scholarly journals Neuronal Cell Death Induces Depressive Disorder in Rats Depression-Like Behaviors Caused by Chronic Stress

2020 ◽  
Vol 1 (2) ◽  
pp. 16-24
Author(s):  
Rachmat Hidayat ◽  
Mgs Irsan Saleh ◽  
Nita Parisa
Keyword(s):  
Animal Model ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Cell Apoptosis ◽  
Neuronal Cells ◽  
Neuronal Cell ◽  
Normal Group ◽  
Experimental Animals ◽  
The Brain

Abstract Introduction Depression is believed to be a disorder in which an increase in serotonin activity in the brain. This has implications for the development of various antidepressant drugs that work to increase serotonin levels, by inhibiting serotonin reuptake. However, management with antidepressants is still believed to be not optimal, there are still various problems that have not been able to be solved only by increasing serotonin levels in the brain. Therefore, it is necessary to do further exploration to find out other possible pathophysiology of depressive disorders. This study intended to explore the role of apoptosis of neuronal cells in the prefrontal cortex to answer the hypothesis that depression was not only caused by increased serotonin levels but also  there was a role of dead neuronal cells in the prefrontal cortex which will trigger the body's homeostatic efforts to compensate by increasing serotonin levels.   Methods A total of 30 male Wistar rats (200 ± 20 g) were obtained from Eureka Research Laboratory (Palembang, Indonesia). Experimental animals were placed in cages under controlled conditions (12 hours of light / dark cycles with temperatures of 22 ± 1˚C and humidity of 40-60%), fed and drank ad libitum. Experimental animals with depression model were induced using Chronic Mild Stress (CMS). CMS procedures were performed with mild stressors such as repeated cold stress (4 ° C), space reduction in the homecage, changed cages and social interaction with other animals of the CMS group. To assess wether animal were being depression or not, the animal were tested using Forced Swimming Test (FST). After induction, rats were randomly divided into two groups which each contained 15 animals: the normal control group (not induced CMS) and the CMS group (negative control). Furthermore, the animal model was performed perfusion to maintain organ when evacuation was done, cell damage did not occur. To evaluate cell organ, immunohistochemistry examination and ELISA examination was performed. All data are presented as mean ± standard deviation and all statistical analyzes are performed with the SPSS 25 (IBM) program. Result This research showed that CMS animal model has a greater duration of immobility than the normal group and serotonin level in CMS animal models decreased almost threefold compared to the normal group. In addition, there were increased expression of caspase-3 indicates that more neuronal cells suffered from apoptosis. So, in this research, it was clearly stated that in depressive disorder, there were elevation of neuronal cell apoptosis in the prefrontal cortex. Conclusion Neuronal cell apoptosis in the prefrontal cortex plays a role in the pathophysiology of depression through activation of negative feedback on serotonin production.

The Neuropsycho–Pharmacology of Attention

2014 ◽  
Author(s):  
Trevor Robbins
Keyword(s):  
Prefrontal Cortex ◽  
Gamma Oscillations ◽  
Psychoactive Drugs ◽  
The Novel ◽  
Experimental Animals ◽  
Chemical Systems ◽  
New Directions ◽  
Network Properties ◽  
The Brain

Pharmacological influences on cognition and behaviour are often accompanied by effects on different aspects of attention. The actions of many psychoactive drugs (often used in the treatment of psychiatric disorders) depend on effects exerted on the classical chemical modulatory neurotransmitter systems including acetylcholine, and the monoamines, dopamine, noradrenaline and serotonin (or 5-hydroxytryptamine, 5-HT). These chemical systems originate in the reticular core of the brain and modulate attention by actions on forebrain structures including the thalamus, striatum, and the neocortex (especially the prefrontal cortex). Current research is attempting to dissect separable functions of these chemical neurotransmitters in mediating attention in relation to states of arousal and stress in comparable test paradigms in experimental animals and humans. New directions in research in this area are also identified, including the functions of the novel neurotransmitter orexin, and the role of GABA and glutamate in gamma oscillations and the network properties of the neocortex.

Application of Perfluorooctylbromide Nanoparticles with Ulinastatin for Early Brain Injury Caused by Carbon Monoxide Poisoning

2021 ◽  
Vol 13 (7) ◽  
pp. 1383-1390
Author(s):  
Guangcong Li ◽  
Dan Li
Keyword(s):  
Carbon Monoxide ◽  
Particle Size ◽  
Treatment Group ◽  
Cell Apoptosis ◽  
High Speed ◽  
Carbon Monoxide Poisoning ◽  
Neuronal Cell ◽  
Early Brain Injury ◽  
Group A ◽  
The Brain

ABSTRACTThis study aimed to explore the mechanism of perfluorooctylbromide (PFOB) nanoparticles (NPs) combined with ulinastatin (UTI) on early brain injury (EBI) caused by carbon monoxide poisoning (CMP). Firstly, PFOB NPs were prepared by high-speed dispersion and high-speed homogenization. The physicochemical characteristics of the particle size distribution and Zeta potential distribution of the NPs were analyzed using a laser particle size analyzer. The thermal and photoinduced phase transition characteristics of the NPs were analyzed under heating and laser irradiation conditions. Then, 50 Sprague Dawley (SD) rats were deemed as the research objects to establish the CMP rat models using hyperbaric oxygen chambers. According to different treatment methods, they were rolled into a healthy control group, a carbon monoxide (CO) model group, a PTOB treatment group, an UTI treatment group, and a PTOB + UTI treatment group. The brain tissues of each group of rats were collected 3 days after treatment. The neuronal cell apoptosis, expression of Caspase-3, messenger ribonucleic acid (mRNA) of inflammatory factors interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in rat brain tissue were detected through immunohistochemical staining, in situ cell apoptosis detection, Reverse transcription-polymerase chain reaction (RT-PCR), and Western blotting, so did the relative expression of target proteins B-cell lymphoma-2 (Bcl-2), Bcl2-Associated X (Bax) and myelin basic protein (MBP). As a result, the average particle size and the average Zeta potential of the prepared PFOB NPs was 103±31 nm and −23 ± 15 mV, respectively. When the PFOB NPs were heated to 80 °C, the particle size increased greatly and cracks appeared. The particle size of PFOB NPs also increased obviously after laser irradiation, and the PFOB inside the particles changed into gas phase. Compared to CO group, expression of Caspase-3, neuronal cell apoptosis rate, mRNA expression of IL-1β and TNF-α, and protein expression of Bax and Bcl-2 in the brain tissue of PTOB group, UTI group, and PFOB + UTI group were notably decreased (P < 0.05), while the MBP protein expression increased considerably (P < 0.05). Changes in PFOB + UTI group were more obvious than those in PTOB group and UTI group, and those indicators weren’t considerably different from the controls. In summary, PFOB NPs were successfully prepared with favorable phase transition characteristics. Moreover, PFOB NPs combined with UTI could reduce the apoptosis of brain neurons after CMP, improve the inflammatory response, and play a protective effect on EBI of CMP.

scholarly journals Effects of omega-3 supplementation on interleukin and neurotrophin levels in an animal model of schizophrenia

2015 ◽  
Vol 87 (2 suppl) ◽  
pp. 1475-1486 ◽  
Author(s):  
ALEXANDRA I. ZUGNO ◽  
LARA CANEVER ◽  
GUSTAVO MASTELLA ◽  
ALEXANDRA S. HEYLMANN ◽  
MARIANA B. OLIVEIRA ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Animal Model ◽  
Prefrontal Cortex ◽  
Immune System ◽  
Mechanism Of Action ◽  
Neurotrophic Factor ◽  
Concomitant Treatment ◽  
Omega 3 ◽  
Preventive Effect

ABSTRACTNew studies suggest that polyunsaturated fatty acids, such as omega-3, may reduce the symptoms of schizophrenia. The present study evaluated the preventive effect of omega-3 on interleukines (IL) and neurotrophin brain-derived neurotrophic factor (BDNF) levels in the brains of young rats subjected to a model of schizophrenia. Treatment was performed over 21 days, starting on the 30th day of rat's life. After 14 days of treatment with omega-3 or vehicle, a concomitant treatment with saline or ketamine (25 mg/kg) was started and maintained until the last day of the experiment. BDNF levels in the rat's prefrontal cortex were decreased at 1 h and 24 h after the last administration of ketamine, whereas the group administered with ketamine and omega-3 showed a decrease in BDNF levels only after 24 h. In contrast, both interventions induced similar responses in levels of IL-1β and IL6. These findings suggest that the similarity of IL-1β and IL6 levels in our experimental groups is due to the mechanism of action of ketamine on the immune system. More studies have to be carried out to explain this pathology. In conclusion, according to previous studies and considering the current study, we could suggest a prophylactic role of omega-3 against the outcome of symptoms associated with schizophrenia.

A metabolomics-based approach for ranking the depressive level in a chronic unpredictable mild stress rat model

RSC Advances ◽  
2016 ◽  
Vol 6 (31) ◽  
pp. 25751-25765 ◽  
Author(s):  
Xinyu Yu ◽  
Shanlei Qiao ◽  
Di Wang ◽  
Jiayong Dai ◽  
Jun Wang ◽  
...  
Keyword(s):  
Animal Model ◽  
Major Depressive Disorder ◽  
Prefrontal Cortex ◽  
Depressive Disorder ◽  
Rat Model ◽  
Untargeted Metabolomics ◽  
Mild Stress ◽  
Chronic Unpredictable Mild Stress ◽  
Major Depressive ◽  
Metabolomics Study

An untargeted metabolomics study to investigate the metabolome change in plasma, hippocampus and prefrontal cortex (PFC) in an animal model with a major depressive disorder (MDD) had been conducted.

scholarly journals Haloperidol and Risperidone Induce Apoptosis Neuronal Cell : Invivo Study

2020 ◽  
Vol 1 (1) ◽  
Author(s):  
Ester G Panserga ◽  
Cecep S Kristanto ◽  
Budi Pratiti ◽  
Patricia Wulandari
Keyword(s):  
Cell Apoptosis ◽  
Wistar Rats ◽  
Caspase 3 ◽  
Neuronal Cells ◽  
Neuronal Cell ◽  
Total Percentage ◽  
White Rats ◽  
Male Wistar Rats ◽  
Group B

Abstract Introduction Antipsychotics are drugs that are widely prescribed for mental disorders, such as schizophrenia and psychosis. Recent in vitro studies show antipsychotics play a role in the initiation of neuronal cell apoptosis. This study aims to determine the effect of haloperidol and risperidone on neuronal cell apoptosis in Wistar white rats. Methods Male wistar rats aged 8 weeks (n = 30) were used in this study. Wistar rats were randomized into 6 groups. Group A: 5 wistar rats as a control without induced schizophrenia, aquades and drugs. Group B: 5 Wistar-induced psychotic mice (using 30 mg / kgBB ketamine, intraperitoneal injection for 5 days) and aquadest. Group C: 5 rats were induced psychotic and were given haloperidol or 0.05 mg / kgBB orally, for 28 days. Group D: 5 mice were induced psychotic and were given haloperidol 0.1 mg / kg orally, for 28 days. Group E: 5 mice were induced psychotic and were given risperidone 0.05 mg / kgBB orally, for 28 days. Group F: 5 mice were induced psychotic and given risperidone 0.1 mg / kgBB orally, for 28 days. Apoptosis of neuronal cells in the ventral tegmental area was assessed by caspase-3 immunohistochemistry. The colored area will be calculated as a total percentage using the imageJ program. Results Risperidone and haloperidol increase caspase-3 activity, but haloperidol increases caspase-3 activity more than risperidone. Conclussion Risperidone and haloperidol induce apoptosis of neuronal cells and tardive dyskinesia in Wistar rats with psychotic models.

scholarly journals Regulation of the p75 Neurotrophin Receptor Attenuates Neuroinflammation and Stimulates Hippocampal Neurogenesis in Experimental Streptococcus Pneumoniae Meningitis

2021 ◽  
Author(s):  
Dandan Zhang ◽  
Shengnan Zhao ◽  
Zhijie Zhang ◽  
Danfeng Xu ◽  
Di Lian ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Streptococcus Pneumoniae ◽  
Cell Apoptosis ◽  
Neuronal Cell ◽  
Hippocampal Neurogenesis ◽  
Clinical Severity ◽  
Neurotrophin Receptor ◽  
Double Labeling

Abstract Background: Streptococcus pneumoniae meningitis is a destructive central nervous system (CNS) infection with acute and long-term neurological disorders. Compelling evidence provided by previous studies suggests that p75NTR signaling influences cell survival, apoptosis, and proliferation in brain-injured conditions. However, the role of p75NTR signaling in regulating pneumococcal meningitis (PM)-induced neuroinflammation and altered neurogenesis remains largely to be elucidated.Methods: p75NTR signaling activation in the pathological process of PM was assessed. During acute PM, a small-molecule p75NTR modulator LM11A-31 or vehicle was intranasally administered for 3 days prior to S.pneumoniae exposure. At 24h post-infection, clinical severity, histopathology, astrocytes/microglia activation, neuronal cell apoptosis and death, inflammation-related transcription factors and inflammatory factors were evaluated. Additionally, p75NTR was knocked down by the adenovirus-mediated short-hairpin RNA (shRNA) to ascertain the role of p75NTR in PM. During long-term PM, the intranasal administration of LM11A-31 or vehicle was continued for 7 days after successfully establishing the PM model. Hippocampal neurogenesis was evaluated by double-labeling immunofluorescence with EdU, DCX and NeuN. Results: Our results revealed that both 24h (acute) and 7,14,28day (long-term) groups of infected rats demonstrated increased p75NTR expression in the brain. During acute PM, modulation of p75NTR through pretreatment of PM model with LM11A-31 significantly alleviated S.pneumoniae-induced clinical severity, histopathological injury and the activation of astrocytes and microglia. LM11A-31 pretreatment also significantly ameliorated neuronal cell apoptosis and death. Moreover, we found that blocking p75NTR with LM11A-31 decreased the expression of inflammation-related transcription factors (NF-κBp65, C/EBPβ) and proinflammatory cytokine (IL-1β, TNF-α, IL-6 and iNOS) in the cortex and hippocampus. Furthermore, p75NTR knockdown induced significant changes in histopathology and inflammation-related transcription factors expression. Importantly, combined LM11A-31 adjuvant therapy significantly improved hippocampal neurogenesis.Conclusion: Our findings suggest that the p75NTR signaling plays an essential role in the pathogenesis of PM. Targeting p75NTR has benefit effects on PM rats by alleviating neuroinflammation and promoting hippocampal neurogenesis. Thus, the p75NTR signaling may be a potential therapeutic target to improve the outcome of PM.

Mitochondrial respiratory chain activity in an animal model of mania induced by ouabain

2011 ◽  
Vol 23 (3) ◽  
pp. 106-111 ◽  
Author(s):  
Tiago P. Freitas ◽  
Gislaine T. Rezin ◽  
Daiane B. Fraga ◽  
Morgana Moretti ◽  
Julia S. Vieira ◽  
...  
Keyword(s):  
Animal Model ◽  
Prefrontal Cortex ◽  
Respiratory Chain ◽  
Rebound Effect ◽  
Mitochondrial Respiratory Chain ◽  
Face Validity ◽  
Mitochondrial Respiratory Chain Activity ◽  
Respiratory Chain Activity ◽  
The Brain ◽  
Mitochondrial Respiratory

Objectives: Bipolar disorder (BD) is a mental illness associated with higher rates of suicide. The present study aims to investigate the brain mitochondrial respiratory chain activity in an animal model of mania induced by ouabain.Methods: Adult male Wistar rats received a single intracerebroventricular administration of ouabain (10−3 and 10−2 M) or vehicle. Locomotor activity was measured using the open field test. Mitochondrial respiratory chain activity was measured in the brain of rats 1 h and 7 days after ouabain administration.Results: Our results showed that spontaneous locomotion was increased 1 h and 7 days after ouabain administration. Complexes I, III and IV activities were increased in the prefrontal cortex, hippocampus and striatum immediately after the administration of ouabain, at the concentration of 10−3 and 10−2 M. Moreover, complex II activity was increased only in the prefrontal cortex at the concentration of 10−2 M. On the other hand, no significant alterations were observed in complex I activity 7 days after ouabain administration. However, an increase in complexes II, III and IV activities was observed only in the prefrontal cortex at the concentration of 10−2 M.Conclusion: Our findings suggest an increase in the activities of mitochondrial respiratory chain in this model of mania. A possible explanation is that these findings occur as a rebound effect trying to compensate for a decrease of ATP deprivation in BD. The present findings suggest that this model may present good face validity and a limitation in construct validity.

scholarly journals Reducing future fears by suppressing the brain mechanisms underlying episodic simulation

2016 ◽  
Vol 113 (52) ◽  
pp. E8492-E8501 ◽  
Author(s):  
Roland G. Benoit ◽  
Daniel J. Davies ◽  
Michael C. Anderson
Keyword(s):  
Prefrontal Cortex ◽  
Dorsolateral Prefrontal Cortex ◽  
Ventromedial Prefrontal Cortex ◽  
Episodic Simulation ◽  
Dorsolateral Prefrontal ◽  
Future Events ◽  
The Right ◽  
Development Of Anxiety ◽  
The Brain

Imagining future events conveys adaptive benefits, yet recurrent simulations of feared situations may help to maintain anxiety. In two studies, we tested the hypothesis that people can attenuate future fears by suppressing anticipatory simulations of dreaded events. Participants repeatedly imagined upsetting episodes that they feared might happen to them and suppressed imaginings of other such events. Suppressing imagination engaged the right dorsolateral prefrontal cortex, which modulated activation in the hippocampus and in the ventromedial prefrontal cortex (vmPFC). Consistent with the role of the vmPFC in providing access to details that are typical for an event, stronger inhibition of this region was associated with greater forgetting of such details. Suppression further hindered participants’ ability to later freely envision suppressed episodes. Critically, it also reduced feelings of apprehensiveness about the feared scenario, and individuals who were particularly successful at down-regulating fears were also less trait-anxious. Attenuating apprehensiveness by suppressing simulations of feared events may thus be an effective coping strategy, suggesting that a deficiency in this mechanism could contribute to the development of anxiety.

The protective role of oxymatrine on neuronal cell apoptosis in the hemorrhagic rat brain

2012 ◽  
Vol 143 (1) ◽  
pp. 228-235 ◽  
Author(s):  
Man Huang ◽  
Yue-Yu Hu ◽  
Xiao-Qiao Dong ◽  
Qiu-Ping Xu ◽  
Wen-Hua Yu ◽  
...  
Keyword(s):  
Rat Brain ◽  
Cell Apoptosis ◽  
Neuronal Cell ◽  
Protective Role

Physical activity as a protective factor for successful aging

2019 ◽  
Vol 29 (87) ◽  
pp. 47-52
Author(s):  
Andrzej Jopkiewicz ◽  
Monika Królicka–Czerniak ◽  
Anita Zaręba
Keyword(s):  
Physical Activity ◽  
Prefrontal Cortex ◽  
Cognitive Processes ◽  
Cognitive Aging ◽  
Successful Aging ◽  
Protective Factor ◽  
Protective Role ◽  
Factors Affecting ◽  
The Brain

To divide the types of aging (successful, usual and impaired), as well as factors affecting this process, the protective role of physical activity was discussed in the literature. It was emphasized that physical activity is also a very important protective factor for cognitive aging - mainly executive function and memory. The prefrontal cortex and hippocampus, i.e. the regions of the brain responsible for the control and course of cognitive processes, show susceptibility to stimulation, which is movement exercises, which are prevention of degenerative changes within the brain.

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