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Peripheral-type benzodiazepine receptors on platelets are correlated with the degrees of anxiety in normal human subjects

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Abstract

Rationale. Anxiety is the one of the main symptoms of psychiatric disorders. Psychosocial stressors have been shown to be related to the onset of anxious episodes. Peripheral-type benzodiazepine receptors (PBR) are involved in regulating stress responses. The sensitivity of PBR to acute or chronic stress has been demonstrated in various situations. The State-Trait Anxiety Inventory (STAI) is one of the longest standing and most frequently used measures of anxiety. The development, evaluation, and use of biological markers with anxious conditions in psychiatry are extremely important.

Objectives. The aims of this survey are to see whether PBR can be used in screening the degrees of anxiety which occur when normal persons are placed in the stressful conditions.

Methods. Twenty-four healthy volunteers (14 men, 10 women; mean age 46 years) participated in this study. We administered the STAI to all the volunteers. The binding of the radioactive PBR antagonist [3H]PK 11195 to platelet membranes was determined for these volunteers.

Results. The mean STAI scores were 40.3±8.0 for trait anxiety and 39.0±8.9 for state anxiety. Bmax of the platelet PBR binding was 2845±2109 fmol/mg protein. Pearson correlational analyses revealed that Bmax values were significantly and positively correlated with scores for trait anxiety but not significantly correlated with scores for state anxiety.

Conclusions. PBR on platelets are correlated with trait anxiety scales of the STAI in healthy normal subjects. It is therefore suggested that the density of platelet PBR is highly associated with these personality traits for anxiety tolerance. PBR density in platelet could also be used as a promising biological marker of stressful conditions.

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Nakamura, K., Fukunishi, I., Nakamoto, Y. et al. Peripheral-type benzodiazepine receptors on platelets are correlated with the degrees of anxiety in normal human subjects. Psychopharmacology 162, 301–303 (2002). https://doi.org/10.1007/s00213-002-1098-y

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  • DOI: https://doi.org/10.1007/s00213-002-1098-y

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