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Hyperserotonemia in autism: activity of 5HT-associated platelet proteins

  • Biological Psychiatry - Original Article
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Abstract

Disturbances in serotonin (5HT) neurotransmission have been indicated as biological substrates in several neuropsychiatric disorders including autism. Blood 5HT concentrations, elevated in about one-third of autistic subjects, are regulated through the action of peripheral 5HT-associated proteins. We have measured the activity of two platelet 5HT-associated proteins: 5HT transporter (5HTT) and monoamine oxidase B (MAOB), and indirectly studied the activity of 5HT2A receptor (5HT2Ar) in 15 hyperserotonemic (HS) and 17 normoserotonemic (NS) autistic subjects, and 15 healthy controls (C). While mean velocities of 5HTT kinetics did not significantly differ among the groups, significant elevation in the mean velocity of MAOB kinetics was observed in NS subjects and was even more pronounced in HS subjects in comparison to controls. Also, a decrease in adenosine 5′-diphosphate-induced platelet aggregation of borderline significance was observed in NS subjects, compared to C subjects. The results suggest a possibility of upregulation of monoaminergic synthesis/degradation and, probably consequential, downregulation of 5HT2Ar in autistic subjects.

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Acknowledgment

This study was supported by the grants “Neurobiological basis of autism: the role of serotonin system” (119-1081870-2396) and “Serotonergic neurotransmission: genes, proteins and behavior” (098-1081870-2395), both funded by the Ministry of Science Education and Sports of the Republic of Croatia. The authors wish to thank Mrs Drina Bagaric, a medical laboratory engineer, for her skillful, kind and gentle approach to the patients during blood sampling, and to Mrs Katarina Karlo, a senior technician, for her assistance in PSL and MAOB measurements.

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Correspondence to Dubravka Hranilović.

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Hranilović, D., Bujas-Petković, Z., Tomičić, M. et al. Hyperserotonemia in autism: activity of 5HT-associated platelet proteins. J Neural Transm 116, 493–501 (2009). https://doi.org/10.1007/s00702-009-0192-2

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