Platelet studies in panic disorder: A review

1997 ◽  
Vol 14 (4) ◽  
pp. 139-143 ◽  
Author(s):  
Laura Mannion ◽  
Desmond Nugent ◽  
Brian Leonard
Keyword(s):  
Panic Disorder ◽  
Platelet Function ◽  
Blood Platelet ◽  
Serotonin Uptake ◽  
Central Neurons ◽  
Paroxetine Binding ◽  
Platelet Monoamine Oxidase ◽  
Methodological Considerations ◽  
Insight Into

AbstractObjective: The blood platelet has been proposed as a model of central neurons and may therefore be used as a peripheral marker of psychiatric illness. One method of investigating serotonin function in panic disorder has relied on the use of the platelet as a model of serotonergic neurons. This article reviews the studies of platelet function in panic disorder.Method: A literature search and review of relevant papers was undertaken.Result: Studies examining platelet serotonin uptake and concentration in panic disorder patients have to date yielded conflicting results, with some investigators reporting increased serotonin uptake, others reduced uptake. Similarly studies of platelet 3H-imipramine binding have also yielded conflicting results. Two studies of platelet 3H-paroxetine binding have shown a reduction in the density of binding sites (Bmax) in patients with panic disorder. Platelet monoamine oxidase activity in anxiety disorders has been reported to be increased by some investigators but decreased by others. Methodological considerations may have been responsible for these differences. Finally, studies of α2 adrenoceptor density have also produced contrasting findings.Conclusion: The findings of these studies indicate that platelet function is altered in panic disorder. Such changes may allow an insight into the biochemical aetiology of the illness. Further studies are required to delineate the role of serotonin and non-adrenaline in panic disorder.

Maternal Perception of Infants’ Expressions of Emotion

2010 ◽  
Vol 24 (3) ◽  
pp. 173-185 ◽  
Author(s):  
Martin Krippl ◽  
Stephanie Ast-Scheitenberger ◽  
Ina Bovenschen ◽  
Gottfried Spangler
Keyword(s):  
Response Pattern ◽  
Electrodermal Activity ◽  
Startle Amplitude ◽  
Caregiving System ◽  
Parental Caregiving ◽  
Opponent Process ◽  
Opponent Process Theory ◽  
Valence And Arousal ◽  
Methodological Considerations

In light of Lang’s differentiation of the aversive and the approach system – and assumptions stemming from attachment theory – this study investigates the role of the approach or caregiving system for processing infant emotional stimuli by comparing IAPS pictures, infant pictures, and videos. IAPS pictures, infant pictures, and infant videos of positive, neutral, or negative content were presented to 69 mothers, accompanied by randomized startle probes. The assessment of emotional responses included subjective ratings of valence and arousal, corrugator activity, the startle amplitude, and electrodermal activity. In line with Lang’s original conception, the typical startle response pattern was found for IAPS pictures, whereas no startle modulation was observed for infant pictures. Moreover, the startle amplitudes during negative video scenes depicting crying infants were reduced. The results are discussed with respect to several theoretical and methodological considerations, including Lang’s theory, emotion regulation, opponent process theory, and the parental caregiving system.

Challenges of Fear Conditioning Research in the Age of RDoC

2017 ◽  
Vol 225 (3) ◽  
pp. 189-199 ◽  
Author(s):  
Tina B. Lonsdorf ◽  
Jan Richter
Keyword(s):  
Fear Conditioning ◽  
Clinical Diagnosis ◽  
Research Domain Criteria ◽  
Major Focus ◽  
The Future ◽  
Definition Of ◽  
Methodological Considerations ◽  
Research Domain

Abstract. As the criticism of the definition of the phenotype (i.e., clinical diagnosis) represents the major focus of the Research Domain Criteria (RDoC) initiative, it is somewhat surprising that discussions have not yet focused more on specific conceptual and procedural considerations of the suggested RDoC constructs, sub-constructs, and associated paradigms. We argue that we need more precise thinking as well as a conceptual and methodological discussion of RDoC domains and constructs, their interrelationships as well as their experimental operationalization and nomenclature. The present work is intended to start such a debate using fear conditioning as an example. Thereby, we aim to provide thought-provoking impulses on the role of fear conditioning in the age of RDoC as well as conceptual and methodological considerations and suggestions to guide RDoC-based fear conditioning research in the future.

Does Increased Platelet Release Normalize During Anti-Hypertensive Treatment?

1987 ◽  
Vol 58 (03) ◽  
pp. 834-838
Author(s):  
Knut Lande ◽  
Sverre Erik Kjeldsen ◽  
Ivar Eide ◽  
Paul Leren ◽  
Knut Gjesdal
Keyword(s):  
Platelet Function ◽  
Adrenergic Receptor ◽  
Blood Platelet ◽  
Placebo Treatment ◽  
Sampling Procedure ◽  
Β Blocker ◽  
Platelet Release ◽  
Hypertensive Drug ◽  
Second Period ◽  
Release Product

SummaryBlood platelet function was evaluated in 10 men, all 50 years old, with untreated, mild hypertension. Each patient was examined four times: At the beginning of the study, after 5 weeks on placebo treatment, after the following 5 weeks on propranolol 160 mg daily, and finally after a second period of 5 weeks on placebo. At baseline the plasma level of the platelet release product (β-thromboglobulin (BTG) was 41.6 (30.5-57.0) μg/l (median and 95% confidence interval). During the first placebo period BTG was normalized to 21.0 (14.1-25.9) μg/l. While systolic blood pressure and heart rate fell during β-adrenergic receptor blockade, BTG remained unchanged throughout the rest of the observation periods. Platelet size increased significantly during treatment with β-blocker. The present study indicates that the normalization of elevated platelet function which previously has been reported to occur during anti-hypertensive drug therapy, may be explained by patient adaptation to the blood sampling procedure.

Effect of Dipyridamole on Spontaneous Platelet Aggregation in Whole Blood Decreases with the Time After Venepuncture: Evidence for the Role of ADP

1987 ◽  
Vol 58 (02) ◽  
pp. 744-748 ◽  
Author(s):  
A R Saniabadi ◽  
G D O Lowe ◽  
J C Barbenel ◽  
C D Forbes
Keyword(s):  
Platelet Aggregation ◽  
Correlation Coefficient ◽  
Whole Blood ◽  
Blood Platelet ◽  
Inhibitory Effect ◽  
Time Interval ◽  
Adp Receptor ◽  
Spontaneous Platelet Aggregation

SummarySpontaneous platelet aggregation (SPA) was studied in human whole blood at 3, 5, 10, 20, 30, 40 and 60 minutes after venepuncture. Using a whole blood platelet counter, SPA was quantified by measuring the fall in single platelet count upon rollermixing aliquots of citrated blood at 37° C. The extent of SPA increased with the time after venepuncture, with a correlation coefficient of 0.819. The inhibitory effect of dipyridamole (Dipy) on SPA was studied: (a) 10 μM at each time interval; (b) 0.5-100 μM at 3 and 30 minutes and (c) 15 μM in combination with 100 μM adenosine, 8 μM 2-chloroadenosine (2ClAd, an ADP receptor blocker) and 50 μM aspirin. There was a rapid decrease in the inhibitory effect of Dipy with the time after venepuncture; the correlation coefficient was -0.533. At all the concentrations studied, Dipy was more effective at 3 minutes than at 30 minutes after venepuncture. A combination of Dipy with adenosine, 2ClAd or aspirin was a more effective inhibitor of SPA than either drug alone. However, when 15 μM Dipy and 10 μM Ad were added together, the inhibitory effect of Dipy was not increased significantly, suggesting that Dipy inhibits platelet aggregation independent of Ad. The increase in SPA with the time after venepuncture was abolished when blood was taken directly into the anticoagulant containing 5 μM 2ClAd. It is suggested that ADP released from the red blood cells is responsible for the increased platelet aggregability with the time after venepuncture and makes a serious contribution to the artifacts of in vitro platelet function studies.

Plasminogen Activation In Vivo upon Intravenous Infusion of DDAVP

1992 ◽  
Vol 67 (01) ◽  
pp. 111-116 ◽  
Author(s):  
Marcel Levi ◽  
Jan Paul de Boer ◽  
Dorina Roem ◽  
Jan Wouter ten Cate ◽  
C Erik Hack
Keyword(s):  
Monoclonal Antibodies ◽  
Plasminogen Activator ◽  
Plasma Levels ◽  
Fold Increase ◽  
Fibrinolytic System ◽  
Plasminogen Activation ◽  
Plasminogen Activator Activity ◽  
Insight Into

SummaryInfusion of desamino-d-arginine vasopressin (DDAVP) results in an increase in plasma plasminogen activator activity. Whether this increase results in the generation of plasmin in vivo has never been established.A novel sensitive radioimmunoassay (RIA) for the measurement of the complex between plasmin and its main inhibitor α2 antiplasmin (PAP complex) was developed using monoclonal antibodies preferentially reacting with complexed and inactivated α2-antiplasmin and monoclonal antibodies against plasmin. The assay was validated in healthy volunteers and in patients with an activated fibrinolytic system.Infusion of DDAVP in a randomized placebo controlled crossover study resulted in all volunteers in a 6.6-fold increase in PAP complex, which was maximal between 15 and 30 min after the start of the infusion. Hereafter, plasma levels of PAP complex decreased with an apparent half-life of disappearance of about 120 min. Infusion of DDAVP did not induce generation of thrombin, as measured by plasma levels of prothrombin fragment F1+2 and thrombin-antithrombin III (TAT) complex.We conclude that the increase in plasminogen activator activity upon the infusion of DDAVP results in the in vivo generation of plasmin, in the absence of coagulation activation. Studying the DDAVP induced increase in PAP complex of patients with thromboembolic disease and a defective plasminogen activator response upon DDAVP may provide more insight into the role of the fibrinolytic system in the pathogenesis of thrombosis.

Platelet Aggregation in Whole Blood: The Role of Thromboxane A2 and Adenosine Diphosphate

1985 ◽  
Vol 54 (03) ◽  
pp. 612-616 ◽  
Author(s):  
A J Carter ◽  
S Heptinstall
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Adenosine Diphosphate ◽  
Blood Platelet ◽  
Thromboxane B2 ◽  
Lipoxygenase Inhibitor ◽  
Thromboxane Synthase Inhibitor ◽  
Synthase Inhibitor

SummaryThe platelet aggregation that occurred in whole blood in response to several aggregating agents (collagen, arachidonic acid, adenosine diphosphate, adrenaline and thrombin) was measured using an Ultra-Flo 100 Whole Blood Platelet Counter. The amounts of thromboxane B2 produced were measured by radioimmunoassay. The effects of various inhibitors of thromboxane synthesis and the effects of apyrase, an enzyme that destroys adenosine diphosphate, were determined.Platelet aggregation was always accompanied by the production of thromboxane B2, and the amounts produced depended on the nature and concentration of the aggregating agent used. The various inhibitors of thromboxane synthesis - aspirin and flurbiprofen (cyclo-oxygenase inhibitors), BW755C (a cyclo-oxygenase and lipoxygenase inhibitor) and dazoxiben (a selective thromboxane synthase inhibitor) - did not markedly inhibit aggregation. Results obtained using apyrase showed that adenosine diphosphate contributed to the aggregation process, and that its role must be acknowledged when devising means of inhibiting platelet aggregation in vivo.

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