Platelet serotonin transporter function predicts default-mode network activity

PLoS One. 2014 Mar 25;9(3):e92543. doi: 10.1371/journal.pone.0092543. eCollection 2014.

Abstract

Background: The serotonin transporter (5-HTT) is abundantly expressed in humans by the serotonin transporter gene SLC6A4 and removes serotonin (5-HT) from extracellular space. A blood-brain relationship between platelet and synaptosomal 5-HT reuptake has been suggested, but it is unknown today, if platelet 5-HT uptake can predict neural activation of human brain networks that are known to be under serotonergic influence.

Methods: A functional magnetic resonance study was performed in 48 healthy subjects and maximal 5-HT uptake velocity (Vmax) was assessed in blood platelets. We used a mixed-effects multilevel analysis technique (MEMA) to test for linear relationships between whole-brain, blood-oxygen-level dependent (BOLD) activity and platelet Vmax.

Results: The present study demonstrates that increases in platelet Vmax significantly predict default-mode network (DMN) suppression in healthy subjects independent of genetic variation within SLC6A4. Furthermore, functional connectivity analyses indicate that platelet Vmax is related to global DMN activation and not intrinsic DMN connectivity.

Conclusion: This study provides evidence that platelet Vmax predicts global DMN activation changes in healthy subjects. Given previous reports on platelet-synaptosomal Vmax coupling, results further suggest an important role of neuronal 5-HT reuptake in DMN regulation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Blood Platelets / physiology*
  • Brain / physiology*
  • Connectome*
  • Female
  • Functional Neuroimaging
  • Genetic Variation
  • Humans
  • Magnetic Resonance Imaging
  • Male
  • Neural Pathways*
  • Serotonin / metabolism*
  • Serotonin Plasma Membrane Transport Proteins / genetics*
  • Young Adult

Substances

  • SLC6A4 protein, human
  • Serotonin Plasma Membrane Transport Proteins
  • Serotonin

Grants and funding

This work was supported by the Special Research Project SFB-35 (Project No. F3514-B11, F3510-B11 and F3506-B11 to LP, MF and HHS, respectively) of the Austrian Science Fund (FWF) and the Institute for Study of Affective Neuroscience (ISAN) as well as by grants of the Austrian National Bank (OeNB P11903 to L. Pezawas and OeNB P13214 to R. Lanzenberger). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.