Platelet Serotonin Pathway in Menstrual Migraine

Fioroni, L.; D’Andrea, Giovanni; Alecci, M.; Cananzi, A.R.; Facchinetti, Fabio

doi:10.1046/j.1468-2982.1996.1606427.x

Cited by 33 publications

(21 citation statements)

References 25 publications

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“…Changes in serotonin content were also noticed in women with menstrual migraine, in relation to the cyclic hormonal variations. In these women, platelet serotonin levels peaked in the follicular period and decreased in the luteal phase, when 5HIAA values were particularly increased [16,17]. These data suggest an aberration in menstrual cycle-related changes of serotonin in women migraineurs, possibly due to increased catabolism or reduced synthesis which predisposes these patients to migraine attacks.…”

Section: Monamine Metabolism In Migraine: Focus On Serotoninmentioning

confidence: 76%

“…The latter finding was supported by early studies which demonstrated Hedman et al [1] 1988 MA Decreased beta-adrenoreceptor response to stimulation with isoprenaline Herman et al [2] 1989 MA and MwA Decreased sensitivity of platelets to PAF Takeshima et al [3] 1989 Migraine, type not specified Increased activation during cold pressure test Kovacs et al [4] 1990 MA Increased activation to ADP and PAF D'Andrea et al [5] 1994 MA and MwA Decreased collagen-induced aggregation Kitano et al [6] 1994 MA and MwA Continuous activation measured as increased values of 11-dehydrothromboxane B2 Tozzi et al [7] 1996 MA and MwA Perturbed platelet viscosity; Decreased stimulation-induced influx of external calcium through the platelet membrane; Hyperaggregation to adenosine diphosphate and collagen MA, migraine with aura; MwA, migraine without aura; PAF, platelet-activating factor S63 a reduced platelet content of serotonin that was attributed to an unidentified plasma releasing factor. The principal data on serotonin metabolism in migraine outside the attacks are summarized in Table 2 [9][10][11][12][13][14][15][16][17]. Differences in platelet serotonin content have been observed between migraine with aura and migraine without aura patients assessed between attacks [15].…”

Section: Monamine Metabolism In Migraine: Focus On Serotoninmentioning

confidence: 99%

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Platelets in migraine

Sarchielli

Gallai

2001

J Headache Pain

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Modification in platelet activation and aggregation has been demonstrated in migraine patients both during and between attacks. A different pattern in the secretion of platelet products has also been observed in patients affected by migraine compared with controls. The most important variation concerns a hyposecretion of dense body products. Platelets share structural and functional analogies with monoaminergic neurons, in particular serotoninergic neurons, and have been used as a peripheral model to study monaminergic function in migraine patients. A reduced turnover of serotonin has been shown in migraine patients in the interictal period, whereas a reduced content of this monoamine was detected in patients with chronic daily headache (CDH), particularly in those with analgesic abuse. Nitric oxide metabolism was also studied in platelets of migraine patients between and during attacks. An increased activity of nitric oxide synthase (NOS), which was more accentuated during attacks, was found in these patients compared to healthy individuals. The increase in platelet NOS activity was also confirmed in CDH patients in association with a reduction of serotonin content and increased calcium levels. Variations in aggregation to different agents and secretion may not, at the moment, be indicative of similar changes in cerebral circulation of migraine patients. Its occurrence should be confirmed in samples of jugular venous blood during attacks to establish a definite link with migraine pathogenesis. Moreover changes in serotonin and NO metabolism observed in platelets of migraine patients may only indirectly suggest similar modifications in the neuronal pathways involved in inducing and maintaining head pain in migraineurs.

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Section: Monamine Metabolism In Migraine: Focus On Serotoninmentioning

confidence: 76%

Section: Monamine Metabolism In Migraine: Focus On Serotoninmentioning

confidence: 99%

Platelets in migraine

Sarchielli

Gallai

2001

J Headache Pain

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“…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]. Differences may relate to factors including cigarette smoking [10,49] and hormonal status [9,47] that independently affect MAO levels and have not been accounted for in most studies.…”

Section: Discussionmentioning

confidence: 99%

“…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]. Differences may relate to factors including cigarette smoking [10,49] and hormonal status [9,47] that independently affect MAO levels and have not been accounted for in most studies.…”

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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“…As far as the 5-HT system and MM are concerned, hypersensitivity of the 5-HT system to gonadal steroid modulation has been described, since platelet MAO-B activity, a good indicator of central 5-HT, is significantly increased in the LP of women with MM in comparison with asymptomatic controls [34]. Moreover, the mean values of platelet 5-HT drop significantly during migraine attack in comparison to baseline, while serum 5-HT increases [35].…”

Section: Discussionmentioning

confidence: 99%

Neuroendocrine Response to the Serotonin Agonist M-Chlorophenylpiperazine in Women with Menstrual Status migrainosus

et al. 2003

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To assess the neuroendocrine correlates of menstrual status migrainosus (MSM) and menstrual migraine (MM), we evaluated the prolactin (PRL) and cortisol responses to the direct central serotoninergic (5-HT) agonist meta-chlorophenylpiperazine (m-CPP) administered orally (0.5 mg/kg) during the follicular (FP: +6, +8) and luteal phases (LP: –4, –6) of the same menstrual cycle. Ten women with MSM (migraine attacks occurring within 2 days of the onset of menstrual bleeding but lasting more than 72 h) and 9 women with MM (migraine occurring within 2 days of the onset of menstrual bleeding with a typical duration of attacks) were studied. Six healthy women served as controls. Blood samples were taken at times –30, 0 and every 30 min over 4 h. Statistical analysis was performed using MANOVA followed by Duncan’s post hoc comparisons. We found that the PRL response to the m-CPP test was significantly blunted in MSM compared with MM and controls in both phases of the menstrual cycle (F = 4.6; p < 0.001). Indeed, the PRL area under the curve (AUC) after m-CPP was higher in both MM and controls compared with MSM (F = 12.7; p < 0.001). The m-CPP-induced cortisol response was absent in MSM compared with MM and controls in both FP and LP (F = 4.1; p < 0.001). On the other hand, the pattern of the plasma cortisol response to m-CPP was similar in MM and controls throughout the menstrual cycle. In addition, the basal plasma cortisol levels were significantly higher in MSM compared with controls (p < 0.001) and MM (p < 0.001) during FP, but not in LP, and progressively decreased over time. Thus, no significant effect of the menstrual cycle phase and diagnosis on the cortisol AUC was found, while a significant diagnosis effect (F = 25.6; p < 0.001) on %Δ_max plasma cortisol levels was evident and consistent with the lack of cortisol response to m-CPP in MSM during the FP and LP compared with MM and controls. A derangement in central 5-HT control of pituitary PRL, and even more so in cortisol release, is present in women with MSM, but not with MM, regardless of the phase of the menstrual cycle, suggesting the involvement of some 5-HT₁ and 5-HT₂ receptor subtypes in the occurrence of extremely severe migraine attacks triggered by menstruation.

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Platelet Serotonin Pathway in Menstrual Migraine

Cited by 33 publications

References 25 publications

Platelets in migraine

Platelets in migraine

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

Neuroendocrine Response to the Serotonin Agonist M-Chlorophenylpiperazine in Women with Menstrual Status migrainosus

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