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Platelet aggregation and dense granule secretion in schizophrenia
J K Yao1, D P van Kammen, J Gurklis
1Neurochemistry and Psychopharmacology Laboratory, Highland Drive Department of Veterans Affairs Medical Center (DVAMC), Pittsburgh, PA, USA.
Insights
Schizophrenia patients exhibit altered platelet aggregation and adenosine triphosphate (ATP) release, suggesting impaired platelet function. These changes correlate with psychosis severity but not medication levels.
Area of Science:
- Neuroscience
- Hematology
- Psychiatry
Background:
- Platelet function may be altered in schizophrenia.
- Antipsychotic medications could influence platelet activity.
Purpose of the Study:
- To investigate platelet aggregation and adenosine triphosphate (ATP) release in schizophrenic patients.
- To compare platelet function between treated and untreated schizophrenic patients and healthy controls.
- To explore correlations between platelet function and clinical parameters.
Main Methods:
- Assessed platelet aggregation and ATP release in response to collagen, arachidonic acid (AA), and adenosine diphosphate (ADP).
- Compared functional states in normal controls, haloperidol-treated schizophrenic patients, and drug-free schizophrenic patients.
- Correlated platelet function with psychosis ratings, medication dosage, and illness duration.
Main Results:
- Platelet aggregation was higher in both patient groups compared to controls (collagen-induced).
- AA-induced ATP release was lower in haloperidol-treated patients versus controls.
- ATP release was higher in drug-free patients than when they were on haloperidol.
- Collagen-induced platelet function correlated negatively with psychosis ratings.
Conclusions:
- Schizophrenia is associated with distinct alterations in platelet function, including impaired ATP release.
- Haloperidol treatment may affect platelet adenosine triphosphate (ATP) secretion.
- Platelet dysfunction in schizophrenia correlates with psychosis severity, independent of medication dosage or illness duration.
Abstract:
The functional state of platelets and their possible impairment in response to various stimuli were assessed in saline-diluted citrated blood samples of normal male control subjects (n = 27), and in schizophrenic patients with (n = 34) and without (n = 23) haloperidol treatment. In response to collagen, but not to arachidonic acid (AA) and adenosine diphosphate, platelet aggregation (as measured by changes in impedance) was significantly higher in both haloperidol-treated and drug-free schizophrenic patients than in normal control subjects. Comparison of the secretion traces, however, indicated that only AA-induced adenosine triphosphate (ATP) release was significantly lower in haloperidol-treated schizophrenic patients than in normal control subjects. In response to thrombin, collagen, and AA, the mean values of ATP release from drug-free patients were significantly higher than those from the same individuals when they were receiving haloperidol. Furthermore, there was a trend toward increased ATP release (in response to thrombin or collagen) in the nonrelapsed group of drug-free schizophrenic patients as compared with the relapsed group. The collagen-induced platelet aggregation or dense granule secretion in drug-free patients was correlated significantly and negatively with psychosis ratings. Such changes in platelet function of schizophrenic patients were not correlated significantly with daily haloperidol dose, plasma haloperidol levels, age of subjects, age of onset, or duration of illness.