Altered behavior and alcohol tolerance in transgenic mice lacking MAO A: a comparison with effects of MAO A inhibitor clorgyline

Попова, Н. К.; Vishnivetskaya, G. B.; Ivanova, Elena; Skrinskaya, Julia A.; Seif, Isabelle

doi:10.1016/s0091-3057(00)00417-2

Cited by 49 publications

(26 citation statements)

References 25 publications

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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

249

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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Section: Serotonin Degradationmentioning

confidence: 99%

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

Holmes

2008

Neuroscience & Biobehavioral Reviews

249

166

View full text Add to dashboard Cite

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“…Meanwhile, antidepressants have been used in treatment of alcohol addiction, and antidepressants and MAO inhibitors have been used in chronic pain management. It has also been noted that MAO inhibitors increase tolerance to alcohol in mice (Popova et al, 2000), and that tobacco smoke exposure increases alcohol consumption in adolescent C56BL/6 mice (Burns and Proctor, 2013). Acetaldehyde is produced in high concentrations when cigarettes are burned.…”

Section: Nicotinementioning

confidence: 99%

Mechanisms of Action and Persistent Neuroplasticity by Drugs of Abuse

Korpi¹,

Hollander²,

Farooq

et al. 2015

Pharmacological Reviews

130

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“…There is reduction in neuronal reuptake of noradrenaline and lower levels of monoamine oxidase A (MAO A ) in type 2 diabetes mellitus resulting in increased central sympathetic outflow (Straznicky et al, 2012) in tandem with decrease in ethanol-induced sleep in transgenic mice lacking MAO A (Popova et al, 2000). Cerebro-spinal fluid norepinephrine metabolite (3-methoxy-4-hydroxyphenylglycol (MHPG) is elevated in mania patients compared to the dopamine metabolite, homovanillic acid (HVA) or the serotonin metabolite, 5-hydroxyindoleacetic acid (HIAA) implying an excessive, abnormal noradrenergic activity in mania (Swan et al, 1983).…”

Section: Noradrenergic Mechanisms In Insulin Resistance Substance Usmentioning

confidence: 99%

Type 2 diabetes mellitus, drug addiction, bipolar disorder and epilepsy display overlapping aetiopathogenic mechanisms: Implication for prevention and pharmacotherapy

Oriaifo¹

2015

J. Med. Med. Sci

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The prevalence of diabetes and co-morbid diseases, especially in developing countries, may have already exceeded estimates. Accumulating reports indicate considerable underpinnings in the mechanisms of the aetiopathogenesis of metabolic syndrome, bipolar disorder, epilepsy and, recently, substance addiction. Continuing evidence incriminates dysfunction in genetic, mitochondrial and inflammatory cascade mechanisms as contributory factors to the dysregulation of neurotrophic, serotonergic, dopaminergic, adrenergic, glutamatergic, GABAergic and autophagic pathways. There may also be co-incident dysregulation of the global anti-oxidant network, the endogenous digitalis system, the vasopressin signalling and the hypothalamo-pituitary-adrenal axis. Nuclear factor-kappa B (NF-kappa B) signaling and reactive oxygen species lead to activation of the mammalian target of rapamycin complex I (mTORCI) and this process may be central to the aetiopathogenesis of drug addiction, obesity, foetal programming, diabetes mellitus, epilepsy and bipolar disorder. Antiglycaemics such as cannabinoid CB2 agonists, metformin, artesunate and valproate; insulin-mimetics such as glucagon-like peptide-I (GLP-I) and its analogues; phytomedicines from garlic and curcumin are now shown to exhibit neuroprotective effects. These agents which may down-regulate inflammatory cytokines, upregulate endothelial nitric oxide (eNOS) and peroxisome proliferator-activated receptor alpha (PPAR-α) signalling, attenuate mitochondrial dysfunction, enhance the actions of glucagon-like peptide-I (GLP-I), inhibit mTOR, NF-kappa B, interleukin-I β and glycogen synthase kinase-3 β stand to be of benefit in these illnesses which demonstrate considerable overlay in their aetopathogenic mechanisms. Underpinnings and bidirectional relationships between the metabolic syndrome and mental health disorders may pave way for common new fronts to drug development in translational cardiovascular psychiatry and neurology.

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Altered behavior and alcohol tolerance in transgenic mice lacking MAO A: a comparison with effects of MAO A inhibitor clorgyline

Cited by 49 publications

References 25 publications

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

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

Mechanisms of Action and Persistent Neuroplasticity by Drugs of Abuse

Type 2 diabetes mellitus, drug addiction, bipolar disorder and epilepsy display overlapping aetiopathogenic mechanisms: Implication for prevention and pharmacotherapy

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