The Human Platelet

Stahl, Stephen M.

doi:10.1001/archpsyc.1977.01770170019001

Cited by 364 publications

(25 citation statements)

References 88 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%

“…In local cerebral ischemia, one of the pathogenetic mechanisms affecting neuroplasticity is related to metabolic changes in biogenic monoamines such as serotonin and dopamine [2,10,12]. 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].…”

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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%

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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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“…Total blood 5-HT is a measure of platelet 5-HT content which, in turn, is widely accepted as a peripheral model for central serotonergic neurons (Stahl, 1977). Cerebrospinal fluid (CSF) 5-HIAA was found to be decreased in alcoholic patients only in the case of pronounced withdrawal symptoms (Takahashi, 1974).…”

Section: Introductionmentioning

confidence: 99%

Factors influencing monoamine metabolites and tryptophan in patients with alcohol dependence

Bánki¹

1981

J. Neural Transmission

103

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Cerebrospinal fluid 5-hydroxyindoleacetic acid (5-HIAA), homovanillic acid (HVA) and tryptophan (TRY) were measured in 36 female patients with alcohol dependence defined by strict operational criteria. Results were compared with a control group of 32 women hospitalized in a neurological unit for peripheral diseases. Several disorders presumably interfering with monoamine metabolism were excluded and diet, psychomotor activity, diurnal variation, nutritional state and similar nonspecific variables controlled in both groups. Only 5-HIAA was found to be decreased in development patients as compared to controls. Since 5-HIAA--but neither HVA nor TRY--correlated with body height in both groups, we eliminated its effect by analysis of covariance: as a result 5-HIAA difference became statistically significant but the other two biochemical measures remained unchanged. A multivariate regression analysis with five independent clinical variables (body height, age, weight, years of alcohol abuse and days of abstinence) yielded significant determination coefficient R2 only for 5-HIAA. Regarding its components only body height and days of abstinence proved to be significantly correlated with 5-HIAA. Severity of withdrawal symptoms assessed on a rating scale in 14 patients with 4 days or less of abstinence correlated marginally with HVA but not with 5-HIAA. This latter metabolite decreased only in patients with 5 days or more of abstinence; the difference between 5-HIAA levels of short-term and long-term abstinence subgroups was statistically highly significant.

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“…The blood platelet is known to be able to take up and store 5-hydroxytryptamine (5-HT) (Pletscher, 1968) and it has been suggested that the platelet might provide a readily accessible model for aminergic nerve terminals in the brain both with respect to amines and their related enzymes (Sneddon, 1973;Stahl, 1977). Recently an inbred strain of rats has been described (Tschopp & Zucker, 1972) which have a prolonged bleeding time and a deficiency of platelet 5-HT, ADP and ATP in many ways similar to that found in platelets from humans with 'storage pool disease', a congenital disorder of haemostasis Weiss, Tschopp, Rogers & Brand, 1974).…”

Section: Introductionmentioning

confidence: 99%

Brain Tryptophan Metabolism on the 5‐hydroxytryptamine and Kynurenine Pathways in a Strain of Rats With a Deficiency in Platelet 5‐ht

Joseph

1978

British J Pharmacology

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Brain 5‐hydroxytryptamine (5‐HT) metabolism has been compared in albino (Sprague‐Dawley; SD) and in Fawn‐Hooded (FH) rats, which have an inherited platelet 5‐HT deficiency. It was confirmed that blood 5‐HT levels in the FH rats were about one quarter of those in the SD rats. Brain 5‐HT and 5‐HIAA were however higher in FH rats on a per gram basis; there was no difference between the strains on a per brain basis, because of the smaller brain weights of the FH rats. Brain and plasma tryptophan were not significantly different in the two strains. Plasma kynur‐enine was higher in the FH rats, and brain kynurenine was also higher either on a per gram or on a per brain basis. The reserpine‐releasable brain 5‐HT was the same proportion of total brain 5‐HT in the two strains. Experiments with pargyline suggested that the turnover of 5‐HT was somewhat higher in the FH rats on a per gram basis, but not significantly so on a per brain basis. It is concluded that although brain tryptophan metabolism may be somewhat accelerated along both the 5‐HT and kynurenine pathways in the FH rats there is no gross deficiency in the binding of 5‐HT in their brains analogous to that found in their platelets.

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The Human Platelet

Cited by 364 publications

References 88 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

Factors influencing monoamine metabolites and tryptophan in patients with alcohol dependence

Brain Tryptophan Metabolism on the 5‐hydroxytryptamine and Kynurenine Pathways in a Strain of Rats With a Deficiency in Platelet 5‐ht

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