Transitory Decrease in Platelet Monoamine-Oxidase Activity During Migraine Attacks

Glover, Vivette; Sandler, M.; Grant, Ellen C. G.; Fc, Rose; Orton, David; Wilkinson, Marcia; Stevens, D.

doi:10.1016/s0140-6736(77)92604-6

Cited by 70 publications

(34 citation statements)

References 22 publications

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“…Nor were we able to demonstrate any connection between activity and drug administration, confirming our earlier study. 13 A recurring problem with studies of platelet MAO activity in both migraine19 and other diseases such as schizophrenia is an apparent lack of reproducibility.20 Although a reduction in platelet MAO activity in migraine patients outside an attack has been recorded in some studies, others, including our previous one,13 have failed to confirm it. A likely explanation for this is biochemical heterogeneity.…”

Section: Discussionmentioning

confidence: 94%

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Platelet monoamine oxidase activity and headache.

Glover¹,

Peatfield²,

Zammit-Pace³

et al. 1981

Journal of Neurology, Neurosurgery & Psychiatry

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Section: Discussionmentioning

confidence: 94%

“…First there can be transient changes during a migraine attack as noted in our previous study. 13 Secondly, there may be some individuals with permanently low MAO activity. Some publications have noted a significant reduction in mean platelet MAO activity in headachefree migraine patients" 12 but others have failed to confirm this finding.1314…”

mentioning

confidence: 99%

Platelet monoamine oxidase activity and headache.

Glover¹,

Peatfield²,

Zammit-Pace³

et al. 1981

Journal of Neurology, Neurosurgery & Psychiatry

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“…In theory, lower levels of MAOB in the peripheral circulation should result in a higher fraction of PEA that reaches cerebral vessels. Several investigators have reported a 20-40% decrease in platelet MAOB activity in subjects with migraine headaches [3,4,22,41,44,49], as well as decreases in MAOB activity during the course of an acute episode [16,44]. Such findings, however, remain controversial with some authors reporting decreases only in a subpopulation of migraine patients [15], and others reporting 'increases' [9] or 'no change' [35,46].…”

Section: Discussionmentioning

confidence: 99%

Cerebral cortical blood flow maps are reorganized in MAOB-deficient mice

Scremin

Holschneider

Chen³

et al. 1999

Brain Research

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Cerebral cortical blood flow (CBF) was measured autoradiographically in conscious mice without the monoamine oxidase B (MAOB) gene (KO, n = 11) and the corresponding wild-type animals (WILD, n = 11). Subgroups of animals of each genotype received a continuous intravenous infusion over 30 min of phenylethylamine (PEA), an endogenous substrate of MAOB, (8 nmol g −1 min −1 in normal saline at a volume rate of 0.11 μl g −1 min −1 ) or saline at the same volume rate. Maps of relative CBF distribution showed predominance of midline motor and sensory area CBF in KO mice over WILD mice that received saline. PEA enhanced CBF in lateral frontal and piriform cortex in both KO and WILD mice. These changes may reflect a differential activation due to chronic and acute PEA elevations on motor and olfactory function, as well as on the anxiogenic effects of this amine. In addition to its effects on regional CBF distribution, PEA decreased CBF globally in KO mice (range −31% to −41% decrease from control levels) with a lesser effect in WILD mice. It is concluded that MAOB may normally regulate CBF distribution and its response to blood PEA.

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“…Alterations in the activity of this intraneuronal enzyme can affect free intracellular amine levels and uptake from the intrasynaptic cleft (Hughes, 1972). Platelet monoamine oxidase activity may be altered in diseases affecting the central nervous system, for example, Parkinson's disease (Zeller et al, 1976), migraine (Sicuteri et al, 1972;Glover et al, 1977a) affective disorders (Murphy and Weiss, 1972;Landowski et al, 1975), and schizophrenia (Wyatt and Murphy, 1976). These conditions have amine disorders as a common suggested feature.…”

mentioning

confidence: 99%