Lack of protection from ischemic injury of monoamine oxidase B-deficient mice following middle cerebral artery occlusion

Holschneider, Daniel P.; Scremin, Oscar U.; Huynh, Ly; Chen, K.; Shih, Jean C.

doi:10.1016/s0304-3940(98)00819-2

Cited by 18 publications

(9 citation statements)

References 18 publications

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“…These results demonstrate pronounced activation of deamination due to increased monoamine activity in patients with IS. Similar results were obtained in experimental studies on various models of IS [7,[9][10][11]. The levels of dopamine and serotonin deamination products are shown to increase greatly in the postischemic period during brain reperfusion.…”

Section: Resultssupporting

confidence: 82%

“…Monoamine oxidase (MAO) as a key enzyme inactivating serotonin and dopamine via oxidative deamination determining the functional status of monoaminergic systems [2][3][4][5]10,11]. Pronounced activation of serotonin and dopamine oxidative deamination by MAO was revealed in different brain structures during postischemic (acute) stage of the experimental IS [7,10,12]. Change in MAO activity is probably a pathogenetic factor affecting neuroplasticity during IS, but we found no clinical trials on this issue.…”

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confidence: 99%

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Change in platelet monoamine oxidase activity in the acutest period of ischemic stroke is associated with the degree of neurological recovery

et al. 2011

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We studied monoamine oxidase activity (MAO) in platelets of patients in the acute period of ischemic stroke. Neurological deficit was evaluated by the data of clinical examinations and scales. In 80% patients MAO activity was considerably increased on 3-5 day after stroke. We found a correlation between increased MAO activity on 3-5 day after ischemic stroke and regression of neurological deficit on day 21 after ischemic stroke. The increase in MAO activity during the acute period of ischemic stroke is presumably a compensatory response aimed at stabilization of tissue homeostasis.

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Section: Resultssupporting

confidence: 82%

mentioning

confidence: 99%

Change in platelet monoamine oxidase activity in the acutest period of ischemic stroke is associated with the degree of neurological recovery

et al. 2011

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“…The mechanism underlying the role of MAO-B in 5-HT depletion has, however, not been clarified, whereas MDMA is a potent MAO-A inhibitor. Specific binding of [ 3 H-methyl]-L-deprenyl to brain tissue was abolished by MAO-B knockout mice (Ekblom et al 1998), as was the protection afforded by selegiline in ischemic infarction, cerebral edema and neurological impairment (Holschneider et al 1999). To elucidate the role of MAO isoenzymes in neuronal death, however, these results must be further explored in MAO-A knockout animals exposed to other neurological and neurotoxic insults.…”

Section: The Role Of Mao-a and Mao-b In Neuronal Lossmentioning

confidence: 99%

Modulation of monoamine oxidase (MAO) expression in neuropsychiatric disorders: genetic and environmental factors involved in type A MAO expression

2015

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Monoamine oxidase types A and B (MAO-A, MAO-B) regulate the levels of monoamine neurotransmitters in the brain, and their dysfunction may be involved in the pathogenesis and influence the clinical phenotypes of neuropsychiatric disorders. Reversible MAO-A inhibitors, such as moclobemide and befloxatone, are currently employed in the treatment of emotional disorders by inhibiting the enzymatic degradation of dopamine, serotonin and norepinephrine in the central nervous system (CNS). It has been suggested that the irreversible MAO-B inhibitors selegiline and rasagiline exert a neuroprotective effect in Parkinson's and Alzheimer's diseases. This effect, however, is not related to their inhibition of MAO activity; in animal and cellular models, selegiline and rasagiline protect neuronal cells through their anti-apoptotic activity and induction of pro-survival genes. There is increasing evidence that MAO-A activity, but not that of MAO-B, is implicated in the pathophysiology of neurodegenerative disorders, but also in gene induction by MAO-B inhibitors; on the other hand, selegiline and rasagiline increase MAO-A mRNA, protein, and enzyme activity levels. Taken together, these results suggest that each MAO subtype exerts effects that modulate the expression and activity of the other isoenzyme. The roles of MAO-A and -B in the CNS should therefore be re-evaluated with respect to the "type-specificity" of their inhibitors, which may not be unconditional during chronic treatment. Mao-a expression, in particular, may be implicated in pathogenesis and phenotypes in neuropsychiatric disorders. MAO-A expression is modified by mao polymorphisms affecting its transcriptional efficiency, as well as by mutations and polymorphism of parkin, Sirt1, FOXO, microRNA, presenilin-1, and other regulatory proteins. In addition, childhood maltreatment has been shown to have an impact upon adolescent social behavior in children with mao-a polymorphisms of low transcriptional activity. Low MAO-A activity may increase the levels of serotonin and norepinephrine, resulting in disturbed neurotransmitter system development and behavior. This review discusses genetic and environmental factors involved in the regulation of MAO-A expression, in the contexts of neuropsychiatric function and of the regulation of neuronal survival and death.

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“…Inhibition of MAO B by L-deprenyl decreases the production of H 2 O 2 [59], and it has been hypothesized that this may attenuate neuronal damage by H 2 O 2 or the highly toxic hydroxyl radical which can be formed from H 2 O 2 by iron-mediated Fenton reactions. To examine the role of MAO B in cerebral ischemia, we subjected MAO B KO and wild-type mice to unilateral middle cerebral artery occlusion [30]. No significant genotypic differences were detected in infarct volume or in the extent of brain edema.…”

Section: Physiological Changesmentioning

confidence: 99%

“…No increase in aggressive behavior [27] Normal visual-spatial learning in adult and in aged animals in the Morris Water Maze [28] Intact working memory as tested in a Y-maze [27] Increased mobility in the Porsolt Forced Swim Test [27] Normal response in the Elevated Plus-Maze [27] Normal exploratory activity in the Open Field [27] Physiologic Decreased blood pressure and heart rate in the resting, restrained state [72] Exaggerated hypertensive response to PEA [72] Regional cerebral cortical blood flow: Higher in midline motor cortex and medial portions of somatosensory and visual cortex; lower in piriform and anterolateral frontal cortex [72] No difference from wild-type mice in infarct volume or extent of brain edema following middle cerebral artery occlusion [30] Lack of MPTP toxicity in brain [27] Normal body weight [30,72] * Includes data from unpublished observations.…”

Section: Adultmentioning

confidence: 99%

Biochemical, behavioral, physiologic, and neurodevelopmental changes in mice deficient in monoamine oxidase A or B

Holschneider

Chen²,

Seif

et al. 2001

Brain Research Bulletin

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The availability of mutant mice that lack either MAO A or MAO B has created unique profiles in the central and peripheral availability of serotonin, norepinephrine, dopamine, and phenylethylamine. This paper summarizes some of the current known phenotypic findings in MAO A knock-out mice and contrast these with those of MAO B knock-out mice. Differences are discussed in relation to the biochemical, behavioral, and physiologic changes investigated to date, as well as the role played by redundancy mechanisms, adaptational responses, and alterations in neurodevelopment.

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Lack of protection from ischemic injury of monoamine oxidase B-deficient mice following middle cerebral artery occlusion

Cited by 18 publications

References 18 publications

Change in platelet monoamine oxidase activity in the acutest period of ischemic stroke is associated with the degree of neurological recovery

Change in platelet monoamine oxidase activity in the acutest period of ischemic stroke is associated with the degree of neurological recovery

Modulation of monoamine oxidase (MAO) expression in neuropsychiatric disorders: genetic and environmental factors involved in type A MAO expression

Biochemical, behavioral, physiologic, and neurodevelopmental changes in mice deficient in monoamine oxidase A or B

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