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Serotoninergic dysfunction in bipolar disorder.

D Marazziti1, A Lenzi, G B Cassano

  • 1Institute of Psychiatry, University of Pisa, Italy.

Pharmacopsychiatry
|September 1, 1991
PubMed
Summary
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Bipolar disorder patients show altered serotonin transporter function. While imipramine binding was similar, platelet serotonin uptake was reduced, suggesting changes in the serotonin transporter complex in bipolarity.

Area of Science:

  • Neuroscience
  • Psychiatry
  • Biochemistry

Background:

  • Peripheral markers offer insights into central neurotransmitter systems in psychiatric research.
  • Human platelets serve as a model for presynaptic serotoninergic neurons, aiding mood disorder research.
  • Platelets exhibit serotonin and 3H-imipramine uptake, mirroring cerebral binding sites.

Purpose of the Study:

  • To investigate the role of the serotonin system in bipolar disorder pathophysiology.
  • To compare 3H-imipramine binding and 14C-serotonin uptake in bipolar patients versus healthy controls.

Main Methods:

  • Evaluated 3H-imipramine binding in 30 bipolar patients and healthy controls.
  • Measured platelet 14C-serotonin (14C-5HT) uptake in 20 bipolar patients.

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Main Results:

  • No significant differences in 3H-imipramine binding parameters were observed between groups.
  • Bipolar patients exhibited a significantly lower Vmax for 14C-5HT uptake compared to controls.

Conclusions:

  • Bipolar disorder is associated with alterations in the serotonin transporter complex within platelets.
  • Reduced serotonin uptake, not imipramine binding, may be a key indicator of serotonergic dysfunction in bipolarity.