lithium-chloride and Depressive-Disorder

About 30% of people with depression do not respond to an antidepressant at the recommended dose and can be described as having treatment-refractory depression.. To summarise the findings from all randomised controlled trials (RCTs) that have assessed the efficacy of a pharmacological or psychological intervention for treatment-refractory depression.. We used a systematic search strategy to identify RCTs that included adults aged 18-75 years with a diagnosis of unipolar depression that had not responded to a 4-week course of a recommended dose of an antidepressant.. We identified 16 RCTs. None of the included trials assessed the efficacy of psychotherapy. All the trials were too small to detect an important clinical response. We found only two trials on lithium augmentation, which randomised 50 subjects in total.. There is little evidence to guide the management of depression that has not responded to a course of antidepressants. Treatment-refractory depression is an important public health problem and large pragmatic trials are needed to inform clinical practice.

Topics: Antidepressive Agents; Antimanic Agents; Depressive Disorder; Humans; Lithium Chloride; Randomized Controlled Trials as Topic; Research Design

To compare the relative efficacy of electroconvulsive therapy (ECT) in psychotic and nonpsychotic patients with unipolar major depression.. The outcome of an acute ECT course in 253 patients with nonpsychotic (n = 176) and psychotic (n = 77) unipolar major depression was assessed in the first phase of an ongoing National Institute of Mental Health-supported four-hospital collaborative study of continuation treatments after successful ECT courses. ECT was administered with bilateral electrode placement at 50% above the titrated seizure threshold. The remission criteria were rigorous: a score

Topics: Adult; Aged; Antidepressive Agents, Tricyclic; Antimanic Agents; Depressive Disorder; Electroconvulsive Therapy; Electrodes; Female; Humans; Lithium Chloride; Male; Middle Aged; Nortriptyline; Psychiatric Status Rating Scales; Psychotic Disorders; Severity of Illness Index; Treatment Outcome

Most previous studies of long-term maintenance therapy for bipolar illness simply compared proportions of patients experiencing recurrences. This method is inadequate because the length of time until a recurrence is not taken into account and because data from patients who withdraw prematurely from the study without a recurrence are either ignored or analyzed improperly. More appropriate survival analytic techniques were applied to the data from the National Institute of Mental Health Collaborative Study of bipolar patients treated with lithium carbonate, imipramine hydrochloride, or both. An interaction between treatment and the nature of the index episode (the episode that brought the patients into the study) was found. In patients with manic index episodes, both lithium and the combination were superior to imipramine. In patients with depressive index episodes, the combination was significantly superior to imipramine, whereas lithium was indistinguishable from imipramine. The latter finding differs from the original analysis, which found the combination to be no different from the other two treatments for patients with a depressive index episode.

Topics: Actuarial Analysis; Bipolar Disorder; Chlorides; Depressive Disorder; Drug Therapy, Combination; Female; Humans; Imipramine; Lithium; Lithium Chloride; Male; Models, Statistical; Multicenter Studies as Topic; Outcome and Process Assessment, Health Care; Patient Dropouts; Recurrence; Regression Analysis

 To investigate the expression of brain-derived neurotrophic factor(BDNF) and tyrosine kinase B (TrkB) protein in the hippocampus of model rats of comorbid epilepsy and depression.. A rat model of epilepsy was established using lithium chloride.pilocarpine. Among these epileptic rats, those with comorbid depression were selected by a battery of behavioral tests starting on the 14th day after establishing the epilepsy model. A depression group was established by unpredicted chronic mild stress (UCMS) and separate housing. These treatment groups were compared to an untreated control group. Thirteen rats per group were examined by immunofluorescence staining with optical density quantitation to determine the distribution of BDNF- and TrkB-positive cells in the hippocampus and by western blotting to estimate total protein expression levels during the 4th week after establishing the models. Immunofluorescence staining for NeuN was also conducted in hippocampus to evaluate neuronal survival. Depression-like behaviors were also assessed..  Compared to the untreated control group and the epilepsy alone group, the comorbid group exhibited lower average optical densities of BDNF- and TrkB-immunopositive cells as well as lower total BDNF and TrkB protein expression levels (all P = 0.000). The comorbid group exhibited lower behavioral scores compared to all other groups (all P=0.000). Numbers of NeuN-positive cells were lower in the hippocampus of all three experimental groups compared to the untreated control group (all P = 0.000)..  These results suggest that hypofunctional BDNF-TrkB signaling may contribute to depression in epilepsy.. BDNF: Brain-derived neurotrophic factor; TrkB: tyrosine kinase B; UCMS: unpredicted chronic mild stress; PBS: phosphate-buffered saline; HS: Hippocampal sclerosis.

Topics: Animals; Brain-Derived Neurotrophic Factor; Cell Survival; Comorbidity; Depressive Disorder; Disease Models, Animal; Down-Regulation; Epilepsy; Female; Hippocampus; Lithium Chloride; Neurons; Pilocarpine; Random Allocation; Rats, Sprague-Dawley; Receptor, trkB

This study aimed to investigate whether 1-trifluoromethoxyphenyl-3-(1-propionylpiperidin-4-yl) urea (TPPU), a soluble epoxide hydrolase inhibitor with anti-inflammatory effects, could alleviate spontaneous recurrent seizures (SRS) and epilepsy-associated depressive behaviours in the lithium chloride (LiCl)-pilocarpine-induced post-status epilepticus (SE) rat model.. The rats were intraperitoneally (IP) injected with LiCl (127 mg/kg) and pilocarpine (40 mg/kg) to induce SE. A video surveillance system was used to monitor SRS in the post-SE model for 6 weeks (from the onset of the 2nd week to the end of the 7th week after SE induction). TPPU (0.1 mg/kg/d) was intragastrically given for 4 weeks from the 21st day after SE induction in the SRS + 0.1 TPPU group. The SRS + PEG 400 group was given the vehicle (40% polyethylene glycol 400) instead, and the control group was given LiCl and PEG 400 but not pilocarpine. The sucrose preference test (SPT) and forced swim test (FST) were conducted to evaluate the depression-like behaviours of rats. Immunofluorescent staining, enzyme-linked immunosorbent assay, and western blot analysis were performed to measure astrocytic and microglial gliosis, neuronal loss, and levels of soluble epoxide hydrolase (sEH), cytokines [tumour necrosis factor alpha (TNF-α), interleukin (IL)-1β, and IL-6], and cyclic adenosine monophosphate (cAMP)-response element binding protein (CREB).. The frequency of SRS was significantly decreased at 6 weeks and 7 weeks after SE induction in the 0.1TPP U group compared with the SRS + PEG 400 group. The immobility time (IMT) evaluated by FST was significantly decreased, whereas the climbing time (CMT) was increased, and the sucrose preference rate (SPR) evaluated by SPT was in an increasing trend. The levels of sEH, TNF-α, IL-1β, and IL-6 in the hippocampus (Hip) and prefrontal cortex (PFC) were all significantly increased in the SRS + PEG 400 group compared with the control group; neuronal loss, astrogliosis, and microglial activation were also observed. The astrocytic and microglial activation and levels of the pro-inflammatory cytokines in the Hip and PFC were significantly attenuated in the TPPU group compared with the SRS + PEG 400 group; moreover, neuronal loss and the decreased CREB expression were significantly alleviated as well.. TPPU treatment after SE attenuates SRS and epilepsy-associated depressive behaviours in the LiCl-pilocarpine induced post-SE rat model, and it also exerts anti-inflammatory effects in the brain. Our findings suggest a new therapeutic approach for epilepsy and its comorbidities, especially depression.

Topics: Animals; Astrocytes; Brain; Depression; Depressive Disorder; Disease Models, Animal; Epilepsy; Epoxide Hydrolases; Hippocampus; Lithium Chloride; Male; Microglia; Neurons; Phenylurea Compounds; Pilocarpine; Piperidines; Rats; Rats, Sprague-Dawley; Seizures; Status Epilepticus; Tumor Necrosis Factor-alpha

Depression is a common comorbidity in patients with epilepsy with unclear mechanisms. This study is to explore the role of glutamate N-methyl-D-aspartate (NMDA) receptor NR1, NR2A and NR2B subunits in epilepsy-associated depression. Lithium chloride (Licl)-pilocarpine chronic rat epilepsy model was established and rats were divided into epilepsy with depression (EWD) and epilepsy without depression (EWND) subgroups based on forced swim test. Expression of NMDA receptor NR1, NR2A and NR2B subunits was measured by western blot and immunofluorescence methods. The immobility time (IMT) was significantly greater in Licl-pilocarpine model group than in Control group, which was also greater in EWD group than in EWND group. No differences of spontaneous recurrent seizure (SRS) counts over two weeks and latency were found between EWD and EWND groups. The number of NeuN positive cells was significantly less in Licl-pilocarpine model group than in Control group, but had no difference between EWD and EWND groups. The ratios of phosphorylated NR1 (p-NR1)/NR1 and p-NR2B/NR2B were significantly greater in the hippocampus in EWD group than in EWND group. Moreover, the expression of p-NR1 and p-NR2B in the CA1 subfield of hippocampus were both greater in Licl-pilocarpine model group than Control group. Selective blockage of NR2B subunit with ifenprodil could alleviate depression-like behaviours of Licl-pilocarpine rat epilepsy model. In conclusion, glutamate NMDA receptor NR2B subunit was involved in promoting depression-like behaviours in the Licl-pilocarpine chronic rat epilepsy model and might be a target for treating epilepsy-associated depression.

Topics: Animals; Antigens, Nuclear; Chronic Disease; Depressive Disorder; Disease Models, Animal; Epilepsy; Hippocampus; Lithium Chloride; Male; Nerve Tissue Proteins; Neurons; Phosphorylation; Pilocarpine; Rats, Sprague-Dawley; Receptors, N-Methyl-D-Aspartate; Seizures

Changes in brain derived neurotrophic factor (BDNF) expression have been associated with mood disorders and cognitive dysfunction. Transgenic models that overexpress or underexpress BDNF demonstrate similar deficits in cognition and mood. We explored the hypothesis that BDNF expression is controlled by balancing the activity of BDNF promoter IV (BP4) with a negative regulatory region containing a polymorphism associated with cognitive dysfunction and mood disorders.. We used comparative genomics, transgenic mouse production, and magnetofection of primary neurons with luciferase reporters and signal transduction agonist treatments to identify novel polymorphic cis-regulatory regions that control BP4 activity.. We show that BP4 is active in the hippocampus, the cortex, and the amygdala and responds strongly to stimuli such as potassium chloride, lithium chloride, and protein kinase C agonists. We also identified a highly conserved sequence 21 kilobase 5' of BP4 that we called BE5.2, which contains rs12273363, a polymorphism associated with decreased BDNF expression, mood disorders, and cognitive decline. BE5.2 modulated the ability of BP4 to respond to different stimuli. Intriguingly, the rarer disease associated allele, BE5.2(C), acted as a significantly stronger repressor of BP4 activity than the more common BE5.2(T) allele.. This study shows that the C allele of rs12273363, which is associated with mood disorder, modulates BP4 activity in an allele-specific manner following cell depolarization or the combined activity of protein kinase A and protein kinase C pathways. The relevance of these findings to the role of BDNF misexpression in mood disorders and cognitive decline is discussed.

Topics: Alleles; Amygdala; Animals; Brain-Derived Neurotrophic Factor; Cerebral Cortex; Colforsin; Depressive Disorder; Gene Expression Regulation; Genomics; Hippocampus; Humans; Lithium Chloride; Mice; Mice, Transgenic; Phorbol Esters; Polymorphism, Single Nucleotide; Potassium Chloride; Primary Cell Culture; Promoter Regions, Genetic; Protein Kinase C; Rats; Rats, Sprague-Dawley; Signal Transduction

Topics: Adult; Antidepressive Agents; Antimanic Agents; Bipolar Disorder; Depressive Disorder; Female; Humans; Lithium Chloride; Treatment Outcome

Depression represents one of the most common comorbidities of temporal lobe epilepsy (TLE), and has profound negative impact on the quality of life of patients with TLE. However, causes and mechanisms of depression in TLE remain poorly understood, and effective therapies are lacking. We examined whether a commonly used model of TLE in rats could be used as a model of comorbidity between epilepsy and depression suitable for both mechanistic studies and for the development of mechanism-based antidepressant therapies. We established that animals that had been subjected to lithium chloride and pilocarpine status epilepticus (SE) and developed spontaneous recurrent seizures, exhibited a set of impairments congruent with a depressive state: behavioral equivalents of anhedonia and despair, dysregulation of the hypothalamus-pituitary-adrenal (HPA) axis, and compromised raphe-hippocampal serotonergic transmission. Pharmacologic studies have suggested that depressive impairments following SE develop as a result of enhanced interleukin-1beta signaling in the hippocampus, which leads to depression via inducing perturbations in the HPA axis and subsequent deficit in the raphe-hippocampal serotonergic transmission.

Topics: Animals; Convulsants; Depressive Disorder; Disease Models, Animal; Epilepsy, Temporal Lobe; Hippocampus; Humans; Hypothalamo-Hypophyseal System; Interleukin-1beta; Lithium Chloride; Pilocarpine; Pituitary-Adrenal System; Raphe Nuclei; Rats; Receptors, Glucocorticoid; Serotonin; Signal Transduction; Status Epilepticus; Synaptic Transmission

A previous study aimed at revealing the prevalence and determinants of lithium induced polyuria suggested an increased risk of polyuria (urine volume > or =3 L/24 h) in those using serotonergic antidepressants next to lithium.. The objective of our study was to re-evaluate this secondary finding in another study population.. We performed a multicenter medical chart review study in patients using lithium in whom a 24-hour urine volume had been determined.. We included 116 patients, twelve (26%)of the 46 patients with polyuria used serotonergic antidepressants compared to ten (14%) of the 70 patients without polyuria. We found an increased risk of polyuria in lithium users concurrently using serotonergic antidepressants (oddsratio 2.86; 95% confidence interval 1.00-8.21), adjusted for age, gender, use of antiepileptics and thyreomimetics.. Our results confirm the previous secondary finding of an increased risk of polyuria in patients using serotonergic antidepressants next to lithium. Physicians should take this into account when evaluating polyuria in patients using lithium and when choosing an antidepressant in patients using lithium.

Topics: Adolescent; Adult; Antidepressive Agents; Association; Cross-Sectional Studies; Depressive Disorder; Female; Humans; Lithium Chloride; Logistic Models; Male; Middle Aged; Odds Ratio; Polyuria; Treatment Outcome

Mood disorders are the most common psychiatric disorders. Although the mechanisms implicated in the genesis of mood disorders are still unclear, stress is known to predispose to depression, and recently, studies have related hippocampal neurogenesis and apoptosis to depression. In the present study we first examined the balance between cell birth-death in the hippocampus and subventricular zone (SVZ) of pre-pubertal and adult rats subjected to chronic-mild-stress (CMS). CMS led to increased corticosterone secretion and induced depressive-like symptoms (assessed in the forced-swimming test); these endocrine and behavioral effects were paralleled by decreased hippocampal, but not SVZ, cell proliferation/differentiation and by increased apoptotic rate. In order to determine if lithium, a known mood stabilizer with antidepressant properties, could prevent the stress-induced events, we analyzed the same parameters in a group of rats treated with lithium during the stress exposure period (CMS+Li) and observed that the hormonal, behavioral and cell turnover effects of CMS were abrogated in these animals. Subsequently, to search for possible pathways through which CMS and lithium influence behavior, cell fate and synaptic plasticity, we analyzed the expression of glycogen-synthase-kinase-3beta (GSK-3beta), as well as some of its downstream targets (B-cell-CLL/lymphoma2-associated athanonege (BAG-1) and synapsin-I). CMS increased GSK-3beta and decreased synapsin-I and BAG-1 expression in the hippocampus. Interestingly, co-administration of lithium precluded the CMS-induced effects in GSK-3beta, synapsin-I and BAG-1 expression. Our observation that specific inhibition of this kinase with AR-A014418 blocked the effects of CMS in depressive-like behavior and in BAG-1 and synapsin-I expression confirmed the involvement of the GSK-3beta pathway in stress-induced effects. In summary, these results reveal that lithium, by regulating the activity of GSK-3beta, prevents the deleterious effects of stress on behavior and cellular functions.

Topics: Adrenal Glands; Animals; Antimanic Agents; Behavior, Animal; Body Weight; Cell Proliferation; Cell Survival; Corticosterone; Depressive Disorder; Disease Models, Animal; DNA-Binding Proteins; Enzyme Inhibitors; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Hippocampus; Lithium Chloride; Male; Neuronal Plasticity; Neurons; Rats; Rats, Wistar; Stem Cells; Stress, Psychological; Synapsins; Synaptic Transmission; Transcription Factors; Up-Regulation

Circumstantial evidence has suggested that activated microglia may be associated with the pathogenesis of depression. Pro-inflammatory cytokines may also be involved. Therefore, we examined the effects of various types of antidepressants, as well as the mood-stabilizer lithium chloride, on interferon-gamma (IFN-gamma)-induced microglial production of the pro-inflammatory mediators interleukin-6 (IL-6) and nitric oxide (NO). Treatment of the murine microglial 6-3 cells with 100 U/ml of IFN-gamma resulted in an eightfold increase in IL-6 and a tenfold increase in NO into the culture medium. Pretreatment with the selective serotonin reuptake inhibitor fluvoxamine, the relatively selective noradrenaline reuptake inhibitor reboxetine, or the non-selective monoaminergic reuptake inhibitor imipramine, significantly inhibited IL-6 and NO production in a dose-dependent manner. These inhibitions were reversed significantly by SQ 22536, a cyclic adenosine monophosphate (cAMP) inhibitor, and, except for reboxetine, by the protein kinase A (PKA) inhibitor Rp-adenosine3',5'-cyclic monophosphorothioate triethylammonium salt (Rp-3',5'-cAMPS). Lithium chloride, which is believed to act by inhibiting the calcium-dependent release of noradrenaline, had a different spectrum of action on microglial 6-3 cells. It enhanced IFN-gamma-stimulated IL-6 production and inhibited NO production. The inhibitory effect of lithium chloride was not reversed by either SQ 22536 or Rp-3',5'-cAMPS. These results suggest that antidepressants have inhibitory effects on IFN-gamma-activated microglia and these effects are, at least partially, mediated by the cAMP-dependent PKA pathway. On the other hand, the mood stabilizer and anti-manic agent lithium chloride has mixed effects on IFN-gamma-induced microglial activation.

Topics: Animals; Antidepressive Agents; Antimanic Agents; Antiviral Agents; Brain; Cell Line; Cyclic AMP; Cyclic AMP-Dependent Protein Kinase Type II; Cyclic AMP-Dependent Protein Kinases; Depressive Disorder; Dose-Response Relationship, Drug; Enzyme Inhibitors; Interferon-gamma; Interleukin-6; Lithium Chloride; MAP Kinase Signaling System; Mice; Mice, Inbred C57BL; Microglia; Neurotransmitter Uptake Inhibitors; Nitric Oxide; Up-Regulation

Glycogen synthase kinase 3-beta (GSK3B) is a serine/threonine kinase which is directly inhibited by lithium. A -50T/C single nucleotide polymorphism (SNP) localized within the promoter region of the GSK3B gene has previously been shown to be associated with response to lithium prophylaxis in bipolar disorder. This study investigates the association of the GSK3B -50T/C SNP and response to lithium augmentation in acutely depressed antidepressant nonresponders.. Eighty-one patients who had not responded to at least one adequate trial of antidepressant monotherapy underwent a standardized trial of lithium augmentation for up to 8 weeks. We genotyped for the GSK3B -50T/C SNP using polymerase chain reaction and restriction fragment length polymorphism methods and investigated the association with remission.. The allele frequencies in our sample were CC 14.8%, CT 48.2% and TT 37% (no deviation from the Hardy-Weinberg equilibrium). Carriers of the C-allele of the -50T/C SNP showed a significantly better response to lithium augmentation (hazard ratio: 2.70, p = .007), with a mean remission rate of 56.25% after 4 weeks compared to 31% in patients with the TT-genotype (chi(2) = 4.1; p = .04).. Our results support the finding of recent studies demonstrating a superior response of C-allele carriers with bipolar disorder to lithium prophylaxis.

Topics: Adult; Antidepressive Agents; Antimanic Agents; Depressive Disorder; Drug Resistance; Drug Therapy, Combination; Female; Genotype; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Humans; Lithium Chloride; Male; Middle Aged; Polymorphism, Restriction Fragment Length; Polymorphism, Single Nucleotide; Psychiatric Status Rating Scales; Regression Analysis; Survival Analysis

Topics: Depressive Disorder; History, 20th Century; History, 21st Century; Humans; Lithium Chloride; Psychiatry

To study the effectiveness of adding lamotrigine to the treatment of inpatient geriatric patients with bipolar disorder (BD) who were in the depressed phase and had been on lithium and valproate for at least 3 months.. Lamotrigine was started at 25 mg given at bedtime, with weekly incremental increases of 12.5 mg daily until a total dosage of either 75 mg or 100 mg was obtained. Improvement was measured by clinical interview and Hamilton Depression Rating Scale (HDRS) scores. Patients were reassessed at 6 weeks, and if their HDRS score had decreased by at least 50%, they were considered to have improved.. The study group comprised 5 women with an average age of 71.5 years (range 65 to 85). Four had rapid-cycling BD, and 1 had mixed BD. All patients had early age of onset, as judged by their first contact with a psychiatrist or their first hospitalization. The average initial HDRS score was 27 (range 20 to 35). Of the patients, 3 out of the 5 had remission of symptoms, as judged by clinical interview and reduction of their HDRS score by 50%. At 3 months follow-up, these 3 patients had not required rehospitalization and were doing well. Lamotrigine was well tolerated, and none of the patients developed a rash. One patient did develop coarse hand tremor that improved when the lamotrigine dosage was decreased.. Lamotrigine in conjunction with lithium and valproate may be effective in treating geriatric patients with BD and depression.

Topics: Aged; Aged, 80 and over; Antimanic Agents; Bipolar Disorder; Depressive Disorder; Dose-Response Relationship, Drug; Drug Administration Schedule; Drug Therapy, Combination; Female; Humans; Lamotrigine; Lithium Chloride; Male; Triazines; Valproic Acid

The aim of this study was to give further support to the available evidence that mood stabilizers can reduce the risk of antidepressant-induced maniform switch phenomena in bipolar I depressed patients.. Medical records of 158 patients with bipolar I depression were analysed for the incidence of switch phenomena from depression to maniform states (mania and hypomania). The impact of mood stabilizers on reducing the risk of switching was analyzed using logistic regression analyses.. Maniform switches during inpatient treatment were observed in 39 (25%) patients out of the total of 158 patients. Results indicate that especially patients receiving tricyclic antidepressants are at risk of switching to maniform states. This risk was shown to be significantly less when patients also received a mood stabilising medication (lithium, carbamazepine or valproic acid).. This was a retrospective study with patients receiving naturalistic treatment. A prospective, double-blind design would probably lead to more conclusive findings.. Treatment with mood stabilizers may be a potent strategy to reduce the risk of antidepressant-induced maniform switches in bipolar I depressed patients.

Topics: Adult; Aged; Antidepressive Agents, Tricyclic; Antimanic Agents; Bipolar Disorder; Carbamazepine; Depressive Disorder; Female; Humans; Lithium Chloride; Male; Middle Aged; Retrospective Studies; Risk Factors; Treatment Outcome; Valproic Acid

This report describes the presentation of neuroleptic malignant syndrome (NMS) in the primary care setting in an older adult with major depression with psychosis. This patient had been stable on a regimen of amoxapine, lithium carbonate, lorazepam, and benztropine. The patient had rigidity, altered sensorium, diaphoresis, autonomic instability, elevated WBC count and urine myoglobin, and creatine phosphokinase (CPK) reaching 1331 U/I. He was successfully treated with bromocriptine.

Topics: Amoxapine; Antidepressive Agents, Second-Generation; Antimanic Agents; Depressive Disorder; Humans; Lithium Chloride; Male; Middle Aged; Neuroleptic Malignant Syndrome; Psychotic Disorders

Topics: Adolescent; Antidepressive Agents; Antimanic Agents; Child; Conduct Disorder; Depressive Disorder; Ethics, Medical; Female; Humans; Lithium Chloride; Male; Mental Disorders; Mentally Ill Persons; Placebos; Randomized Controlled Trials as Topic; Research Design

A random sample of patients (n = 43) had been investigated to detect any difference in response of bright light therapy in lithium-treated inpatients (n = 18) suffering from depression. Only 27% of the lithium-based inpatients respond to bright light therapy, but 73% of patients respond who were not treated with lithium. We conclude that lithium therapy reduces the chance of achieving t remission of depression by bright light therapy.

Topics: Adult; Antidepressive Agents; Bipolar Disorder; Combined Modality Therapy; Depressive Disorder; Drug Therapy, Combination; Female; Humans; Lithium Chloride; Middle Aged; Phototherapy; Treatment Outcome

In the olfactory-bulbectomised rat model of depression, neutrophil phagocytosis was significantly decreased and phagocytosis started later in comparison to sham-operated animals. Both desipramine and lithium chloride treatment significantly reversed the depressed neutrophil phagocytosis and shortened the time to commencement of phagocytosis in drug-treated bulbectomised rats. The catalase and glutathione peroxidase (GSH-PX) activities in bulbectomised rats were decreased, while superoxide dismutase (SOD) was significantly increased. Chronic desipramine and lithium chloride treatment slightly improved catalase activity in the bulbectomised rats. Desipramine significantly reversed the reduction in activity of GSH-PX, but failed to reverse the increased activity of SOD. In contrast, lithium chloride significantly reversed SOD activity to normal values, without affecting GSH-PX activity in the bulbectomised rats.

Topics: Animals; Depressive Disorder; Desipramine; Disease Models, Animal; Glutathione Peroxidase; Lithium Chloride; Male; Neutrophils; Olfactory Bulb; Phagocytosis; Rats; Rats, Sprague-Dawley; Superoxide Dismutase