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P.2.b.011 Antidepressant therapy and apoptosis of immnocompetent cells in patients with depressive disorders
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P.2.b Affective disorders and antidepressants – Affective disorders (basic)
lower before treatment and approached the value observed within the control group (7.9±4.1 ng/ml) during 6 weeks of treatment with SSRIs. Conclusions: The blunted PRL response to a challenge with a single-dose of buspirone approaches normal value after 6-weeks SSRI treatment independently of clinical response. Our findings support a role for the 5-HT (1A) receptor in the etiology of MD, specifically at the postsynaptic site. References [1] Meltzer HY, Maes M, 1994, Effects of buspirone on plasma prolactin and cortisol levels in major depressed and normal subjects. Biol Psychiatry 35, 316−23. [2] Moeller FG, Steinberg JL, Fulton M, Kramer G, Petty F, 1994, A preliminary neuroendocrine study with buspirone in major depression. Neuropsychopharmacology 10, 75−83. [3] Navines R, Martin-Santos R, Gomez-Gil E, Martinez de Osaba MJ, Luisa Imaz M, Gasto C, 2007, Effects of citalopram treatment on hypothermic and hormonal responses to the 5-HT(1A) receptor agonist buspirone in patients with major depression and therapeutic response. Psychoneuroendocrinology doi:10.1016/j.psyneuen.2007.01.006.
P.2.b.011 Antidepressant therapy and apoptosis of immnocompetent cells in patients with depressive disorders N. Vyalova1 ° , S. Ivanova1 , G. Simutkin1 , V. Semke2 . 1 Mental Health Research Institute, Laborratory of Cellular and MolecularBiological Investigations, Tomsk, Russia; 2 Mental Health Research Institute, Borderline States Department, Tomsk, Russia Introduction: In last years interdisciplinary investigations of psychoneuroimmunomodulation in clinic and therapy of stressrelated mental diseases are topical. Psychological stress and depressive disorder are associated with several immune alterations, including reduced cell proliferation and natural killer cell activity and disturbances of cytokine levels. Psychotropic (antidepressant) medications can be effect on various immune functions, including normal physiological programmed cell death of lymphocytes. Programmed death of cells by apoptosis is regarded as a protective mechanism of organism against an accumulation and spread of defective cells. Apoptosis is a normal physiological programmed cell death that can be enhanced by a variety of external stimuli, such as stress, viral infections, medications and pathological conditions. This phenomenon can be mediated via various pathways that cause condensation of the cytoplasm and chromatin, nuclear fragmentation, and ultimate sequestration of cellular contents into membrane-bound apoptotic bodies. The aim of this investigation was to study apoptosis of immunocompetent cells in the patients with depression in the process of the antidepressant therapy. Methods: We measured apoptosis in the mononuclears lymphocytes (MNLs) of peripheral blood) of 26 patients with depression and in 20 age- and gender-matched controls. The inclusion criterion was depression (diagnosed according to ICD10: F31 – bipolar affective disorder; F32 – depressive episode; F33 – recurrent affective disorder). The exclusion criteria were any other psychiatric disorder or any immunological disorder. The investigation was carried out in dynamics: before the beginning the pharmacotherapy against the background of depressive symptomatology and after the course of medication with selective serotonin re-uptake inhibitors (fluoxetine). We counted number of leukocytes, percent CD95+ lymphocytes and morphological changes characteristic of apoptosis in lymphocytes and neutrophils.
Results and Discussion: We observed significantly increased apoptosis in the MNLs of depressive patients: the percentage of lymphocytes with expression FAS-receptors was 19.47±1.02% (11.64±0.31% in control, p < 0.05). Level of spontaneous apoptosis of neutrophils in smears in patients with depressive disorder before treatment reliably differed from values observed in healthy persons (1.16±0.38% and 0.40±0.15%, respectively, p < 0.01). Also, we demonstrated a significant increase of lymphocytes with morphological changes characteristic of apoptosis (nuclear condensation, vacuolation, and blebbing) in the depressive patients (2.03±0.72% and 0.88±0.18% in control, p < 0.05). The normalisation of CD95+lymphocytes was observed after the conducted treatment with selective serotonin re-uptake inhibitors. After the treatment, number of neutrophils exposed to apoptosis significantly decreased up to 0.59±0.27%. Also, we demonstrated a significant decrease lymphocytes with fragmented nucleus in schizophrenic patients (0.23±0.08% and 0.88±0.18% in control, p < 0.05). Conclusion: Antidepressant therapy have potent immunomodulatory properties, resulting in decreased levels of expressing receptors to Fas-dependent death and apoptosis realization of immunocompetent cells. Our results can explain findings obtained by others that showed reduced NK activity and lower mitogen stimulation in depressed patients. Some of these observations can be attributed to the increased apoptosis in these cells. It is not yet clear whether this tendency could be attributed to a certain subpopulation of the MNLs or to the MNLs in general.
P.2.b.012 Plasma cortisol levels and resilience in depressed patients G. Camardese ° , F. Adamo, L. Mosca, A. Picello, G. Pizi, B. Mattioli, L. Pucci, P. Bria. University of the Sacred Heart, Institute of Psychiatry, Rome, Italy Introduction: In recent years a large body of evidence has emerged linking stressful life events with an increased vulnerability for affective and anxiety disorders. Stressful events often precede the onset of depression and stress has also been associated with the severity of the illness. Meantime there has been growing interest in the concept of resilience. A current theory views resilience as a measure of stress coping ability and its clinical significance may lie in its ability to function as an index of overall mental health. Resilience is a complex notion that incorporates such dimensions as coping mechanism and personality. Several critical factors are associated with a successful adaptation to stressful events: some of these include temperament, personality traits, cognitive factors, genetic traits, and other attribute, such a sense of humour and social support. Existing literature highlights a correlation between PTSD and low resilience. Furthermore, resilience can be used as a measure of treatment outcome in patients suffering of post-traumatic stress. Regarding mood disorders there is a lack of information on the correlation between resilience and treatment outcome. An analysis of the biological mechanisms underlying both resilience and depression shows the implication of common features. Several biochemical mediators of response to extreme stress may be related to resilience or vulnerability, and the release of cortisol may tend to undermine resilience. The present study analyses the correlation between resilience and plasma cortisol levels in depressed patients during treatment.
P.2.b Affective disorders and antidepressants – Affective disorders (basic)
lower before treatment and approached the value observed within the control group (7.9±4.1 ng/ml) during 6 weeks of treatment with SSRIs. Conclusions: The blunted PRL response to a challenge with a single-dose of buspirone approaches normal value after 6-weeks SSRI treatment independently of clinical response. Our findings support a role for the 5-HT (1A) receptor in the etiology of MD, specifically at the postsynaptic site. References [1] Meltzer HY, Maes M, 1994, Effects of buspirone on plasma prolactin and cortisol levels in major depressed and normal subjects. Biol Psychiatry 35, 316−23. [2] Moeller FG, Steinberg JL, Fulton M, Kramer G, Petty F, 1994, A preliminary neuroendocrine study with buspirone in major depression. Neuropsychopharmacology 10, 75−83. [3] Navines R, Martin-Santos R, Gomez-Gil E, Martinez de Osaba MJ, Luisa Imaz M, Gasto C, 2007, Effects of citalopram treatment on hypothermic and hormonal responses to the 5-HT(1A) receptor agonist buspirone in patients with major depression and therapeutic response. Psychoneuroendocrinology doi:10.1016/j.psyneuen.2007.01.006.
P.2.b.011 Antidepressant therapy and apoptosis of immnocompetent cells in patients with depressive disorders N. Vyalova1 ° , S. Ivanova1 , G. Simutkin1 , V. Semke2 . 1 Mental Health Research Institute, Laborratory of Cellular and MolecularBiological Investigations, Tomsk, Russia; 2 Mental Health Research Institute, Borderline States Department, Tomsk, Russia Introduction: In last years interdisciplinary investigations of psychoneuroimmunomodulation in clinic and therapy of stressrelated mental diseases are topical. Psychological stress and depressive disorder are associated with several immune alterations, including reduced cell proliferation and natural killer cell activity and disturbances of cytokine levels. Psychotropic (antidepressant) medications can be effect on various immune functions, including normal physiological programmed cell death of lymphocytes. Programmed death of cells by apoptosis is regarded as a protective mechanism of organism against an accumulation and spread of defective cells. Apoptosis is a normal physiological programmed cell death that can be enhanced by a variety of external stimuli, such as stress, viral infections, medications and pathological conditions. This phenomenon can be mediated via various pathways that cause condensation of the cytoplasm and chromatin, nuclear fragmentation, and ultimate sequestration of cellular contents into membrane-bound apoptotic bodies. The aim of this investigation was to study apoptosis of immunocompetent cells in the patients with depression in the process of the antidepressant therapy. Methods: We measured apoptosis in the mononuclears lymphocytes (MNLs) of peripheral blood) of 26 patients with depression and in 20 age- and gender-matched controls. The inclusion criterion was depression (diagnosed according to ICD10: F31 – bipolar affective disorder; F32 – depressive episode; F33 – recurrent affective disorder). The exclusion criteria were any other psychiatric disorder or any immunological disorder. The investigation was carried out in dynamics: before the beginning the pharmacotherapy against the background of depressive symptomatology and after the course of medication with selective serotonin re-uptake inhibitors (fluoxetine). We counted number of leukocytes, percent CD95+ lymphocytes and morphological changes characteristic of apoptosis in lymphocytes and neutrophils.
Results and Discussion: We observed significantly increased apoptosis in the MNLs of depressive patients: the percentage of lymphocytes with expression FAS-receptors was 19.47±1.02% (11.64±0.31% in control, p < 0.05). Level of spontaneous apoptosis of neutrophils in smears in patients with depressive disorder before treatment reliably differed from values observed in healthy persons (1.16±0.38% and 0.40±0.15%, respectively, p < 0.01). Also, we demonstrated a significant increase of lymphocytes with morphological changes characteristic of apoptosis (nuclear condensation, vacuolation, and blebbing) in the depressive patients (2.03±0.72% and 0.88±0.18% in control, p < 0.05). The normalisation of CD95+lymphocytes was observed after the conducted treatment with selective serotonin re-uptake inhibitors. After the treatment, number of neutrophils exposed to apoptosis significantly decreased up to 0.59±0.27%. Also, we demonstrated a significant decrease lymphocytes with fragmented nucleus in schizophrenic patients (0.23±0.08% and 0.88±0.18% in control, p < 0.05). Conclusion: Antidepressant therapy have potent immunomodulatory properties, resulting in decreased levels of expressing receptors to Fas-dependent death and apoptosis realization of immunocompetent cells. Our results can explain findings obtained by others that showed reduced NK activity and lower mitogen stimulation in depressed patients. Some of these observations can be attributed to the increased apoptosis in these cells. It is not yet clear whether this tendency could be attributed to a certain subpopulation of the MNLs or to the MNLs in general.
P.2.b.012 Plasma cortisol levels and resilience in depressed patients G. Camardese ° , F. Adamo, L. Mosca, A. Picello, G. Pizi, B. Mattioli, L. Pucci, P. Bria. University of the Sacred Heart, Institute of Psychiatry, Rome, Italy Introduction: In recent years a large body of evidence has emerged linking stressful life events with an increased vulnerability for affective and anxiety disorders. Stressful events often precede the onset of depression and stress has also been associated with the severity of the illness. Meantime there has been growing interest in the concept of resilience. A current theory views resilience as a measure of stress coping ability and its clinical significance may lie in its ability to function as an index of overall mental health. Resilience is a complex notion that incorporates such dimensions as coping mechanism and personality. Several critical factors are associated with a successful adaptation to stressful events: some of these include temperament, personality traits, cognitive factors, genetic traits, and other attribute, such a sense of humour and social support. Existing literature highlights a correlation between PTSD and low resilience. Furthermore, resilience can be used as a measure of treatment outcome in patients suffering of post-traumatic stress. Regarding mood disorders there is a lack of information on the correlation between resilience and treatment outcome. An analysis of the biological mechanisms underlying both resilience and depression shows the implication of common features. Several biochemical mediators of response to extreme stress may be related to resilience or vulnerability, and the release of cortisol may tend to undermine resilience. The present study analyses the correlation between resilience and plasma cortisol levels in depressed patients during treatment.