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I. H. Gotlib and C.L. Hammen's (1992) psychopathology model of depression was used as a conceptual framework for studying the process of change in an effective course of cognitive therapy (CT) for depression. Archived CT transcripts from 30 depressed outpatients in the Cognitive-Pharmaco-therapy Treatment project (S. D. Hollon et al., 1992) were studied. An observational coding system was used to assess whether therapists focused on the cognitive, interpersonal, and developmental vulnerabilities of depression and whether these interventions were associated with symptom reduction. Therapists maintained a primarily cognitive focus, but it was interventions that addressed the interpersonal and developmental domains that were associated with improvement. A developmental focus also predicted a longer time of recovery and better global functioning over the 24-month followup period. These findings are consistent with recent theoretical developments in cognitive therapy and with the psychopathology research on depression.
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The influence of pregnenolone-16 alpha-carbonitrile (PCN) upon the biliary and urinary excretion of unchanged imipramine and some of its metabolites was investigated in female rats. The substrate and its metabolites were identified and quantified by thin-layer chromatography and/or gas-liquid chromatography. PCN augmented urinary excretion of desipramine and the imipramine- and desipramine-glucuronides. PCN pretreatment also diminished the urinary elimination of imipramine N-oxide whereas proadifen hydrochloride had an inverse effect, suggesting a shift in the metabolic pathways of imipramine. The biliary excretion of the imipramine and desipramine glucuronides was not significantly altered by PCN.
Given the absence of high quality evidence and the inability to draw firm conclusions based on that evidence, the use of SAMe for the treatment of depression in adults should be investigated further. Future trials should be in the form of large randomised controlled clinical trials of high methodological quality, with particular attention given to randomisation, allocation concealment, blinding and the handling of missing data. Comparator antidepressants from all classes should be used. Adverse events should be detailed for each participant, bearing in mind that induction of mania is of particular interest.
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The aim of the study was to investigate the influence of selected antidepressants and neuroleptics on the protein level and activity of cytochrome P450 2D (CYP2D) in rat brain. The obtained results showed that imipramine, fluoxetine, nefazodone, thioridazine and perazine, added to brain microsomes of control rats, inhibited CYP2D activity to a lower extent (K(i)=255-485μM) than when added to liver microsomes (K(i)=1-45μM), which may result from their stronger affinity for liver CYP2D2 (K(i)=2.7 and 1.25μM for imipramine and fluoxetine, respectively) than for brain CYP2D4 (K(i)=25 and 10μM for imipramine and fluoxetine, respectively), as well as from their high non-specific binding in brain microsomes. Two-week treatment with fluoxetine evoked decreases in the level and activity of CYP2D in the striatum and the nucleus accumbens. In contrast, fluoxetine increased CYP2D expression in the cerebellum, while nefazodone considerably enhanced the activity (but not the protein level) of CYP2D in the truncus cerebri. Imipramine and mirtazapine (active in the liver) did not affect brain CYP2D. Chronic thioridazine decreased CYP2D activity in the substantia nigra and nucleus accumbens, but significantly increased that activity in the striatum and cerebellum. Clozapine significantly enhanced CYP2D activity in the truncus cerebri. In conclusion, psychotropics influence CYP2D in the brain, but their effect is different than in the liver and depends on the cerebral structure. The observed psychotropics-brain CYP2D interactions may be important for the metabolism of neurosteroids and monoaminergic neurotransmitters, and for the local biotransformation of drugs.
Imipramine was taken up by rat cerebellar neurons in primary culture. The process was dependent on time, temperature and pH and was reduced in the presence of the adenosine triphosphatase (ATPase) inhibitor dicyclohexylcarbodiimide or in the absence of glucose. Uptake approached saturation at 100 microM imipramine where approximately 42 nmol of the drug accumulated intracellularly per mg cell protein. Propranolol, but not serotonin, competed for imipramine uptake and uptake was inhibited by the 'lysosomotropic' amine chloroquine and by the Na+/H+ ionophore monensin, both of which dissipate proton gradients. Neurons were fractionated on Percoll gradients and the fractions exposed to [3H]imipramine. MgATP-dependent accumulation of [3H]imipramine was found mainly in fractions enriched for dense lysosomes. We conclude that imipramine was taken up by cerebellar neurons in primary culture and accumulated at high concentrations in intracellular compartments.
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We used positron emission tomography to monitor the distribution of radioactivity in dog brain and muscle following i.v. administration of 11C-labelled antipyrine, imipramine, and quinidine. Twenty-five sequential scans of a transaxial slice of the head were performed within 90 min; radioactivity in plasma was measured in a gamma-counter. Following i.v. injection of [11C]antipyrine (50 mg kg-1; 9-68 mCi; n = 10), the decay of plasma activity was accompanied by rapid uptake in brain and variable uptake in muscle, immediately followed by a redistribution leading to equalization of the radioactivity in the tissues. Administration of [11C]imipramine (4 mg kg-1; 30-110 mCi; n = 8) was followed by a rapid build-up of a sustained gradient between high brain, and low plasma and muscle radioactivity. After i.v. injection of [11C]quinidine (1 mg kg-1; 11-87 mCi; n = 10), radioactivity in brain was low, with higher activity in plasma and muscle throughout the experiment. Positron emission tomography thus revealed for each drug a distinct pattern of distribution consistent with established properties of the compounds. This technique seems promising for the study of early drug distribution, notwithstanding certain limitations.
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Fluoxetine administered intraperitoneally to sham-operated or adrenalectomized/castrated (ADX/CX) male rats dose-dependently (2.9-58 mumol/kg i.p.) increased the brain content of the neurosteroid 3 alpha-hydroxy-5 alpha-pregnan-20-one (allopregnanolone, 3 alpha, 5 alpha-TH PROG). The increase of brain 3 alpha, 5 alpha-TH PROG content elicited by 58 mumol/kg fluoxetine lasted more than 2 hr and the range of its extent was comparable in sham-operated (approximately 3-10 pmol/g) and ADX/CX rats (2-9 pmol/g) and was associated with a decrease (from 2.8 to 1.1 pmol/g) in the 5 alpha-pregnan-3,20-dione (5 alpha-dihydroprogesterone, 5 alpha-DH PROG) content. The pregnenolone, progesterone, and dehydroepiandrosterone content failed to change in rats receiving fluoxetine. The extent of 3 alpha, 5 alpha-TH PROG accumulation elicited by fluoxetine treatment differed in various brain regions, with the highest increase occurring in the olfactory bulb. Importantly, fluoxetine failed to change the 3 alpha, 5 alpha-TH PROG levels in plasma, which in ADX/CX rats were at least two orders of magnitude lower than in the brain. Two other serotonin re-uptake inhibitors, paroxetine and imipramine, in doses equipotent to those of fluoxetine in inhibiting brain serotonin uptake, were either significantly less potent than fluoxetine (paroxetine) or failed to increase (imipramine) 3 alpha, 5 alpha-TH PROG brain content. The addition of 10 microM of 5 alpha-DH PROG to brain slices of ADX/CX rats preincubated with fluoxetine (10 microM, 15 min) elicited an accumulation of 3 alpha, 5 alpha-TH PROG greater than in slices preincubated with vehicle. A fluoxetine stimulation of brain 3 alpha, 5 alpha-TH PROG biosynthesis might be operative in the anxiolytic and antidysphoric actions of this drug.
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The effects of captopril, an inhibitor of angiotensin-converting enzyme, on sinus rate and atrial contraction were investigated in 10 isolated dog atria and in 3 intact anesthetized donor dogs. Captopril (10-1,000 micrograms) caused an increase in heart rate and the development of atrial contractile tension when injected into the sinus node artery of the isolated atrium perfused with arterial blood of the anesthetized dog. At extremely high doses (1-3 mg), captopril produced brief negative effects followed by positive ones. The positive effects were completely blocked by 10 micrograms of propranolol, after which the negative ones became more evident. The positive effects were also significantly suppressed by 30 micrograms of imipramine, whereas the negative ones were not influenced by treatment with atropine. In all 3 cases when captopril (0.3 mg/Kg) was administered intravenously to donor dogs, the blood pressure decreased and a slight tachycardia usually appeared. In contrast, no significant change was observed in sinus rate and contractile tension of isolated atria. Thus, it is concluded that only at extremely high doses does captopril cause a release of catecholamine by a tyramine-like action which may have a slight depressive action on the sinus node and contractility.
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A significant percentage of psychiatric patients who are treated with antipsychotics are treated with more than one antipsychotic drug in the clinic. Thus, it is advantageous to use a rapid and reliable assay that is suitable for determination of multiple antipsychotic drugs in plasma in a single run. A simple and sensitive HPLC-UV method was developed and validated for simultaneous quantification of olanzapine, haloperidol, chlorpromazine, ziprasidone, risperidone and its active metabolite 9-hydroxyrisperidone in rat plasma using imipramine as an internal standard (I.S.). The analytes were extracted from rat plasma using a single step liquid-liquid acid solution back extraction technique with wash procedure, which provided the very clear baseline for blank plasma extraction. The compounds were separated on an Agilent Eclipse XDB C8 (150 mm x 4.6 mm i.d., 5 microm) column using a mobile phase of acetonitrile/30 mM ammonium acetate including 0.05% triethylamine (pH 5.86 adjusted with acetic acid) with gradient elution. All of the analytes were monitored using UV detection. The method was validated and the linearity, lower limit of quantitation (LLOQ), precision, accuracy, recoveries, selectivity and stability were determined. The LLOQ was 2.0 ng/ml and correlation coefficient (R(2)) values for the linear range of 2.0-500.0 ng/ml were 0.998 or greater for all the analytes. The precision and accuracy for intra-day and inter-day were better than 7.44%. The recovery was above 74.8% for all of the analytes. This validated method has been successfully used to quantify the plasma concentration of the analytes for pharmacological and toxicological studies following chronic treatment with antipsychotic drugs in the rat.
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Imipramine is a tricyclic antidepressant that has been demonstrated to be useful in the treatment of certain voiding dysfunctions. Imipramine has a variety of pharmacological effects including direct antimuscarinic activity, inhibition of catecholamine reuptake, direct muscle relaxant, and calcium antagonism. Using the in-vitro whole bladder model we have studied the effect of imipramine on the rate and magnitude of both intravesical pressure generation and bladder emptying in response to field stimulation. The results can be summarized as follows: at concentrations as low as 1 mumol/l imipramine causes a significant inhibition of volume expulsion without significantly affecting pressure generation. Imipramine produced a dose-dependent inhibition of both pressure development and percent volume emptying; however, it was substantially more potent in inhibiting the ability of the bladder to empty than to generate pressure.
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The present study examined the effect of combined exposure to repeated challenge using low doses of lipopolysaccharide (LPS) and chronic mild stress (CMS) together. This combined exposure is thought to expose the animals to more realistic challenges, testable on different levels (behavioral, neurochemical, immunohistochemical and gene expression). The role of glial cells was examined, as well. Additionally, the effects of chronic administration of the tricyclic antidepressant imipramine and the anti-TNF-α pentoxyphylline were investigated.
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Too often, providers reassure patients of a healthy heart because of normal coronary arteries despite persistent chest pain and ST segment changes on the electrocardiogram. Chest pain, one of the primary signs and symptoms of CSX, can be reduced through common medications and interventions if the diagnosis of CSX is initiated.
There is accumulating evidence suggesting that depression is a risk factor for cardiovascular diseases. This study aimed to examine the hypothesis that the proinflammatory cytokine TNF-α would partially explain the link between depression and atherosclerotic endothelial changes. Rats were distributed among 6 groups: (i) control group; (ii) group subjected to chronic mild stress (CMS); (iii) group fed a cholesterol-cholic acid-thiouracil (CCT diet); and (iv) CMS group fed the CCT diet and treated with the vehicle for 8 weeks. The last 2 groups were subjected to CMS-CCT and received thalidomide (THAL) or imipramine (IMIP). Rats were assessed behaviorally (sucrose preference, open field, and forced-swimming tests). TNF-α protein was assessed from the serum, aorta, and liver. Aortic TNF-α gene expression (assessed using RT-PCR), serum lipid profile, and insulin levels were measured. Endothelial function was assessed in isolated aortic rings. The THAL and IMIP groups showed ameliorated CMS-CCT-related behavioral changes. CMS-CCT-induced metabolic and endothelial dysfunctions were improved in the THAL group but were worsened in the IMIP group. RT-PCR showed a significant reduction of aortic TNF-α mRNA expression in the THAL and IMIP treatment groups. These data paralleled the findings for aortic immunohistochemistry. The THAL group, but not the IMIP group, showed improved CMS-CCT-induced changes in the vascular reactivity of the aortic rings. Thus, TNF-α provides a target link between depression, metabolic syndrome, and endothelial dysfunction. This could open a new therapeutic approach to address the comorbidities of depression.
Delusion of parasitosis is a rare condition in which the patient has a strong conviction that he or she is infested by small organisms. The condition may exist as an isolated phenomenon, or may occur in association with other psychiatric syndromes. We report a single case of a rare form of this phenomenon. A middle-aged woman who met forth edition of diagnostic and statistical manual of mental disorders criteria for major depressive disorder with psychotic features is described. She had delusions of oral parasitosis. She felt lizards and small organisms in her mouth. To the best of our knowledge, there has been only one previous report of delusions of oral parasitosis to date. We discuss the interesting aspects of this case.
One hundred ninety-five patients in a primary care practice were screened with the National Institute of Mental Health Diagnostic Interview Schedule, a structured psychiatric interview, so that the epidemiology of panic disorder could be studied. Thirteen percent of the patients met criteria described in the Diagnostic and Statistical Manual of Mental Disorders, ed 3 (DSM-III) for panic disorder (6.7 percent if the DSM-III exclusionary criteria are used). An additional 8.7 percent of patients, labeled in the study as having simple panic, had four or more autonomic symptoms of panic disorder but did not meet DSM-III criteria (three panic attacks in a three-week period). Compared with controls, patients with panic disorder or simple panic had a significantly higher lifetime risk of major depression, multiple phobias, and avoidance behavior and higher scores on their psychological distress scales. Patients with panic disorder and simple panic often misinterpreted their symptoms as being due to a physical illness and had significantly higher scores on the somatization scale of the SCL-90 and on a medical review of symptoms than did the controls with no panic disorder. It is important to diagnose panic disorder accurately because double-blind placebo-controlled studies have demonstrated the efficacy of psychopharmacologic treatments, including tricyclic antidepressants (notably imipramine and desipramine), the high-potency benzodiazepine (alprazolam) and monoamine oxidase inhibitors (phenelzine). Primary care physicians, by screening patients with complaints of tension and anxiety, as well as multiple unexplained somatic complaints for panic disorder, may be able to reduce somatic preoccupation and disease phobia by instituting effective therapy.
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Platelet 3H-imipramine binding values from 45 normal controls and 20 depressed subjects were collected over a 2-year period. During this time, wide inter-individual variations in the affinity constant (Kd) and maximal number of binding sites (Bmax) were observed in the control population; however, we failed to observe a seasonal change in platelet 3H-imipramine binding. The Kd and Bmax values of depressed subjects were not significantly different from those of controls.
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The acute and subchronic effects of two dosages of a new serotonergic antidepressant, nefazodone, and those of the tricyclic imipramine were examined in a double-blind, crossover, placebo-controlled study. Twenty-four healthy subjects from two age groups (12 adults and 12 elderly from both sexes) received the four treatments (nefazodone, 100 and 200 mg twice daily; imipramine, 50 mg twice daily; and placebo) for 7 days with a 7-day washout period. Measurements were performed after the morning doses on day 1 and day 7. These included a standard over-the-road highway driving test, a psychomotor test battery, and sleep latency tests. Blood samples were taken on both days and analyzed to determine concentrations of parent drugs and their major metabolites. The main results showed that the reference drug, imipramine, had a detrimental effect after a single dose on lateral position control in the driving test, primarily in the adult group, that diminished after repeated dosing. Minor impairment on psychomotor test performance was found with both days. On the other hand, a single administration of both doses of nefazodone did not impair highway driving performance (even showed some improvement) and had no or only minor effects on psychomotor performance. After repeated dosing, nefazodone 200 mg twice daily (but not the 100-mg dose) produced slight impairment of lateral position control; dose-related impairment of cognitive and memory functions was found. The effects of nefazodone were generally in the same direction in both age groups. Significant correlations were found between steady-state concentrations of nefazodone in plasma (200-mg, twice-daily condition) as well as imipramine, and reaction time changes in a memory scanning task. Neither drug appeared to induce daytime sleepiness as measured by the sleep latency tests.
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There are multiple pathways by which individuals begin to emerge from depression; these pathways can be identified empirically. Variables from diverse psychobiologic domains can be used to predict which persons are likely to advance along which trajectories toward recovery.
We aimed to assess the effect of three drugs belonging to amphiphilic cations, imipramine, amitriptyline and propranolol, on lipid synthesis and intracellular calcium homeostasis in glioma C6 cells. Antidepressants, imipramine and amitriptyline, had a stimulatory effect on [14C]serine incorporation into phosphatidylserine. Similar effect was induced by propranolol, antidysrhythmic drug and an antagonist of beta-adrenergic receptor, but not by isoproterenol, a selective agonist of this receptor. Stimulation of serine base-exchange activity by amphiphilic cations occured at concentration as low as 5-25 microM that may be reached during clinical treatment. At much higher concentration (250 microM), those drugs also stimulated phospholipase D-mediated synthesis of [14C]phosphatidylethanol and blocked phorbol ester-induced, protein kinase C-dependent phospholipase D activity. The latter effect already occurred at low (25 microM) concentration of drugs. We have also shown that treatment of the cells with amphiphilic cations (1 mM) produced only a weak increase in the intracellular Ca2+ concentration and did not affect Ca2+ release from the intracellular stores evoked by nucleotide receptor agonists, ATP and ADP. In contrast, this treatment strongly diminished an unspecific leak of Ca2+ from the endoplasmic reticulum caused by thapsigargin and ionomycin. Mianserin, which is not cationic amphiphilic drug, did not affect phosphatidylserine synthesis and phospholipase D activity and produced heterogenous and chaotic Ca2+ responses. Our results suggest that imipramine, amitriptyline and propranolol may modulate lipid synthesis and intracellular calcium signaling independently of their action on membrane receptors, most probably by modification of the physicochemical properties of cell membranes.
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An Amberlite XAD-2 (XAD2) and titanium dioxide nanoparticles (TNPs) modified glassy carbon paste electrode (XAD2-TNP-GCPE) was developed for the determination of imipramine (IMI), trimipramine (TRI) and desipramine (DES). The electrochemical behavior of these molecules was investigated employing cyclic voltammetry (CV), chronocoulometry (CC), electrochemical impedance spectroscopy (EIS) and adsorptive stripping differential pulse voltammetry (AdSDPV). After optimization of analytical conditions using a XAD2-TNP-GCPE electrode at pH 6.0 phosphate buffer (0.1 M), the peak currents were found to vary linearly with its concentration in the range of 1.30 × 10(-9) to 6.23 × 10(-6) M for IMI, 1.16 × 10(-9) to 6.87 × 10(-6) M for TRI and 1.43 × 10(-9) to 5.68 × 10(-6) M for DES. The detection limits (S/N = 3) of 3.93 × 10(-10), 3.51 × 10(-10) and 4.35 × 10(-10) M were obtained for IMI, TRI and DES respectively using AdSDPV. The prepared modified electrode showed several advantages such as a simple preparation method, high sensitivity, very low detection limits and excellent reproducibility. The proposed method was employed for the determination of IMI, TRI and DES in pharmaceutical formulations, blood serum and urine samples.
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We assessed the functional expression of the norepinephrine (NE) transporter (NET) in cultured rat cortical astrocytes. Specific [3H]NE uptake increased in a time-dependent manner, and this uptake involves temperature- and Na+-sensitive mechanisms. The Na+-dependent [3H]NE uptake was saturable, and the Km for the process was 539.3 +/- 55.4 nm and the Vmax was 1.41 +/- 0.03 pmol/mg protein/min. Ouabain, a Na+-K+ ATPase inhibitor, significantly inhibited Na+-dependent [3H]NE uptake. The selective NE uptake inhibitor nisoxetine, the tricyclic antidepressants desipramine and imipramine, and the serotonin and NE reuptake inhibitor (SNRI) milnacipran very potently inhibited Na+-dependent [3H]NE uptake. On the other hand, GBR-12935 (a selective dopamine uptake inhibitor), fluvoxamine (a selective serotonin reuptake inhibitor), venlafaxine (a SNRI) and cocaine had weaker inhibitory activities. RT-PCR demonstrated that astrocytes expressed mRNA for the cloned NET protein, which was characterized as neuronal NET. Western blots indicated that anti-NET polyclonal antibody recognized a major band of 80 kDa in astrocytes. These data indicate that the neuronal NET is functionally expressed in cultured rat astrocytes. Glial cells may exert significant control of noradrenergic activity by inactivating NE that escapes neuronal re-uptake in sites distant from terminals, and are thus cellular targets for antidepressant drugs that inhibit NE uptake.
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The special extract of St. John's wort, LI 160, exhibited a superior antidepressant efficacy compared to placebo in several controlled trials. Two further trials demonstrated a similar reduction of depressive symptomatology under LI 160 compared to tricyclics. All these trials were performed in mildly to moderately depressed patients. The present investigation was a randomized, controlled, multicentre, 6-week trial comparing 1800 mg LI 160/die to 150 mg imipramine/die in severely depressed patients according to ICD-10. The main efficacy parameter, a reduction of the total score of the Hamilton Depression Scale, proved both treatment regimens very effective at the end of the 6 week treatment period (mean values 25.3 to 14.5 in the LI 160 group and 26.1 to 13.6 in the imipramine group), but not statistically equivalent within a a-priori defined 25% interval of deviation. The analysis of subgroups with more than a 33% and 50% reduction of the HAMD total score justified the assumption of equivalence within a 25% deviation interval. This view was also supported by the global efficacy ratings from patients and investigators. Regarding adverse events, the nonrejection of the nonequivalence hypothesis denotes a superiority of the herbal antidepressant. These main result indicate that LI 160 might be a treatment alternative to the synthetic tricyclic antidepressant imipramine in the majority of severe forms of depressions. However, more studies of this type must be performed before a stronger recommendation can be made.
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The effects of chronic antidepressant (AD) administration (amitryptiline 12 mg/Kg i.p., 20 days) on cerebral cortical [3H] imipramine binding sites were examined in control rats and in serotonergic denervated animals. Both treatments independently reduced the density of [3H] imipramine binding sites by 33-40%. Animals submitted to both treatments showed a slightly higher decrease in the Bmax (-50%). No alterations were observed in the apparent dissociation constant. Preincubation of cerebral cortical synaptosomal membranes with Triton X-100 (0.2% v/v), which preferentially dissolves the presynaptic component of the synaptosomes, reduced by 40% the maximal number of [3H] imipramine binding sites in control rats. In chronic AD treated rats or in serotonergic lesioned rats, membranes preincubated with Triton X-100 showed a 30% decrease in the number of [3H] imipramine sites in comparison to the sham group. The combination of both treatments produced an even larger decrease in the density of [3H] imipramine binding sites in Triton X-100 treated membranes (-55%) compared to the sham group. Taken together, these results strongly suggest that cerebral cortical [3H] imipramine binding sites located both pre- and postsynaptically, are down regulated by the long term AD administration independently of the integrity of the central serotonergic system.
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The relationship between social support, depressive symptoms and the maximal binding capacity of [3H]imipramine (Bmax) in platelets was examined in medical students during and after a period of examination stress. There was a positive correlation between the students' perception of their social support and [3H]imipramine Bmax values during examinations, and their perception of social support contributed significantly to the prediction of Bmax by depressive symptomatology. The results suggest that psychosocial factors may be associated with alterations in serotonergic neurotransmission, rendering an individual more physiologically vulnerable to psychological disturbances.
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The effect of dopamine (DA) agonists (apomorphine, quinpirole) and three antidepressants (selegiline, nomifensine, imipramine), given in a single dose, on the electric footshock-induced fighting behavior was investigated in the control and chronically stressed rats. It was found that 48 h after the last session of chronic stress (various stressors applied for 16 days) the number of shock-induced fighting attacks was reduced by 50-70% in comparison with the control value. The drugs (except for imipramine), given in a single dose, 48 h after the last session of chronic stress, increased the number of fighting attacks and restored it to the control or above the control value. The same drugs at doses used, changed neither the intensity of fighting in the control (unstressed) rats nor the exploratory activity in both groups of animals. It is concluded that the short-lasting dopaminergic activation facilitates the aggressiveness reduced by chronic stress and that this effect does not depend on the locomotor activity level.