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      Platelet serotonin level and its correlation with finger length relation

      research-article
      Indian Journal of Psychiatry
      Medknow Publications
      Finger lengths (4D and 5D), neuroticism, personality, serotonin

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          Abstract

          Background:

          Serotonin is one of the neurotransmitters implicated in normal personality. Many psychobiological models of personality include some dimensions related to serotonin. Moreover, platelets have long been proposed as easily obtainable, neurological models of serotonergic neurons.

          Aim:

          This study was done to examine whether measurement for platelet serotonin could aid as a marker for increased neuroticism trait amongst (arbitrarily named Group C) males and females having the tip of the little fingers below the distal finger mark on the adjacent ring fingers in both their outstretched hands compared to (arbitrarily named Group A) the males and females who have the tip of the little fingers above the distal finger mark on the adjacent ring fingers in both their outstretched hands.

          Materials and Methods:

          Platelet serotonin estimation was done by Elisa Method (LDN, Germany Kit) from randomly selected 48 healthy subjects [24 males (12 males belonging to Group A and 12 belonging to Group C) and 24 females (12 females belonging to group A and 12 females belonging to Group C)].

          Results:

          Preliminary results showed that the platelet serotonin levels were significantly lower (level of significance: 0.05 in t-Test analysis) in Group C males compared to those observed in Group A males and the platelet serotonin levels were also significantly lower (level of significance: 0.05 in t-Test analysis) in Group C females compared to those observed in Group A females.

          Conclusion:

          Thus, it may be inferred that the platelet serotonin may be used as a biochemical marker for increased neuroticism trait in Group C subjects.

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          Most cited references32

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          Central serotonin and impulsive aggression.

          E Coccaro (1989)
          The role of central serotonergic (5-HT) system dysfunction in the regulation of aggression in both animals and man has been investigated for more than the past two decades. Evidence for reduced central 5-HT in the mediation of aggression comes from both behavioural and correlative studies. Functional reduction and augmentation of 5-HT activity is respectively associated with increased and decreased aggression in various animal models of aggression. While similar studies in man have not been performed, strong and consistent associations between indices reflecting reduced pre-synaptic 5-HT activity and aggression have been reported. Evidence of post-synaptic receptor upregulation in the brains of suicide victims has also been reported leaving the functional status 5-HT activity in such patients an open question. However, reduced neuroendocrine (i.e. prolactin) responses to fenfluramine, a 5-HT uptake inhibitor/releaser, which activates both pre- and post-synaptic sides of the 5-HT synapse, strongly suggest that overall central 5-HT activity is reduced in mood and/or personality disorder patients with history of suicidal and/or impulsive aggressive behaviour. Preliminary data with the 5-HT receptor agonist m-chlorophenylpiperazine further suggest that reduced activity of post-synaptic 5-HT receptors may be an important correlate of impulsive aggressive behaviour. Pharmacological agents with potent 5-HT pre- and/or post-synaptic augmenting effects should be tested clinically to determine their efficacy in the treatment of impulsive aggressive behaviour in psychiatric patients.
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            Forced swimming test and fluoxetine treatment: in vivo evidence that peripheral 5-HT in rat platelet-rich plasma mirrors cerebral extracellular 5-HT levels, whilst 5-HT in isolated platelets mirrors neuronal 5-HT changes.

            Low levels of central serotonin (5-HT) have been related to the state of depression, and 5-HT is the major target of the newer antidepressant drugs such as selective serotonin reuptake inhibitors (SSRIs). Neurons and platelets display structural and functional similarities, so that the latter have been proposed as a peripheral model of central functions. In particular, in blood more than 99% of 5-HT is contained in platelets, so that one could consider changes in 5-HT levels in platelets as a mirror of changes in central 5-HT. Here, this hypothesis has been studied via the analysis of the influence of: (1) the forced swimming test (FST, which has been proved to be of utility to predict the clinical efficacy of antidepressants in rodents) and (2) treatment with the SSRI fluoxetine upon 5-HT levels monitored in brain regions and in peripheral platelets by means of electrochemical in vivo and ex vivo measurements. The results obtained confirm that the FST increases immobility; furthermore they show a parallel and significant decrease in cerebral (brain homogenate) and peripheral (in platelet-rich plasma, PRP) voltammetric 5-HT levels following the FST in naive rats. In addition, subchronic treatment with fluoxetine was followed by a significant increase in 5-HT levels in PRP, while the same SSRI treatment performed within the FST resulted in a decrease in the 5-HT levels in PRP. However, this decrease was inferior to that observed without SSRI treatment. These data suggest that there is an inverse relationship between immobility and the levels of 5-HT in PRP and that these peripheral 5-HT levels are sensitive to: (1) the FST, (2) the treatment with fluoxetine and (3) the combination of both treatments, i.e. SSRI + FST. It has been reported that SSRI treatment at first inhibits the 5-HT transporter in brain, resulting in increased extracellular 5-HT, while following sustained SSRI treatments decreased intracellular levels of central 5-HT were observed. Accordingly, the present data show that the initial block of 5-HT reuptake is revealed by the selective increase in 5-HT levels (extracellular content) measured in PRP (not in insulated platelets, IPs) the 1st day of fluoxetine treatment. The initial action of this SSRI upon the 5-HT transporter in brain has also been confirmed by in vivo voltammetric data showing selective increase in the serotonergic signal following local injection of fluoxetine into the brain region studied. Successively, the major effect monitored is a decrease in 5-HT levels, which is more evident in IPs than in PRP. However, it is known that following 2 weeks treatment with an SSRI, 5-HT autoreceptors are desensitized and the serotonin synthesis is restored, together with the intracellular 5-HT levels. The present data showing that the levels of 5-HT in IPs tend to return to control values 12 days after the beginning of chronic fluoxetine treatment suggest that 5-HT levels in IPs (intracellular environment) mirror the influence of SSRI treatment upon the central 5-HT system. On the other hand, at day 12 of the chronic fluoxetine treatment, 5-HT content remains low in PRP. Similarly, low levels of 5-HT have been monitored in brain homogenate of rats chronically treated with fluoxetine. This would support the similarity between PRP preparation and brain homogenate as in both cases cells are disrupted by sample preparation. In conclusion this work supports the literature in proposing platelets as a peripheral model of central functions. In particular, the present data support the idea that peripheral 5-HT platelet levels can reflect the state of the central 5-HT system in conditions of depression. Furthermore, the main outcome of this study is that PRP may mirror central extracellular 5-HT levels, whilst IPs mirror neuronal 5-HT changes.
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              The influence of selective serotonin reuptake inhibitors on human platelet serotonin.

              Clinical depression has been proposed to be an independent risk factor for cardiovascular disease. While it is suggested that selective serotonin reuptake inhibitors (SSRIs) reduce the risk of acute cardiovascular problems of depressed patients, the effect of SSRIs on platelets, the only blood cells committed to serotonin (5-HT) transport, remains largely unknown. The goal of this pilot study was to measure the 5-HT levels in platelets of untreated and SSRI-treated depressed patients and normal subjects and to determine whether the interaction of SSRIs with platelets can explain their possible cardiovascular benefit in patients with depression. Platelet 5-HT was determined by an immunocytochemical assay and high-pressure liquid chromatography with electrochemical detection (HPLC-ECD). In normal control subjects without cardiovascular disease, 78 +/- 8% of platelets were 5-HT-positive (n = 14). Depression caused a significant reduction in platelet 5-HT to 46 +/- 21% in untreated patients (n = 13) and 22 +/- 13% in SSRI-treated patients (n = 14). As a class, all selective serotonin reuptake inhibitors significantly reduced the 5-HT concentration in patient platelets. An inverse relationship of 5-HT level and dose of medication might be suggested. These results correlated well with 5-HT data from HPLC (r = 0.8509, p < 0.001). SSRIs did not affect platelet aggregation and dense granule release in response to thrombin, but significantly reduced ADP-induced platelet aggregation and dense granule release in both patient and normal control samples. The active inhibition of platelet aggregation by SSRIs might explain their cardiovascular benefit.
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                Author and article information

                Journal
                Indian J Psychiatry
                IJP
                Indian Journal of Psychiatry
                Medknow Publications (India )
                0019-5545
                1998-3794
                Oct-Dec 2008
                : 50
                : 4
                : 253-256
                Affiliations
                Department of Psychiatry, Rehmatbai Hospital, 82A Raja Ram Mohan Roy Road, Kolkata - 700 082, India
                Author notes
                Correspondence: Dr. Devasis Ghosh, Department of Psychiatry, Rehmatbai Hospital, 82A Raja Ram Mohan Roy Road, Kolkata - 700 082, India. E-mail: devasisghosh@ 123456hotmail.com
                Article
                IJP-50-253
                10.4103/0019-5545.44746
                2755143
                19823609
                656b80a1-11a6-4085-812d-77f144ca2283
                © Indian Journal of Psychiatry

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Original Article

                Clinical Psychology & Psychiatry
                neuroticism,personality,finger lengths (4d and 5d),serotonin
                Clinical Psychology & Psychiatry
                neuroticism, personality, finger lengths (4d and 5d), serotonin

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