Acquisition and extinction of a conditioned passive avoidance reflex in mice with genetic knockout of monoamine oxidase A

Дубровина, Н. И.; Попова, Н. К.; Gilinskii, M. A.; Tomilenko, R. A.; Seif, Isabelle

doi:10.1007/s11055-006-0022-z

Cited by 14 publications

(11 citation statements)

References 24 publications

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“…In particular, KO mice showed exaggerated defensive and neophobic responses to minor or innocuous stimuli (such as unfamiliar objects in their home cage or a mild footshock) (Kim et al, 1997; Godar et al, 2011); furthermore, they displayed lower response to stressful and threatening contingencies, including predator cues, physical restraint and cold temperature (Popova et al, 2006; Godar et al, 2011; Godar et al, 2015). KO mice were also found to exhibit a marked reduction in other measures of risk assessment and threat appraisal (Popova et al, 2001; Bortolato et al, 2011; Godar et al, 2011), as well as greater retention of aversive memories (Kim et al, 1997; Dubrovina et al, 2006). …”

Section: Maoa Deficiency and Aggressionmentioning

confidence: 99%

The role of monoamine oxidase A in aggression: Current translational developments and future challenges

Godar

Fite

McFarlin

et al. 2016

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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Drawing upon the recent resurgence of biological criminology, several studies have highlighted a critical role for genetic factors in the ontogeny of antisocial and violent conduct. In particular, converging lines of evidence have documented that these maladaptive manifestations of aggression are influenced by monoamine oxidase A (MAOA), the enzyme that catalyzes the degradation of brain serotonin, norepinephrine and dopamine. The interest on the link between MAOA and aggression was originally sparked by Han Brunner’s discovery of a syndrome characterized by marked antisocial behaviors in male carriers of a nonsense mutation of this gene. Subsequent studies showed that MAOA allelic variants associated with low enzyme activity moderate the impact of early-life maltreatment on aggression propensity. In spite of overwhelming evidence pointing to the relationship between MAOA and aggression, the neurobiological substrates of this link remain surprisingly elusive; very little is also known about the interventions that may reduce the severity of pathological aggression in genetically predisposed subjects. Animal models offer a unique experimental tool to investigate these issues; in particular, several lines of transgenic mice harboring total or partial loss-of-function Maoa mutations have been shown to recapitulate numerous psychological and neurofunctional endophenotypes observed in humans. This review summarizes the current knowledge on the link between MAOA and aggression; in particular, we will emphasize how an integrated translational strategy coordinating clinical and preclinical research may prove critical to elucidate important aspects of the pathophysiology of aggression, and identify potential targets for its diagnosis, prevention and treatment.

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Section: Maoa Deficiency and Aggressionmentioning

confidence: 99%

The role of monoamine oxidase A in aggression: Current translational developments and future challenges

Godar

Fite

McFarlin

et al. 2016

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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“…MAO A KO mice also exhibit higher retention of aversive or fear-related memories than WT animals, including freezing response after footshock [54] and retention of condition passive avoidance [55]. …”

Section: Genetic Inactivation Of Mao: Mao Knockout (Ko) Micementioning

confidence: 99%

Monoamine oxidase inactivation: From pathophysiology to therapeutics

Bortolato

Chen

Shih

2008

Advanced Drug Delivery Reviews

528

329

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Monoamine oxidases (MAOs) A and B are mitochondrial bound isoenzymes which catalyze the oxidative deamination of dietary amines and monoamine neurotransmitters, such as serotonin, norepinephrine, dopamine, β-phenylethylamine and other trace amines. The rapid degradation of these molecules ensures the proper functioning of synaptic neurotransmission and is critically important for the regulation of emotional behaviors and other brain functions. The byproducts of MAO-mediated reactions include several chemical species with neurotoxic potential, such as hydrogen peroxide, ammonia and aldehydes. As a consequence, it is widely speculated that prolonged excessive activity of these enzymes may be conducive to mitochondrial damages and neurodegenerative disturbances. In keeping with these premises, the development of MAO inhibitors has led to important breakthroughs in the therapy of several neuropsychiatric disorders, ranging from mood disorders to Parkinson’s disease. Furthermore, the characterization of MAO knockout (KO) mice has revealed that the inactivation of this enzyme produces a number of functional and behavioral alterations, some of which may be harnessed for therapeutic aims. In this article, we discuss the intriguing hypothesis that the attenuation of the oxidative stress induced by the inactivation of either MAO isoform may contribute to both antidepressant and antiparkinsonian actions of MAO inhibitors. This possibility further highlights MAO inactivation as a rich source of novel avenues in the treatment of mental disorders.

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“…Maoa knockout mice have increased ECF serotonin in the PFC and hippocampus and display exaggerated unconditioned and conditioned fear behaviors, as well as increased conspecific aggression (Cases et al, 1995;Dubrovina et al, 2006;Evrard et al, 1999;Kim et al, 1997;Popova et al, 2000). However, these mice also display an attenuated glucocorticoid response to acute and chronic stressors that may relate to the significant reduction in dorsal raphe neuron activity observed in these mice (Evrard et al, 1999).…”

Section: Serotonin Degradationmentioning

confidence: 99%

Genetic variation in cortico-amygdala serotonin function and risk for stress-related disease

Holmes

2008

Neuroscience & Biobehavioral Reviews

243

166

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The serotonin system is strongly implicated in the pathophysiology and therapeutic alleviation of stress-related disorders such as anxiety and depression. Serotonergic modulation of the acute response to stress and the adaptation to chronic stress is mediated by a myriad of molecules controlling serotonin neuron development (Pet-1), synthesis (tryptophan hydroxylase 1 and 2 isozymes), packaging (vesicular monoamine transporter 2), actions at presynaptic and postsynaptic receptors (5-HT1A, 5-HT1B, 5-HT2A, 5-HT2C, 5-HT3A, 5-HT4, 5-HT5A, 5-HT6, 5-HT7), reuptake (serotonin transporter), and degradation (monoamine oxidase A). A growing body of evidence from preclinical rodents models, and especially genetically modified mice and inbred mouse strains, has provided significant insight into how genetic variation in these molecules can affect the development and function of a key neural circuit between the dorsal raphe nucleus, medial prefrontal cortex and amygdala. By extension, such variation is hypothesized to have a major influence on individual differences in the stress response and risk for stress-related disease in humans. The current article provides an update on this rapidly evolving field of research.

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Acquisition and extinction of a conditioned passive avoidance reflex in mice with genetic knockout of monoamine oxidase A

Cited by 14 publications

References 24 publications

The role of monoamine oxidase A in aggression: Current translational developments and future challenges

The role of monoamine oxidase A in aggression: Current translational developments and future challenges

Monoamine oxidase inactivation: From pathophysiology to therapeutics

Genetic variation in cortico-amygdala serotonin function and risk for stress-related disease

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