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Related Experiment Videos

Platelet imipramine binding in autistic subjects.

G M Anderson, R B Minderaa, P P van Benthem

    Psychiatry Research
    |February 1, 1984
    PubMed
    Summary

    This study found no differences in serotonin transporter regulation in autistic individuals, suggesting that altered serotonin uptake is not a key factor in autism. This research provides insights into the neurobiology of autism.

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    Area of Science:

    • Neuroscience
    • Biochemistry
    • Autism Spectrum Disorder Research

    Background:

    • Previous studies indicated elevated platelet serotonin (5-HT) in autistic individuals.
    • This suggested potential alterations in platelet 5-HT uptake mechanisms in autism.

    Purpose of the Study:

    • To investigate whether 5-HT uptake is altered in autism.
    • To compare the parameters of 3H-imipramine (IMI) binding in autistic subjects and normal volunteers.

    Main Methods:

    • Measured 3H-imipramine (IMI) binding parameters (Bmax and Kd) in drug-free autistic subjects (n=11) and normal volunteers (n=10).
    • Analyzed the number and affinity of IMI binding sites.

    Main Results:

    • No significant differences were found in the mean Bmax (maximal binding capacity) between autistic subjects (1350 +/- fmole/mg protein) and normal volunteers (1590 +/- 206 fmole/mg protein).

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  • Similarly, no significant differences were observed in the mean Kd (dissociation constant, indicating binding affinity) between groups (autistics: 0.98 +/- 0.10 nM; normals: 0.94 +/- 0.13 nM).
  • Conclusions:

    • The findings suggest that the number and affinity of the IMI binding site, reflecting serotonin transporter regulation, are not different in autism.
    • This indicates that altered serotonin uptake regulation is unlikely to be a primary factor contributing to autism.