgulara benzer sonuçlar sunmaktadır.
Bağımlılık araştırmaları, aşırı tüketim/entoksikasyon, yoksunluk ve aşerme evrelerini yansıtan hayvan modellerinden faydalanır. İntrakranyel self stimülasyon eşik ölçümleri, şartlandırılmış yer tercihi (CPP) ve stres kaynaklı yeniden madde arayışı gibi bağımlı değişkenler, madde kullanımının nasıl arttığını, ödül eşiklerinin nasıl değiştiğini ve nüksetmenin neden meydana geldiğini göstermede kullanılır. Bu yöntemler güçlü prediktif geçerlilik gösterir ve yeni farmakolojik müdahaleleri test etmek için deney ortamı sağlar.
Genel olarak, hayvan modelleri psikiyatrik hastalıkların altında yatan nörobiyolojik ve davranışsal mekanizmalara ışık tutmada yeri doldurulamaz bir alan sunar. Bu modeller geçerliliklerinin kısmi olmasına rağmen; hastalık etyolojisini araştırmak, terapötik hedefleri belirlemek ve klinik araştırmalara rehberlik etmek için elimizdeki iyi birer yöntemdirler. Model tasarımlarını iyileştirerek ve genetik ve çevresel faktörleri entegre ederek; gelecekteki çalışmalar bu modellerin karmaşık psikiyatrik durumlara uygulanabilme gücünü artıracaktır.

Keywords

psikiyatride hayvan modelleri bağımlılık modelleri şizofreni modelleri depresyon modelleri

References

  • Krishnan V, Nestler EJ. Animal models of depression: molecular perspectives. Molecular and functional models in neuropsychiatry. 2011:121-47.
  • Belin D, Belin‐Rauscent A, Everitt BJ, Dalley JW. In search of predictive endophenotypes in addiction: insights from preclinical research. Genes, Brain and Behavior. 2016;15(1):74-88.
  • Nestler EJ, Hyman SE. Animal models of neuropsychiatric disorders. Nature neuroscience. 2010;13(10):1161-9.
  • Willner P, Mitchell P. The validity of animal models of predisposition to depression. Behavioural pharmacology. 2002;13(3):169-88.
  • Willner P. The chronic mild stress (CMS) model of depression: History, evaluation and usage. Neurobiology of stress. 2017;6:78-93.
  • Koob GF. Animal models of drug dependence: motivational perspective. Addiction Medicine: Science and Practice. 2011:333-57.
  • Koob GF. Addiction is a reward deficit and stress surfeit disorder. Frontiers in psychiatry. 2013;4:72.
  • Koob GF, Zimmer A. Animal models of psychiatric disorders. Handbook of clinical neurology. 2012;106:137-66.
  • Geller I, Seifter J. The effects of meprobamate, barbiturates, d-amphetamine and promazine on experimentally induced conflict in the rat. Psychopharmacologia. 1960;1:482-92.
  • Vogel JR, Beer B, Clody DE. A simple and reliable conflict procedure for testing anti-anxiety agents. Psychopharmacologia. 1971;21:1-7.
  • Walf AA, Frye CA. The use of the elevated plus maze as an assay of anxiety-related behavior in rodents. Nature protocols. 2007;2(2):322-8.
  • Basso AM, Spina M, Rivier J, Vale W, Koob GF. Corticotropin-releasing factor antagonist attenuates the “anxiogenic-like” effect in the defensive burying paradigm but not in the elevated plus-maze following chronic cocaine in rats. Psychopharmacology. 1999;145(1):21-30. doi: 10.1007/s002130051028.
  • De Boer SF, Koolhaas JM. Defensive burying in rodents: ethology, neurobiology and psychopharmacology. European Journal of Pharmacology. 2003;463(1):145-61. doi: https://doi.org/10.1016/S0014-2999(03)01278-0.
  • Dyakonova VE, Schürmann FW, Sakharov DA. Effects of Serotonergic and Opioidergic Drugs on Escape Behaviors and Social Status of Male Crickets. Naturwissenschaften. 1999;86(9):435-7. doi: 10.1007/s001140050647.
  • Schöner J, Heinz A, Endres M, Gertz K, Kronenberg G. Post‐traumatic stress disorder and beyond: an overview of rodent stress models. Journal of cellular and molecular medicine. 2017;21(10):2248-56.
  • Korte SM, De Boer SF. A robust animal model of state anxiety: fear-potentiated behaviour in the elevated plus-maze. European journal of pharmacology. 2003;463(1-3):163-75.
  • American Psychiatric Association D, American Psychiatric Association D. Diagnostic and statistical manual of mental disorders: DSM-5: American psychiatric association Washington, DC; 2013.
  • Bell CC. DSM-IV: Diagnostic and Statistical Manual of Mental Disorders. JAMA. 1994;272(10):828-9. doi: 10.1001/jama.1994.03520100096046.
  • Valle R. Schizophrenia in ICD-11: Comparison of ICD-10 and DSM-5. Revista de Psiquiatría y Salud Mental (English Edition). 2020;13(2):95-104. doi: https://doi.org/10.1016/j.rpsmen.2020.01.002.
  • Morgan C, Fisher H. Environment and Schizophrenia: Environmental Factors in Schizophrenia: Childhood Trauma—A Critical Review. Schizophrenia Bulletin. 2006;33(1):3-10. doi: 10.1093/schbul/sbl053.
  • Białoń M, Wąsik A. Advantages and Limitations of Animal Schizophrenia Models. International Journal of Molecular Sciences. 2022;23(11):5968. PubMed PMID: doi:10.3390/ijms23115968.
  • Bitsios P, Giakoumaki SG, Frangou S. The effects of dopamine agonists on prepulse inhibition in healthy men depend on baseline PPI values. Psychopharmacology. 2005;182(1):144-52. doi: 10.1007/s00213-005-0056-x.
  • Gray NS, Pickering AD, Hemsley DR, Dawling S, Gray JA. Abolition of latent inhibition by a single 5 mg dose ofd-amphetamine in man. Psychopharmacology. 1992;107(2):425-30. doi: 10.1007/BF02245170.
  • Tenn CC, Kapur S, Fletcher PJ. Sensitization to amphetamine, but not phencyclidine, disrupts prepulse inhibition and latent inhibition. Psychopharmacology. 2005;180(2):366-76. doi: 10.1007/s00213-005-2253-z.
  • Grayson B, Idris NF, Neill JC. Atypical antipsychotics attenuate a sub-chronic PCP-induced cognitive deficit in the novel object recognition task in the rat. Behavioural Brain Research. 2007;184(1):31-8. doi: https://doi.org/10.1016/j.bbr.2007.06.012.
  • Lipska BK, Aultman JM, Verma A, Weinberger DR, Moghaddam B. Neonatal damage of the ventral hippocampus impairs working memory in the rat. Neuropsychopharmacology. 2002;27(1):47-54.
  • Hikida T, Jaaro-Peled H, Seshadri S, Oishi K, Hookway C, Kong S, et al. Dominant-negative DISC1 transgenic mice display schizophrenia-associated phenotypes detected by measures translatable to humans. Proceedings of the National Academy of Sciences. 2007;104(36):14501-6. doi: doi:10.1073/pnas.0704774104.
  • van den Buuse M. Modeling the Positive Symptoms of Schizophrenia in Genetically Modified Mice: Pharmacology and Methodology Aspects. Schizophrenia Bulletin. 2009;36(2):246-70. doi: 10.1093/schbul/sbp132.
  • Kundakovic M, Jaric I. The Epigenetic Link between Prenatal Adverse Environments and Neurodevelopmental Disorders. Genes. 2017;8(3):104. PubMed PMID: doi:10.3390/genes8030104.
  • Borrell J, Vela JM, Arévalo-Martin A, Molina-Holgado E, Guaza C. Prenatal Immune Challenge Disrupts Sensorimotor Gating in Adult Rats: Implications for the Etiopathogenesis of Schizophrenia. Neuropsychopharmacology. 2002;26(2):204-15. doi: 10.1016/S0893-133X(01)00360-8.
  • Deroche-Gamonet V, Belin D, Piazza PV. Evidence for addiction-like behavior in the rat. Science. 2004;305(5686):1014-7.
  • Creswell KG. Drinking together and drinking alone: A social-contextual framework for examining risk for alcohol use disorder. Current Directions in Psychological Science. 2021;30(1):19-25.
  • Hodebourg R. Intracranial Self-Stimulation: Using the Curve-Shift Paradigm to Assess the Abuse Potential of Drugs. In: Fakhoury M, editor. The Brain Reward System. New York, NY: Springer US; 2021. p. 199-208.
  • Tzschentke TM. Review on CPP: Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade. Addiction biology. 2007;12(3‐4):227-462.
  • Koob GF, Bloom F, Kupfer D. Animal models of drug addiction. Psychopharmacology: The fourth generation in progress/Bloom FE, Kupfer DJ—1995—345 p. 2012.
  • Becker HC, Lopez MF. Animal models of excessive alcohol consumption in rodents. 2024.
  • Murphy JM, Stewart RB, Bell RL, Badia-Elder NE, Carr LG, McBride WJ, et al. Phenotypic and Genotypic Characterization of the Indiana University Rat Lines Selectively Bred for High and Low Alcohol Preference. Behavior Genetics. 2002;32(5):363-88. doi: 10.1023/A:1020266306135.
  • Koob GF, Volkow ND. Neurocircuitry of addiction. Neuropsychopharmacology. 2010;35(1):217-38.
  • Koob G, Kreek MJ. Stress, dysregulation of drug reward pathways, and the transition to drug dependence. Am J Psychiatry. 2007;164(8):1149-59. Epub 2007/08/03. doi: 10.1176/appi.ajp.2007.05030503. PubMed PMID: 17671276; PubMed Central PMCID: PMCPMC2837343.
  • Koob GF. The neurobiology of addiction: a neuroadaptational view relevant for diagnosis. Addiction. 2006;101:23-30.
  • Bossert JM, Marchant NJ, Calu DJ, Shaham Y. The reinstatement model of drug relapse: recent neurobiological findings, emerging research topics, and translational research. Psychopharmacology. 2013;229(3):453-76. doi: 10.1007/s00213-013-3120-y.
  • Namba MD, Tomek SE, Olive MF, Beckmann JS, Gipson CD. The winding road to relapse: forging a new understanding of cue-induced reinstatement models and their associated neural mechanisms. Frontiers in behavioral neuroscience. 2018;12:17.
  • Shaham Y, Stewart J. Stress reinstates heroin-seeking in drug-free animals: An effect mimicking heroin, not withdrawal. Psychopharmacology. 1995;119(3):334-41. doi: 10.1007/BF02246300.
  • Barrus MM, Cherkasova M, Winstanley CA. Skewed by Cues? The Motivational Role of Audiovisual Stimuli in Modelling Substance Use and Gambling Disorders. In: Simpson EH, Balsam PD, editors. Behavioral Neuroscience of Motivation. Cham: Springer International Publishing; 2016. p. 507-29.
  • Ozdemir D, Allain F, Kieffer BL, Darcq E. Advances in the characterization of negative affect caused by acute and protracted opioid withdrawal using animal models. Neuropharmacology. 2023;232:109524. doi: https://doi.org/10.1016/j.neuropharm.2023.109524.

Animal Experimental Models Used In The Study Of Psychiatric Diseases

Year 2025, Volume: 14 Issue: 1, 37 - 51, 30.04.2025

Onur Koçhan

https://doi.org/10.47493/abantmedj.1610414

Abstract

Animal experimental models used for modelling psychiatric diseases and treatments are an indispensable tool. But it is impossible to construct a single animal model which demonstrates every aspect of a psychiatric disease. Thus partial models are preferred. The validity of models are examined for construct, face and prediction dimensions. This evaluation is used together with the similarity with human disease and is of vital importance in terms of obtaining findings that will contribute to clinical applications.
Learned helplessness, forced swim tests and tail suspension test are traditional tools for modelling depression with good predictive but limited construct validity so research shifted away from them. In depression research, animal models focusing on basic formations such as anhedonia comes to the fore. Chronic mild stress (CMS) protocol is used to create anhedonia and dependent variables like sucrose preference, intracranial self-stimulation reward (ICSS) and progressive ratio reward are used to measure the anhedonia with good face and predictive validity. Anxiety models include high plus maze, operant conflict test and social interaction paradigms best used to determine drugs anxiolytic effects.
Modeling schizophrenia is challenging. Complexity of positive, negative, and cognitive symptoms makes it harder to replicate. Pharmacological manipulations like dopaminergic or glutamatergic agents, brain lesion models, and genetic manupulation techniques have been developed in this area. Prepulse inhibition (PPI), latent inhibition, and working memory tests, while not fully valid, provide results similar to humans.
Addiction research utilizes animal models that reflect the stages of binge/intoxication, withdrawal, and craving. Dependent variables such as intracranial self-stimulation threshold (ICSS) measurements, conditioned place preference (CPP), and stress-induced reinstatement are used to demonstrate how substance use escalates, how reward thresholds change, and why relapse occurs. These methods demonstrate strong predictive validity and provide experimental settings for testing new pharmacological interventions.
In general, animal models provide an irreplaceable opportunity for investigating the neurobiological and behavioral mechanisms for psychiatric illness. Despite their partial validity, these models are indispensable for investigating etiology, identifying therapeutic targets, and guiding clinical research. Future studies with improved model designs and incorporated genetic and enviromental factors will increase the applicability to complex psychiatric conditions.

Keywords

Animal models psychiatry schizophrenia models depression models addiction animal models

References

  • Krishnan V, Nestler EJ. Animal models of depression: molecular perspectives. Molecular and functional models in neuropsychiatry. 2011:121-47.
  • Belin D, Belin‐Rauscent A, Everitt BJ, Dalley JW. In search of predictive endophenotypes in addiction: insights from preclinical research. Genes, Brain and Behavior. 2016;15(1):74-88.
  • Nestler EJ, Hyman SE. Animal models of neuropsychiatric disorders. Nature neuroscience. 2010;13(10):1161-9.
  • Willner P, Mitchell P. The validity of animal models of predisposition to depression. Behavioural pharmacology. 2002;13(3):169-88.
  • Willner P. The chronic mild stress (CMS) model of depression: History, evaluation and usage. Neurobiology of stress. 2017;6:78-93.
  • Koob GF. Animal models of drug dependence: motivational perspective. Addiction Medicine: Science and Practice. 2011:333-57.
  • Koob GF. Addiction is a reward deficit and stress surfeit disorder. Frontiers in psychiatry. 2013;4:72.
  • Koob GF, Zimmer A. Animal models of psychiatric disorders. Handbook of clinical neurology. 2012;106:137-66.
  • Geller I, Seifter J. The effects of meprobamate, barbiturates, d-amphetamine and promazine on experimentally induced conflict in the rat. Psychopharmacologia. 1960;1:482-92.
  • Vogel JR, Beer B, Clody DE. A simple and reliable conflict procedure for testing anti-anxiety agents. Psychopharmacologia. 1971;21:1-7.
  • Walf AA, Frye CA. The use of the elevated plus maze as an assay of anxiety-related behavior in rodents. Nature protocols. 2007;2(2):322-8.
  • Basso AM, Spina M, Rivier J, Vale W, Koob GF. Corticotropin-releasing factor antagonist attenuates the “anxiogenic-like” effect in the defensive burying paradigm but not in the elevated plus-maze following chronic cocaine in rats. Psychopharmacology. 1999;145(1):21-30. doi: 10.1007/s002130051028.
  • De Boer SF, Koolhaas JM. Defensive burying in rodents: ethology, neurobiology and psychopharmacology. European Journal of Pharmacology. 2003;463(1):145-61. doi: https://doi.org/10.1016/S0014-2999(03)01278-0.
  • Dyakonova VE, Schürmann FW, Sakharov DA. Effects of Serotonergic and Opioidergic Drugs on Escape Behaviors and Social Status of Male Crickets. Naturwissenschaften. 1999;86(9):435-7. doi: 10.1007/s001140050647.
  • Schöner J, Heinz A, Endres M, Gertz K, Kronenberg G. Post‐traumatic stress disorder and beyond: an overview of rodent stress models. Journal of cellular and molecular medicine. 2017;21(10):2248-56.
  • Korte SM, De Boer SF. A robust animal model of state anxiety: fear-potentiated behaviour in the elevated plus-maze. European journal of pharmacology. 2003;463(1-3):163-75.
  • American Psychiatric Association D, American Psychiatric Association D. Diagnostic and statistical manual of mental disorders: DSM-5: American psychiatric association Washington, DC; 2013.
  • Bell CC. DSM-IV: Diagnostic and Statistical Manual of Mental Disorders. JAMA. 1994;272(10):828-9. doi: 10.1001/jama.1994.03520100096046.
  • Valle R. Schizophrenia in ICD-11: Comparison of ICD-10 and DSM-5. Revista de Psiquiatría y Salud Mental (English Edition). 2020;13(2):95-104. doi: https://doi.org/10.1016/j.rpsmen.2020.01.002.
  • Morgan C, Fisher H. Environment and Schizophrenia: Environmental Factors in Schizophrenia: Childhood Trauma—A Critical Review. Schizophrenia Bulletin. 2006;33(1):3-10. doi: 10.1093/schbul/sbl053.
  • Białoń M, Wąsik A. Advantages and Limitations of Animal Schizophrenia Models. International Journal of Molecular Sciences. 2022;23(11):5968. PubMed PMID: doi:10.3390/ijms23115968.
  • Bitsios P, Giakoumaki SG, Frangou S. The effects of dopamine agonists on prepulse inhibition in healthy men depend on baseline PPI values. Psychopharmacology. 2005;182(1):144-52. doi: 10.1007/s00213-005-0056-x.
  • Gray NS, Pickering AD, Hemsley DR, Dawling S, Gray JA. Abolition of latent inhibition by a single 5 mg dose ofd-amphetamine in man. Psychopharmacology. 1992;107(2):425-30. doi: 10.1007/BF02245170.
  • Tenn CC, Kapur S, Fletcher PJ. Sensitization to amphetamine, but not phencyclidine, disrupts prepulse inhibition and latent inhibition. Psychopharmacology. 2005;180(2):366-76. doi: 10.1007/s00213-005-2253-z.
  • Grayson B, Idris NF, Neill JC. Atypical antipsychotics attenuate a sub-chronic PCP-induced cognitive deficit in the novel object recognition task in the rat. Behavioural Brain Research. 2007;184(1):31-8. doi: https://doi.org/10.1016/j.bbr.2007.06.012.
  • Lipska BK, Aultman JM, Verma A, Weinberger DR, Moghaddam B. Neonatal damage of the ventral hippocampus impairs working memory in the rat. Neuropsychopharmacology. 2002;27(1):47-54.
  • Hikida T, Jaaro-Peled H, Seshadri S, Oishi K, Hookway C, Kong S, et al. Dominant-negative DISC1 transgenic mice display schizophrenia-associated phenotypes detected by measures translatable to humans. Proceedings of the National Academy of Sciences. 2007;104(36):14501-6. doi: doi:10.1073/pnas.0704774104.
  • van den Buuse M. Modeling the Positive Symptoms of Schizophrenia in Genetically Modified Mice: Pharmacology and Methodology Aspects. Schizophrenia Bulletin. 2009;36(2):246-70. doi: 10.1093/schbul/sbp132.
  • Kundakovic M, Jaric I. The Epigenetic Link between Prenatal Adverse Environments and Neurodevelopmental Disorders. Genes. 2017;8(3):104. PubMed PMID: doi:10.3390/genes8030104.
  • Borrell J, Vela JM, Arévalo-Martin A, Molina-Holgado E, Guaza C. Prenatal Immune Challenge Disrupts Sensorimotor Gating in Adult Rats: Implications for the Etiopathogenesis of Schizophrenia. Neuropsychopharmacology. 2002;26(2):204-15. doi: 10.1016/S0893-133X(01)00360-8.
  • Deroche-Gamonet V, Belin D, Piazza PV. Evidence for addiction-like behavior in the rat. Science. 2004;305(5686):1014-7.
  • Creswell KG. Drinking together and drinking alone: A social-contextual framework for examining risk for alcohol use disorder. Current Directions in Psychological Science. 2021;30(1):19-25.
  • Hodebourg R. Intracranial Self-Stimulation: Using the Curve-Shift Paradigm to Assess the Abuse Potential of Drugs. In: Fakhoury M, editor. The Brain Reward System. New York, NY: Springer US; 2021. p. 199-208.
  • Tzschentke TM. Review on CPP: Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade. Addiction biology. 2007;12(3‐4):227-462.
  • Koob GF, Bloom F, Kupfer D. Animal models of drug addiction. Psychopharmacology: The fourth generation in progress/Bloom FE, Kupfer DJ—1995—345 p. 2012.
  • Becker HC, Lopez MF. Animal models of excessive alcohol consumption in rodents. 2024.
  • Murphy JM, Stewart RB, Bell RL, Badia-Elder NE, Carr LG, McBride WJ, et al. Phenotypic and Genotypic Characterization of the Indiana University Rat Lines Selectively Bred for High and Low Alcohol Preference. Behavior Genetics. 2002;32(5):363-88. doi: 10.1023/A:1020266306135.
  • Koob GF, Volkow ND. Neurocircuitry of addiction. Neuropsychopharmacology. 2010;35(1):217-38.
  • Koob G, Kreek MJ. Stress, dysregulation of drug reward pathways, and the transition to drug dependence. Am J Psychiatry. 2007;164(8):1149-59. Epub 2007/08/03. doi: 10.1176/appi.ajp.2007.05030503. PubMed PMID: 17671276; PubMed Central PMCID: PMCPMC2837343.
  • Koob GF. The neurobiology of addiction: a neuroadaptational view relevant for diagnosis. Addiction. 2006;101:23-30.
  • Bossert JM, Marchant NJ, Calu DJ, Shaham Y. The reinstatement model of drug relapse: recent neurobiological findings, emerging research topics, and translational research. Psychopharmacology. 2013;229(3):453-76. doi: 10.1007/s00213-013-3120-y.
  • Namba MD, Tomek SE, Olive MF, Beckmann JS, Gipson CD. The winding road to relapse: forging a new understanding of cue-induced reinstatement models and their associated neural mechanisms. Frontiers in behavioral neuroscience. 2018;12:17.
  • Shaham Y, Stewart J. Stress reinstates heroin-seeking in drug-free animals: An effect mimicking heroin, not withdrawal. Psychopharmacology. 1995;119(3):334-41. doi: 10.1007/BF02246300.
  • Barrus MM, Cherkasova M, Winstanley CA. Skewed by Cues? The Motivational Role of Audiovisual Stimuli in Modelling Substance Use and Gambling Disorders. In: Simpson EH, Balsam PD, editors. Behavioral Neuroscience of Motivation. Cham: Springer International Publishing; 2016. p. 507-29.
  • Ozdemir D, Allain F, Kieffer BL, Darcq E. Advances in the characterization of negative affect caused by acute and protracted opioid withdrawal using animal models. Neuropharmacology. 2023;232:109524. doi: https://doi.org/10.1016/j.neuropharm.2023.109524.
There are 45 citations in total.

Details

Primary Language English
Subjects Psychiatry
Journal Section Review
Authors

Onur Koçhan 0000-0003-3072-0853

Early Pub Date April 29, 2025
Publication Date April 30, 2025
Submission Date December 31, 2024
Acceptance Date March 24, 2025
Published in Issue Year 2025 Volume: 14 Issue: 1

Cite

APA Koçhan, O. (2025). Animal Experimental Models Used In The Study Of Psychiatric Diseases. Abant Medical Journal, 14(1), 37-51. https://doi.org/10.47493/abantmedj.1610414
AMA Koçhan O. Animal Experimental Models Used In The Study Of Psychiatric Diseases. Abant Med J. April 2025;14(1):37-51. doi:10.47493/abantmedj.1610414
Chicago Koçhan, Onur. “Animal Experimental Models Used In The Study Of Psychiatric Diseases”. Abant Medical Journal 14, no. 1 (April 2025): 37-51. https://doi.org/10.47493/abantmedj.1610414.
EndNote Koçhan O (April 1, 2025) Animal Experimental Models Used In The Study Of Psychiatric Diseases. Abant Medical Journal 14 1 37–51.
IEEE O. Koçhan, “Animal Experimental Models Used In The Study Of Psychiatric Diseases”, Abant Med J, vol. 14, no. 1, pp. 37–51, 2025, doi: 10.47493/abantmedj.1610414.
ISNAD Koçhan, Onur. “Animal Experimental Models Used In The Study Of Psychiatric Diseases”. Abant Medical Journal 14/1 (April 2025), 37-51. https://doi.org/10.47493/abantmedj.1610414.
JAMA Koçhan O. Animal Experimental Models Used In The Study Of Psychiatric Diseases. Abant Med J. 2025;14:37–51.
MLA Koçhan, Onur. “Animal Experimental Models Used In The Study Of Psychiatric Diseases”. Abant Medical Journal, vol. 14, no. 1, 2025, pp. 37-51, doi:10.47493/abantmedj.1610414.
Vancouver Koçhan O. Animal Experimental Models Used In The Study Of Psychiatric Diseases. Abant Med J. 2025;14(1):37-51.
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