Brain Laterality as a Source of Individual Differences in Behavior: Animal Models of Depression and Substance Abuse

AbstractUnderstanding the emotional reaction to loss, or frustration, is a critical problem for the field of mental health. Animal models of loss have pointed to the opioid system as a nexus of frustration, physical pain, and substance abuse. However, few attempts have been made to connect the results of animal models of loss to human behavior. Allelic differences in the human mu opioid receptor gene, notably the A118G single nucleotide polymorphism, have been linked to individual differences in pain sensitivity, depressive symptoms, and reward processing. The present study explored the relationship between A118G and behavior in two frustrating tasks in humans. Results showed that carriers of the mutant G-allele were slower to recover behavior following a reward downshift and abandoned a frustrating task earlier than those without the mutation. Additionally, G-carriers were more sensitive to physical pain. These results highlight the overlap between frustration and pain, and suggest that genetic variation in opioid tone may contribute to individual differences in vulnerability and resilience following emotional disturbances.

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Animal models of depression

Comparative Biochemistry and Physiology Part A Physiology ◽

10.1016/0300-9629(90)90708-z ◽

1990 ◽

Vol 96 (2) ◽

pp. 355

Keyword(s):

Animal Models ◽

Animal Models Of Depression

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Elevated Brain Fatty Acid Amide Hydrolase Induces Depressive-Like Phenotypes in Rodent Models: A Review

International Journal of Molecular Sciences ◽

10.3390/ijms22031047 ◽

2021 ◽

Vol 22 (3) ◽

pp. 1047

Author(s):

Dorsa Rafiei ◽

Nathan J. Kolla

Keyword(s):

Depressive Symptoms ◽

Fatty Acid ◽

Animal Models ◽

Fatty Acid Amide Hydrolase ◽

Acid Amide ◽

Endocannabinoid System ◽

Animal Models Of Depression ◽

Amide Hydrolase ◽

Fatty Acid Amide

Altered activity of fatty acid amide hydrolase (FAAH), an enzyme of the endocannabinoid system, has been implicated in several neuropsychiatric disorders, including major depressive disorder (MDD). It is speculated that increased brain FAAH expression is correlated with increased depressive symptoms. The aim of this scoping review was to establish the role of FAAH expression in animal models of depression to determine the translational potential of targeting FAAH in clinical studies. A literature search employing multiple databases was performed; all original articles that assessed FAAH expression in animal models of depression were considered. Of the 216 articles that were screened for eligibility, 24 articles met inclusion criteria and were included in this review. Three key findings emerged: (1) FAAH expression is significantly increased in depressive-like phenotypes; (2) genetic knockout or pharmacological inhibition of FAAH effectively reduces depressive-like behavior, with a dose-dependent effect; and (3) differences in FAAH expression in depressive-like phenotypes were largely localized to animal prefrontal cortex, hippocampus and striatum. We conclude, based on the animal literature, that a positive relationship can be established between brain FAAH level and expression of depressive symptoms. In summary, we suggest that FAAH is a tractable target for developing novel pharmacotherapies for MDD.

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Progesterone after Estradiol Modulates Shuttle-Cage Escape by Facilitating Volition

Journal of Experimental Neuroscience ◽

10.4137/jen.s32735 ◽

2015 ◽

Vol 9s1 ◽

pp. JEN.S32735

Author(s):

Darryl J. Mayeaux ◽

Sarah M. Tandle ◽

Sean M. Cilano ◽

Matthew J. Fitzharris

Keyword(s):

Depressive Symptoms ◽

Animal Models ◽

Electric Shock ◽

Ovarian Hormones ◽

Learning Task ◽

The Other ◽

Female Rats ◽

Animal Models Of Depression ◽

Escape Learning

In animal models of depression, depression is defined as performance on a learning task. That task is typically escaping a mild electric shock in a shuttle cage by moving from one side of the cage to the other. Ovarian hormones influence learning in other kinds of tasks, and these hormones are associated with depressive symptoms in humans. The role of these hormones in shuttle-cage escape learning, however, is less clear. This study manipulated estradiol and progesterone in ovariectomized female rats to examine their performance in shuttle-cage escape learning without intentionally inducing a depressive-like state. Progesterone, not estradiol, within four hours of testing affected latencies to escape. The improvement produced by progesterone was in the decision to act, not in the speed of learning or speed of escaping. This parallels depression in humans in that depressed people are slower in volition, in their decisions to take action.

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