Abnormalities in Platelet 5-Hydroxytryptamine Efflux in Patients with Infantile Autism

Boullin, D. J.; Coleman, Mary; O'Brien, R.A.

doi:10.1038/226371a0

Cited by 82 publications

(30 citation statements)

References 8 publications

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“…A number of studies have specifically examined gene expression patterns in ASD [90][91][92][114][115][116][117][118][119][120][121][122][123]. It should be noted that predating this gush of expression studies in ASD, hyperserotonemia was observed in one third of patients and platelet serotonin was suggested as a marker for this disorder [124][125][126][127].…”

Section: Biomarkers For Autism Spectrum Disordersmentioning

confidence: 99%

Are retinoids potential therapeutic agents in disorders of social cognition including autism?

et al. 2011

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Edited by Sergio Papa, Gianfranco Gilardi and Wilhelm JustKeywords: Autism spectrum disorder (ASD) All-trans retinoic acid (ATRA) CD38 Oxytocin Polymorphism a b s t r a c t Increasing evidence suggests that the nonapeptide, oxytocin (OT), helps shape social and affiliative behaviors not only in lower mammals but also in humans. Recently, an essential mediator of brain OT release has been discovered, ADP-ribosyl cyclase and/or CD38. We have subsequently shown that polymorphisms across the CD38 gene are associated with autism spectrum disorders (ASD). Notably, CD38 expression in lymphoblastoid cells (LBC) is reduced in cell lines derived from ASD subjects compared to parental cell lines. Intriguingly, a correlation was observed between CD38 expression and measures of social function in ASD. Finally, we have shown that all-trans retinoic acid (ATRA), a known inducer of CD38 transcription, can rescue low CD38 expressing LBC lines derived from ASD subjects and restore normal levels of transcription of this ectoenzyme providing 'proof of principle' in a peripheral model that retinoids are potential therapeutic agents in ASD. Ó 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved. OxytocinClassically, the nonapeptide oxytocin (OT) has been viewed as a hypothalamic neuropeptide that is released into the general circulation from the neural lobe of the pituitary, inducing uterine contractions during parturition and milk ejection during lactation. OT is derived from a pre-prohormone precursor that is synthesized in the hypothalamus and stored in vesicles at the posterior pituitary for storage and subsequent release into the bloodstream (see [1] for comprehensive review of the oxytocin receptor system). OT and social behaviorBeyond the long-known peripheral effects of OT, a wealth of animal studies have elaborated the role of OT, or their analogues such as isotocin and vasotocin [2], in molding social behavior from fish to mammals [3]. In the past few years the role of OT has also been examined in our own species, and similar to what has been learned from animal studies, it appears that this nonapeptides also influence social behaviors in humans [4,5]. Indeed, OT has been suggested as the 'great facilitator of life' in a recent review [6].In humans, intranasal administration of OT has been shown to increase trust [7], facilitate mind-reading [8], enhance human memory for social identity [9], increase positive communication between couples [10], increase gaze to the eye region [11] and increase generosity [12]. Intriguingly, OT plasma levels have been linked to individual patterns of maternal-fetal attachment [13] and salivary OT levels were associated with bonding to own parents and inversely related to psychological distress, particularly depressive symptoms [14]. Social anxiety symptom severity, adjusted for age and gender in a healthy group of subjects, was associated with higher plasma oxytocin levels [15]. Imaging studies reinforce the role of OT in influencing human social ...

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Section: Biomarkers For Autism Spectrum Disordersmentioning

confidence: 99%

Are retinoids potential therapeutic agents in disorders of social cognition including autism?

et al. 2011

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“…Anomalies of amine metabolism have been implicated in some behavioral disorders of childhood. Alterations in serotonin metabolism and blood levels were found in certain retarded, schizophrenic and autistic children (Boullin et al, 1970;Coleman, 1973; P age, 1968\Partington et al, 1973Ritvo et al, 1970;Schain and Freedman, 1961;Campbell et al, 1974Campbell et al, , 1975. Others have found abnormalities in catecholamine metabolism in autistic and atypical children (Cohen et al, 1975).…”

mentioning

confidence: 98%

Blood Platelet Monoamine Oxidase Activity in Schizophrenic Children and Their Families

Campbell¹,

Friedman²,

Green³

et al. 1976

Neuropsychobiology

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In this study monoamine oxidase (MAO) activity was measured in blood platelets of 21 individuals (age 2⁶/₁₂^–19 years) who were diagnosed at preschool age as schizophrenics; MAO activity was not significantly different from that found in normals. An insignificant correlation was found between MAO activity in patients and age; a similar correlation for normals was also insignificant. In a sample of 15 families, no significant correlation between MAO activity of patients and their parents was obtained.

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“…Consequently, decreased uptake of 5HT by mongol platelets might be explained by a defect in platelet ATP content or function. A decrease in total ATP concentration has recently been suggested for Down's syndrome patients [5], but this has not been confirmed in other studies [13].…”

Section: Discussionmentioning

confidence: 85%

Down's Syndrome: Transport, Storage, and Metabolism of Serotonin in Blood Platelets

1972

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ExtractSerotonin (5HT) transport and metabolism were studied in platelets from 14 trisomy-21 patients who were matched with 12 sibling and 9 non-sibling control subjects with regard to age, sex, home environment, diet and weight. Endogenous 5HT content, in nanograms per milligram platelet protein, was reduced from 446 ± 66 in the sibling controls and from 492 ± 74 in the non-sibling controls to 158 ± 16 in the Down's syndrome group, a difference of 61% and 68% respectively (P < 0.001). Initial uptake of 14 G-5HT measured after a 3-min incubation period was reduced 35% (P < 0.05) in the platelets from Down's syndrome patients, while the efflux of radiolabeled amine from platelets was not significantly altered in these patients. Since platelets do not synthesize 5HT, the decreased transport found may explain the lower 5HT levels in these patients. Mongols did not differ from control subjects in the activity of platelet monoamine oxidase. SpeculationSimilarities in the uptake, storage, and release of 5HT between the human blood platelet and the serotonergic neuron suggest that the 5HT abnormality observed in mongol platelets may reflect disordered metabolism of the monoamine within the central nervous system.

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Abnormalities in Platelet 5-Hydroxytryptamine Efflux in Patients with Infantile Autism

Cited by 82 publications

References 8 publications

Are retinoids potential therapeutic agents in disorders of social cognition including autism?

Are retinoids potential therapeutic agents in disorders of social cognition including autism?

Blood Platelet Monoamine Oxidase Activity in Schizophrenic Children and Their Families

Down's Syndrome: Transport, Storage, and Metabolism of Serotonin in Blood Platelets

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