Depression-Like Adult Behaviors may be a Long-Term Result of Experimental Pneumococcal Meningitis in Wistar Rats Infants.

Pneumococcal meningitis is a life-threatening infection of the central nervous system (CNS) with a high mortality rate. In addition to causing severe neurological sequelae infectious diseases of the CNS can play a significant role in the pathogenesis of neuropsychiatric disorders. In this study infant Wistar rats, postnatal day 11, received intracerebroventricular (i.c.v.) either artificial cerebrospinal fluid (CSF) or a Streptococcus pneumoniae suspension to a concentration of 1 × 106 colony-forming units (CFU). 18 h later animals received antibiotic treatment as usual during 7 days. On postnatal day 46, the animals received imipramine intraperitoneal (i.p.) or sterile NaCl during 14 days (postnatal days 46-60). Then, on postnatal days 59-60 we evaluated the consumption of sweet food (an index of anhedonia). On postnatal day 60 the animals were submitted to the forced swimming task. 60 min after this task the animals were decapitated and the blood was collected to evaluate adrenocorticotropic hormone (ACTH) and corticosterone. Immediately after blood collection the hippocampus was removed to evaluate brain-derived neurotropic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF). The meningitis group exhibited depressive-like behavior as evidenced by decreased sucrose intake and increased immobility time in the forced swimming task, and BDNF and GDNF decrease in the hippocampus. ACTH levels were increased in the blood. Imipramine treatment reversed depressive-like behaviors, re-established hippocampal BDNF and GDNF expression, and normalized ACTH levels in the blood. Here we demonstrate that meningitis during early life period can trigger depressive-like behavior in adult life of rats.

Folic acid prevented cognitive impairment in experimental pneumococcal meningitis.

Streptococcus pneumoniae is a common cause of bacterial meningitis, with a high mortality rate and neurological sequelae. In contrast, folic acid plays an important role in neuroplasticity and the preservation of neuronal integrity. In the present study, we evaluated the influence of folic acid on memory, oxidative damage, enzymatic defence, and brain-derived neurotrophic factor (BDNF) expression in experimental pneumococcal meningitis. In animals that received folic acid at a dose of 10 or 50 mg, there was a reduction in both crossing and rearing during an open-field task compared with the training session, demonstrating habituation memory. During a step-down inhibitory avoidance task, there was a difference between the training and the test sessions, demonstrating aversive memory. In the hippocampus, BDNF expression decreased in the meningitis group; however, adjuvant treatment with 10 mg of folic acid increased BDNF expression, decreased lipid peroxidation, protein carbonylation, nitrate/nitrite levels, and myeloperoxidase activity and increased superoxide dismutase activity. In frontal cortex adjuvant treatment with 10 mg of folic acid decreased lipid peroxidation and protein carbonylation. There is substantial interest in the role of folic acid and related pathways in nervous system function and in folic acid's potential therapeutic effects. Here, adjuvant treatment with vitamin B9 prevented memory impairment in experimental pneumococcal meningitis.

DARPP-32 expression in rat brain after electroconvulsive stimulation.

Although electroconvulsive therapy (ECT) has been used as a treatment for mental disorder since 1930s, little progress has been made in the mechanisms underlying its therapeutic or adverse effects. The aim of this work was to analyze the expression of DARPP-32 (a protein with a central role in dopaminergic signaling) in striatum, cortex, hippocampus and cerebellum of Wistar rats subjected to acute or chronic electroconvulsive stimulation (ECS). Rats were submitted to a single stimulation (acute) or to a series of eight stimulations, applied one every 48 h (chronic). Animals were killed for collection of tissue samples at time zero, 0.5, 3, 12, 24 and 48 h after stimulation in the acute model and at the same time intervals after the last stimulation in the chronic model. Our results indicated that acute ECS produces smaller changes in the expression of DARPP-32 but, interestingly, chronic ECS increased transient expression of DARPP-32 in several time frames, in striatum and hippocampus, after the last stimulation. Results on the expression of proteins involved in signaling pathways are relevant for neuropsychiatric disorders and treatment, in particular ECT, and can contribute to shed light on the mechanisms related to therapeutic and adverse effects.

Lithium and valproate act on the GSK-3ß signaling pathway to reverse manic-like behavior in an animal model of mania induced by ouabain.

The present study aimed to investigate the effects of mood stabilizers, specifically lithium (Li) and valproate (VPA), on the PI3K/Akt signaling pathway in the brains of rats subjected to the ouabain (OUA)-induced animal model of mania. In addition, the effects of AR-A014418, a GSK-3ß inhibitor, on manic-like behavior induced by OUA were evaluated. In the first experimental protocol Wistar rats received a single ICV injection of OUA or artificial cerebrospinal fluid (aCSF). From the day following ICV injection, the rats were treated for 6 days with intraperitoneal injections of saline, Li or VPA twice a day. In the second experimental protocol, rats received OUA, aCSF, OUA plus AR-A014418, or aCSF plus AR-A014418. On the 7th day after OUA injection, locomotor activity was measured using the open-field test. In addition, we analyzed the levels of p-PI3K, p-MAPK, p-Akt, and p-GSK-3ß in the brain of rats by immunoblot. Li and VPA reversed OUA-related hyperactivity. OUA decreased p-PI3K, p-Akt and p-GSK-3ß levels. Li and VPA improved these OUA-induced cellular dysfunctions; however, the effects of the mood stabilizers were dependent on the protein and brain region analyzed. In addition, AR-A014418 reversed the manic-like behavior induced by OUA. These findings suggest that the manic-like effects of ouabain are associated with the activation of GSK-3ß, and that Li and VPA exert protective effects against OUA-induced inhibition of the GSK-3ß pathway.

Intracerebral Administration of BDNF Protects Rat Brain Against Oxidative Stress Induced by Ouabain in an Animal Model of Mania.

Several studies have suggested that alterations in brain-derived neurotrophic factor (BDNF) and increased oxidative stress have a central role in bipolar disorder (BD). Intracerebroventricular (ICV) injection of ouabain (OUA) in rats alters oxidative stress parameters and decreases BDNF levels in the brain. In this context, the present study aims to investigate the effects of BDNF ICV administration on BDNF levels and oxidative stress parameters in brains of rats submitted to animal model of mania induced by OUA. Wistar rats received an ICV injection of OUA, artificial cerebrospinal fluid (ACSF), OUA plus BDNF, or ACSF plus BDNF. Locomotor activity and risk-taking behavior in the rats were measured using the open-field test. In addition, we analyzed the BDNF levels and oxidative stress parameters (TBARS, Carbonyl, CAT, SOD, GR, and GPx) in the frontal cortex and hippocampus of rats. The BDNF was unable to reverse the ouabain-induced hyperactivity and risk-taking behavior. Nevertheless, BDNF treatment increased BDNF levels, modulated the antioxidant enzymes, and protected the OUA-induced oxidative damage in the brain of rats. These results suggest that BDNF alteration observed in BD patients may be associated with oxidative damage, both seen in this disorder.

Vitamin B6 prevents cognitive impairment in experimental pneumococcal meningitis.

Streptococcus pneumoniae is the relevant cause of bacterial meningitis, with a high-mortality rate and long-term neurological sequelae, affecting up to 50% of survivors. Pneumococcal compounds are pro-inflammatory mediators that induce an innate immune response and tryptophan degradation through the kynurenine pathway. Vitamin B6 acts as a cofactor at the active sites of enzymes that catalyze a great number of reactions involved in the metabolism of tryptophan, preventing the accumulation of neurotoxic intermediates. In the present study, we evaluated the effects of vitamin B6 on memory and on brain-derived neurotrophic factor (BDNF) expression in the brain of adult Wistar rats subjected to pneumococcal meningitis. The animals received either 10 µL of artificial cerebral spinal fluid (CSF) or an equivalent volume of S. pneumoniae suspension. The animals were divided into four groups: control, control treated with vitamin B6, meningitis, and meningitis treated with vitamin B6. Ten days after induction, the animals were subjected to behavioral tests: open-field task and step-down inhibitory avoidance task. In the open-field task, there was a significant reduction in both crossing and rearing in the control group, control/B6 group, and meningitis/B6 group compared with the training session, demonstrating habituation memory. However, the meningitis group showed no difference in motor and exploratory activity between training and test sessions, demonstrating memory impairment. In the step-down inhibitory avoidance task, there was a difference between training and test sessions in the control group, control/B6 group, and meningitis/B6 group, demonstrating aversive memory. In the meningitis group, there was no difference between training and test sessions, demonstrating impairment of aversive memory. In the hippocampus, BDNF expression decreased in the meningitis group when compared to the control group; however, adjuvant treatment with vitamin B6 increased BDNF expression in the meningitis group. Thus, vitamin B6 attenuated the memory impairment in animals subjected to pneumococcal meningitis.

Neonatal Escherichia coli K1 meningitis causes learning and memory impairments in adulthood.

Neonatal Escherichia coli meningitis continues to be an important cause of mortality and morbidity in newborns worldwide. The aim of this study was to investigate the cytokines/chemokines, brain-derived neurotrophic factor (BDNF) levels, blood-brain barrier integrity in neonatal rats following E. coli K1 experimental meningitis infection and subsequent behavioural parameters in adulthood. In the hippocampus, interleukin increased at 96 h, IL-6 at 12, 48 and 96 h, IL-10 at 96 h, cytokine-induced neutrophil chemoattractant-1 at 6, 12, 24, 48 and 96 h, and BDNF at 48 and 96 h. In the cerebrospinal fluid, tumour necrosis factor alpha levels increased at 6, 12, 24, 48 and 96 h. The BBB breakdown occurred at 12 h in the hippocampus, and at 6h in the cortex. We evaluated behavioural parameters in adulthood: habituation to the open-field, step-down inhibitory avoidance, object recognition, continuous multiple-trials step-down inhibitory avoidance and forced swimming tasks. In adulthood, the animals showed habituation and aversive memory impairment. The animals needed a significant increase in the number of training periods to learn and not had depressive-like symptoms.

Anxiety disorders are associated with quality of life impairment in patients with insulin-dependent type 2 diabetes: a case-control study.

OBJECTIVE: To assess the presence of anxiety disorders and quality of life in patients with insulin-dependent type 2 diabetes. METHODS: Case-control study of 996 patients with type 2 diabetes and 2,145 individuals without diabetes. The sole inclusion criterion for the case group was insulin-dependent type 2 diabetes. We compared the case and control groups for sociodemographic variables, laboratory and clinical data, and presence of anxiety disorders. Quality of life was evaluated using the WHOQOL-BREF instrument, and the prevalence of anxiety disorder was evaluated by the Mini International Neuropsychiatric Interview (MINI). RESULTS: Patients with diabetes had a higher prevalence of generalized anxiety disorder, panic disorder, and obsessive-compulsive disorder. The presence of these disorders in combination with type 2 diabetes was associated with worse quality of life in the physical, social, psychological, and environmental domains. CONCLUSIONS: This study demonstrates the importance of diagnosing and treating anxiety disorders in patients with diabetes, so as to prevent more serious complications associated with these comorbidities.

Increased prevalence of mood disorders and suicidal ideation in type 2 diabetic patients.

This study evaluated the association of mood disorders, suicidal ideation and the quality of life in patients with type 2 diabetes. We used a case-control study employing 996 patients suffering with type 2 diabetes (using insulin for over 1 year), and 2.145 individuals without diabetes. The groups were then used to evaluate the presence of different mood disorders and suicidal ideation, beyond quality of life. In addition to this, fasting glucose and glycosylated hemoglobin (Hb1C) were also evaluated. The data were analyzed using the Pearson chi-squared test, logistic regression, ANCOVA and Student's t-tests. We showed an association between type 2 diabetes and depressive episodes (adjusted OR = 1.8, CI 95 % 1.7-2.0, p < 0.001), recurrent depressive episodes (adjusted OR = 2.4, CI 95 % 2.2-2.6, p < 0.001), dysthymia (adjusted OR = 5.2, CI 95 % 4.9-5.5, p < 0.001), mood disorder with psychotic symptoms (adjusted OR = 2.5, CI 95 % 1.5-3.4, p < 0.001) and suicidal ideation (adjusted OR = 3.6, CI 95 % 2.5-4.8, p < 0.001, light; adjusted OR = 4.6, CI 95 % 1.5-7.7, p < 0.01, moderate and severe). The recurrent depression (OR = 1.3, CI 95 % 1.1-1.7, p < 0.05) and psychotic symptoms (OR = 4.1, CI 95 % 1.1-15.1, p < 0.05) were associated with higher levels of Hb1C. Dysthymia was associated with high blood glucose (OR = 1.6, CI 95 % 1.1-2.5, p < 0.05). Patients had lower mean scores in the following domains: physical [36.5 (13.6) × 56.0 (4.9), p < 0.001)], psychological [42.6 (8.6) × 47.9 (8.6), p < 0.001] and environmental [40.0 (8.6) × 49.3 (8.3), p < 0.001], but had higher scores in the area of social relations [50.2 (16.9) × 35.7 (27.9), p < 0.001]. The data demonstrated a worse quality of life, a high comorbidity of type 2 DM with depressive disorders and suicidal ideation. In addition, the poor control of DM is associated with the severity of mood disorders.

Lithium and valproate modulate antioxidant enzymes and prevent ouabain-induced oxidative damage in an animal model of mania.

In this study, we assessed the oxidative stress parameters in rats submitted to an animal model of mania induced by ouabain (OUA), which included the use of lithium (Li) and valproate (VPA). Li and VPA treatment reversed and prevented the OUA-induced damage in these structures, however, this effect varies depending on the brain region and treatment regimen. Moreover, the activity of the antioxidant enzymes, namely, superoxide dismutase (SOD) and catalase (CAT) was found to be increased and decreased, respectively, in the brain of OUA-administered rats. Li and VPA modulated SOD and CAT activities in OUA-subjected rats in both experimental models. Our results support the notion that Li and VPA exert antioxidant-like properties in the brain of rats submitted to animal model of mania induced by ouabain.

Prevalência de transtornos ansiosos e algumas comorbidades em idosos: um estudo de base populacional / Prevalence of anxiety disorders and some comorbidities in elderly: a population-based study

RESUMO Objetivo Avaliar a prevalência de transtornos ansiosos e fatores associados em uma amostra populacional de idosos do Sul de Santa Catarina. Métodos Estudo transversal com base em dados populacionais, que avaliou 1.021 indivíduos idosos entre 60 e 79 anos. Foram realizadas entrevistas domiciliares para aferição de variáveis sobre transtornos ansiosos, por meio do questionário MINI, dados sociodemográficos, hipertensão arterial sistêmica (HAS), infarto agudo do miocárdio (IAM) e dosagem de colesterol. Resultados As prevalências entre os transtornos ansiosos foram de 22,0% para o transtorno de ansiedade generalizada (TAG); 14,8% para fobia social (FS); 10,5% para transtorno do pânico (TP); e 8,5% para o transtorno obsessivo-compulsivo (TOC). Além disso, 40,5% dos indivíduos apresentaram pelo menos um transtorno de ansiedade. A distribuição dos transtornos foi semelhante nos dois gêneros; TAG foi mais prevalente nos indivíduos de menor escolaridade; TOC foi mais presente em indivíduos casados ou em união estável. Em relação às variáveis clínicas, HAS foi associada à presença de TOC; FS foi associada com IAM; TOC e FS foram associados com HDL > 40 mg/dL. Conclusão Os dados demonstram que os quadros de ansiedade são muito frequentes em idosos da comunidade, se sobrepõem de forma significativa e estão associados a algumas variáveis clínicas cardiovasculares.

ABSTRACT Objective This study evaluated the prevalence of anxiety disorders and associated factors in a population sample of elderly from South of Santa Catarina. Methods Cross-sectional study based on population data, which evaluated 1,021 elderly individuals, between 60 and 79 years. Home interviews were conducted to measure the variables of anxiety disorders, through of the MINI questionnaire, sociodemographic data, systemic arterial hypertension (SAH), acute myocardial infarction (AMI) and serum cholesterol measurements. Results The prevalence among anxiety disorders were 22.0% for generalized anxiety disorder (GAD), 14.8% for social phobia (FS); 10.5% for panic disorder (PD); 8.5% for obsessive-compulsive disorder (OCD), and with only, at least one disorder 40.5%. The distribution of the disorders were similar in both genders, GAD was more prevalent among those with lower education; OCD was more prevalent in individuals who were married or in union stable. In relation to clinical variables, SAH was associated with the presence of OCD; FS was associated with AMI; FS and OCD were associated with HDL > 40 mg/dL. Conclusion The data demonstrate that anxiety conditions are very common in older adults, significantly overlap and are associated with cardiovascular clinical variables.

Effects of mood stabilizers on hippocampus and amygdala BDNF levels in an animal model of mania induced by ouabain.

There is a body of evidence suggesting that BDNF is involved in bipolar disorder (BD) pathogenesis. Intracerebroventricular (ICV) injection of ouabain (OUA), a specific Na(+)/K(+) ATPase inhibitor, induces hyperlocomotion in rats, and has been used as an animal model of mania. The present study aims to investigate the effects of the lithium (Li) and valproate (VPT) in an animal model of mania induced by ouabain. In the reversal model, animals received a single ICV injection of OUA or cerebrospinal fluid (aCSF). From the day following the ICV injection, the rats were treated for 6 days with intraperitoneal (IP) injections of saline (SAL), Li or VPT twice a day. In the maintenance treatment (prevention model), the rats received IP injections of Li, VPT, or SAL twice a day for 12 days. In the 7th day of treatment the animals received a single ICV injection of either OUA or aCSF. After the ICV injection, the treatment with the mood stabilizers continued for more 6 days. Locomotor activity was measured using the open-field test and BDNF levels were measured in rat hippocampus and amygdala by sandwich-ELISA. Li and VPT reversed OUA-related hyperactive behavior in the open-field test in both experiments. OUA decreased BDNF levels in first and second experiments in hippocampus and amygdala and Li treatment, but not VPT reversed and prevented the impairment in BDNF expression after OUA administration in these cerebral areas. Our results suggest that the present model fulfills adequate face, construct and predictive validity as an animal model of mania.

DNA damage after intracerebroventricular injection of ouabain in rats.

There is an emerging body of data suggesting that bipolar disorder is associated with DNA damage. Intracerebroventricular (i.c.v.) administration of ouabain in rats results in manic-like alterations. We evaluated DNA damage of peripheral blood, cerebrospinal fluid and hippocampus of rats after i.c.v. ouabain injection. Ouabain-induced hyperlocomotion was examined in an open field. Additionally, we used single cell gel electrophoresis (comet assay) to measure early transient damage in cerebrospinal fluid (CSF), hippocampus and blood; and the micronucleus test to measure persistent damage in total blood samples of rats after ouabain administration. Our findings demonstrated that ouabain induced hyperlocomotion in rats, and this response remained up to 7 days following a single i.c.v. injection. In addition, we observed that the persistent increase in the rat spontaneous locomotion is associated with increased hippocampal and peripheral index of early DNA damage in rats. No significant alterations were observed in the micronucleus frequency in total blood samples of the rats after the ouabain i.c.v. injection. These results suggest that ouabain may induce peripheral and central early DNA damage, but this early damage may be repaired.

Anxiety disorders are associated with quality of life impairment in patients with insulin-dependent type 2 diabetes: a case-control study

Objective: To assess the presence of anxiety disorders and quality of life in patients with insulin-dependent type 2 diabetes. Methods: Case-control study of 996 patients with type 2 diabetes and 2,145 individuals without diabetes. The sole inclusion criterion for the case group was insulin-dependent type 2 diabetes. We compared the case and control groups for sociodemographic variables, laboratory and clinical data, and presence of anxiety disorders. Quality of life was evaluated using the WHOQOL-BREF instrument, and the prevalence of anxiety disorder was evaluated by the Mini International Neuropsychiatric Interview (MINI). Results: Patients with diabetes had a higher prevalence of generalized anxiety disorder, panic disorder, and obsessive-compulsive disorder. The presence of these disorders in combination with type 2 diabetes was associated with worse quality of life in the physical, social, psychological, and environmental domains. Conclusions: This study demonstrates the importance of diagnosing and treating anxiety disorders in patients with diabetes, so as to prevent more serious complications associated with these comorbidities. .

Effects of chronic haloperidol and/or clozapine on oxidative stress parameters in rat brain.

Decreased antioxidant activity is considered as one of the causes of tardive dyskinesia in schizophrenic patients in a prolonged neuroleptic treatment course. Haloperidol (HAL) has been hypothesized to increase oxidative stress, while clozapine (CLO) would produce less oxidative damage. The objective was to determine whether CLO for 28 days could reverse or attenuate HAL-induced oxidative damage in animals previously treated with HAL for 28 days. HAL significantly increased thiobarbituric acid reactive substances levels in the cortex (CX) and striatum and increased protein carbonyls in hippocampus (HP) and CX and this was not attenuated by CLO treatment. In the total radical trapping antioxidant parameter assay there was a decrease in the HP total antioxidant potential induced by HAL and by treatment with HAL + CLO. Our findings demonstrated that the atypical antipsychotic CLO could not revert oxidative damage caused by HAL.

Effects of maintenance electroshock on the oxidative damage parameters in the rat brain.

Although several advances have occurred over the past 20 years concerning refining the use and administration of electroconvulsive therapy to minimize side effects of this treatment, little progress has been made in understanding the mechanisms underlying its therapeutic or adverse effects. This work was performed in order to determine the level of oxidative damage at different times after the maintenance electroconvulsive shock (ECS). Male Wistar rats (250-300 g) received a protocol mimicking therapeutic of maintenance or simulated ECS (Sham) and were subsequently sacrificed immediately after, 48 h and 7 days after the last maintenance electroconvulsive shock. We measured oxidative damage parameters (thiobarbituric acid reactive species for lipid peroxidation and protein carbonyls for protein damage, respectively) in hippocampus, cortex, cerebellum and striatum. We demonstrated no alteration in the lipid peroxidation and protein damage in the four structures studied immediately after, 48 h and 7 days after a last maintenance electroconvulsive shock. Our findings, for the first time, demonstrated that after ECS maintenance we did protocol minimal oxidative damage in the brain regions, predominating absence of damage on the findings.

Decreased BDNF levels in amygdala and hippocampus after intracerebroventricular administration of ouabain / Diminuição dos níveis de BDNF em amígdala e hipocampo após a administração intracerebroventricular de ouabaína

OBJECTIVE: The present study aims to investigate the effects of ouabain intracerebroventricular injection on BDNF levels in the amygdala and hippocampus of Wistar rats.METHODS: Animals received a single intracerebroventricular injection of ouabain (10-3 and 10-2 M) or artificial cerebrospinal fluid and immediately, 1h, 24h, or seven days after injection, BDNF levels were measured in the rat's amygdala and hippocampus by sandwich-ELISA (n = 8 animals per group).RESULTS: When evaluated immediately, 3h, or 24h after injection, ouabain in doses of 10-2 and 10-3 M does not alter BDNF levels in the amygdala and hippocampus. However, when evaluated seven days after injection, ouabain in 10-2 and 10-3 M, showed a significant reduction in BDNF levels in both brain regions evaluated.DISCUSSION: In conclusion, we propose that the ouabain decreased BDNF levels in the hippocampus and amygdala when assessed seven days after administration, supporting the Na/K ATPase hypothesis for bipolar illness.

OBJETIVO: O presente estudo tem como objetivo investigar os efeitos da injeção intracerebroventricular de ouabaína sobre os níveis de BDNF na amígdala e no hipocampo de ratos Wistar.MÉTODOS: Os animais receberam uma única injeção intracerebroventricular de ouabaína (10-3 and 10-2 M) ou fluido cerebroespinhal artificial e, imediatamente, 3h, 24h ou sete dias após a injeção, os níveis de BDNF foram mensurados na amígdala e hipocampo dos ratos por ELISA sandwich (n = 8 animais por grupo).RESULTADOS: Quando avaliados imediatamente após a injeção, 3h ou 24h, ouabaína nas doses 10-2 e 10-3 M não alterou os níveis de BDNF em ambas as estruturas avaliadas. Entretanto, quando avaliados sete dias após a injeção, ouabaína nas doses 10-2 e 10-3 M mostrou uma significante redução nos níveis de BDNF em amígdala e hipocampo.CONCLUSÃO: Em conclusão, propõe-se que a administração de ouabaína diminuiu os níveis de BDNF em amígdala e hipocampo quando avaliados sete dias após a injeção, suportando a hipótese da participação da Na/K ATPase no transtorno bipolar.

NCS-1 expression in rat brain after electroconvulsive stimulation.

Although electroconvulsive therapy (ECT) has been used as a treatment for mental disorder since 1930s, little progress has been made towards understanding the mechanisms underlying its therapeutic and adverse effects. The aim of this work was to analyze the expression of NCS-1 (neuronal calcium sensor 1, a protein that was found to be altered in post-mortem prefrontal cortex of schizophrenic patients) in striatum, cortex, hippocampus and cerebellum of Wistar rats after acute or chronic electroconvulsive stimulation (ECS). Rats were submitted to a single stimulation (acute) or to a series of eight stimulations, applied one every 48 h (chronic). Animals were killed for collection of tissue samples at time zero, 30 min, 3, 12, 24 and 48 h after stimulation in the acute model and at the same time intervals after the last stimulation in the chronic model. Our results indicated that chronic ECS increased the expression of NCS-1 only in cerebellum. Such results on the expression of proteins involved in signaling pathways that are relevant for neuropsychiatric disorders and treatment, in particular ECT, can contribute to shed light on the mechanisms related to therapeutic and adverse effects.

Long lasting effects of electroconvulsive seizures on brain oxidative parameters.

This work was performed in order to determine the level of oxidative damage and antioxidant enzymes activities late after acute and chronic electroconvulsive shock (ECS) in rats. We measured oxidative parameters in hippocampus, cortex, and striatum, at 45, 60, 90 and 120 days after a single or multiple ECS. We demonstrated an increase in lipid peroxidation after multiple ECS in the hippocampus and striatum. This was also the case for protein carbonyls in the single or multiple protocols. In this way, we demonstrated an increase in catalase in cortex in contrast to striatum and hippocampus, were there were decreases sometimes in chronic ECS. The superoxide dismutase activities decrease in different times after single and multiple ECS in the hippocampus. Our findings demonstrated that there is a delayed increase after ECS in oxidative damage and decrease in antioxidant enzymes activities in hippocampus and striatum.