Depression Behavior Research Articles

Positive Effect of 6-Gingerol on Functional Plasticity of Microglia in a rat Model of LPS-induced Depression.

Neuroinflammation has emerged as a crucial factor in the development of depression. Despite the well-known anti-inflammatory properties of 6-gingerol, its potential impact on depression remains poorly understood. This study aimed to investigate the antidepressant effects of 6-gingerol by suppressing microglial activation. In vivo experiments were conducted to evaluate the effect of 6-gingerol on lipopolysaccharide (LPS)-induced behavioral changes and neuroinflammation in rat models. In vitro studies were performed to examine the neuroprotective properties of 6-gingerol against LPS-induced microglial activation. Furthermore, a co-culture system of microglia and neurons was established to assess the influence of 6-gingerol on the expression of synaptic-related proteins, namely synaptophysin (SYP) and postsynaptic density protein 95 (PSD95), which are influenced by microglial activation. In the in vivo experiments, administration of 6-gingerol effectively alleviated LPS-induced depressive behavior in rats. Moreover, it markedly suppressed the activation of rat prefrontal cortex (PFC) microglia induced by LPS and the activation of the NF-κB/NLRP3 inflammatory pathway, while also reducing the levels of inflammatory cytokines IL-1β and IL-18. In the in vitro experiments, 6-gingerol mitigated nuclear translocation of NF-κB p65, NLRP3 activation, and maturation of IL-1β and IL-18, all of which were induced by LPS. Furthermore, in the co-culture system of microglia and neurons, 6-gingerol effectively restored the decreased expression of SYP and PSD95. The findings of this study demonstrate the neuroprotective effects of 6-gingerol in the context of LPS-induced depression-like behavior. These effects are attributed to the inhibition of microglial hyperactivation through the suppression of the NF-κB/NLRP3 inflammatory pathway.

Selective depression and adsorption of a novel eco-friendly depressant on the flotation separation of chalcopyrite from carrollite

Carrollite is often associated with chalcopyrite, and their natural floatability is similar, which makes it difficult to separate the two minerals by flotation in industrial production. In this study, the depression behavior and mechanism of flaxseed gum (FG) introduced as carrollite depressant on carrollite and chalcopyrite in PBX flotation system was investigated through micro-flotation, zeta potential, total organic carbon (TOC), fourier transform infrared (FT-IR), and X-ray photoelectron spectroscopy (XPS). The flotation results indicated that FG was a highly effective depressant to separate 92.39 % chalcopyrite from the mixture with carrollite at pH 9.0 with a reagent scheme of 50 mg/L of FG and 8.0 × 10−5 mol/L of PBX. The zeta potential and TOC analysis results demonstrated that both carrollite and chalcopyrite exhibited a favorable affinity to FG, and pre-treated FG significantly hindered the adsorption of PBX on carrollite, while only slightly decreased that on chalcopyrite, resulting in the considerable difference in floatability between carrollite and chalcopyrite. In addition, FT-IR spectra and XPS detection results further confirmed that the affinity of FG towards carrollite superior to PBX might be due to the bidentate coordination of the carboxyl groups in FG with Co sites on carrollite surface, whereas the interaction between its carboxyl groups and Cu sites on both minerals was very weak or did not happen. Therefore, FG was promising in flotation separation of copper-cobalt sulfide minerals as a new friendly efficient depressant.

EVALUATION OF SUICIDAL BEHAVIOR AND DEPRESSION, INSIGHT AND DISEASE CHARACTERISTICS IN SCHIZOPHRENIA

Introduction: Suicide is a severe public health issue with high rates of morbidity and mortality. Schizophrenia also has a high suicide incidence, which is one of the main factors contributing to rising morbidity and mortality. For strategies to lower suicide rates, it is essential to understand the risk factors for suicide in people with schizophrenia. By evaluating the relationship between the risk of suicidal behavior and demographic factors, disease characteristics, depression, and insight in schizophrenia patients, in the light of literature information, this study aimed at preventing suicide in schizophrenia and set an example for future studies. Method: This study included 103 schizophrenia patients who underwent follow-up for at least 4 years in a community mental health center (CMHC). The study included patients who had the mental capacity to understand and complete the questionnaires, were not experiencing an acute psychotic attack, and gave their consent to participate. The patients were given the Three Components of Insight Scale (TCIS), Scale for Evaluation of Positive Symptoms in Schizophrenia (SAPS), Scale for Evaluation of Negative Symptoms in Schizophrenia (SANS), Calgary Depression Inventory in Schizophrenia (CDIS), and Suicide Behavior Scale (SBS). Results: 47% of patients demonstrated suicidal behavior, and 69% of patients were men. 46% of the group demonstrating suicidal behavior had severe or very severe suicidal ideation. Age and disease duration were revealed to be significant risk factors for suicidal behavior (p=0.033 and p=0.004, respectively), but gender, SBS, CDIS, SANS, SAPS, and TCIS scores had no significant effect. Age and suicidal behavior risk were found to be inversely correlated, with each unit of age increase reducing the risk of suicidal behavior by 0.929 times. The risk of suicidal behavior rises along with the duration of disease. With every one unit increase in the duration of disease, the risk of suicidal behavior increases by 1.133 times. Additionally, the group with severe-very severe suicidal ideation had significantly more severe depression scores than the group with mild-moderate (p=0.01). Discussion: More than half of the patients with schizophrenia who were followed up showed suicidal behavior, and approximately half of the group who had suicidal ideation showed severe suicidal ideation. Suicidal behavior was found to be correlated with age and duration of illness. While suicidal behavior increases age decreases and duration of illness increases.There was no significant correlation between insight, depression, gender, symptom severity and suicidal behavior in this population. In addition, depression scores were found to be statistically significantly higher in the group with severe-very severe suicidal ideation. According to the research, in individuals with schizophrenia who were being monitored, the frequency of suicidal behavior increased along with the severity of depression. Conclusion: It is crucial to identify the risk factors and protective factors for suicide in schizophrenia patients in order to develop interventions for them. Because suicidal behavior is a significant morbidity and mortality factor in schizophrenia.

Evaluation of the protective effect of capric acid on behavioral and biochemical alterations in valproic acid-induced model of autism

Aim and objectiveThe purpose of the study is to determine the neuroprotective effect of capric acid on sodium valproate-induced model of autism. MethodsIn this study, the effect of CA was observed in animals with single dose of valproic acid (600 mg/kg, i. p.) where the disease condition was confirmed by developmental impairment in pups. Behavioral tests that assess anxiety, depression, stereotypical and repetitive behavior, social interaction, learning and memory, and other confounding variables were performed. Subsequently, oxidative stress parameters, pro-inflammatory cytokine levels and mitochondrial complex activities in the selected brain regions were analyzed. ResultsValproic acid successfully produced autism-like symptoms from post-natal day 7 and also demonstrated impairment in social behavior, learning and memory, and anxiety and depression. Valproic acid was found to produce oxidative stress and neuro-inflammation in the hippocampus, prefrontal cortex, and cerebellum. Treatment with capric acid produced a positive effect on the alterations with maximum effects evident at 400 mg/kg, p. o. through amelioration of behavioral as well as biochemical changes. ConclusionThe current study concluded that capric acid could act as a likely candidate for the treatment and management of autism via significant modulation of neurobehavioral parameters, oxidative stress, mitochondrial dysfunction and inflammatory markers.

Early life stress unravels epistatic genetic associations of cortisol pathway genes with depression

Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis represents one of the most consistent pathophysiological findings in depressive disorders. Cortisol signaling is affected by proteins that mediate its cellular responses or alters its availability to mineralocorticoid and glucocorticoid receptors. In our study, we evaluated candidate genes that may influence the risk for depression and suicide due to its involvement in cortisol signaling. The aim of the study was to assess whether the genotypes of these genes are associated with the risk for depression, severity of depressive symptoms, suicidal ideation, and suicide attempts. And whether there is interaction between genes and early-life stress. In this study, 100 healthy controls and 140 individuals with depression were included. The subjects were clinically assessed using the 21-item GRID-Hamilton questionnaires (GRID-HAMD-21), Beck Scale for Suicidal Ideation (BSI), and the Childhood Trauma Questionnaire (CTQ). A robust multifactorial dimensionality reduction analysis was used to characterize the interactions between the genes HSD11B1, NR3C1, NR3C2, and MDR1 and early-life stress. It was found a significant association of the heterozygous genotype of the MDR1 gene rs1128503 polymorphism with reduced risk of at least one suicide attempt (OR: 0.08, p = 0.003*) and a reduction in the number of suicide attempts (β = −0.79, p = 0.006*). Furthermore, it was found that the MDR1 rs1228503 and NR3C2 rs2070951 genes interact with early-life stress resulting in a strong association with depression (p = 0.001). Our findings suggest that polymorphisms in the MDR1 and NR3C2 genes and their interaction with childhood trauma may be important biomarkers for depression and suicidal behaviors.

Ficus platyphylla alleviates seizure severity and neurobehavioral comorbidities in pentylenetetrazole–kindled rats via modulation of oxidative stress

PTZ kindling induces oxidative stress, neuronal cell degeneration, and neurobehavioral alterations in rodents that mimic neuropsychiatric comorbidities of epilepsy, which could be initiated or aggravated by some antiepileptic drugs. Here, we investigated the effects of the methanol extract of Ficus platyphylla (FP) on severity scores for seizures, neuronal cell degeneration, and neurobehavioral alterations in rats kindled with pentylenetetrazole (PTZ) and probed the involvement of oxidative stress in these ameliorative effects of FP. FP (50 and 100 mg/kg, p.o.) ameliorated seizure severity, neuronal cell degeneration, depressive behaviors, cognitive dysfunctions, and oxidative stress in rats kindled with PTZ (42.5 mg/kg, i.p.). The findings from this study give additional insights into the potential values of FP in the treatment of persistent epilepsy and major neuropsychiatric comorbidities via modulation of oxidative stress.

Prophylactic Effects of n-Acethylcysteine on Inflammation-induced Depression-like Behaviors in Mice

Depression, affecting individuals worldwide, is a prevalent mental disease, with an increasing incidence. Numerous studies have been conducted on depression, yet its pathogenesis remains elusive. Recent advancements in research indicate that disturbances in synaptic transmission, synaptic plasticity, and reduced neurotrophic factor expression significantly contribute to depression's pathogenesis. In our study, we utilized adult male C57BL/6J mice. Lipopolysaccharide (LPS) can induce both chronic and acute depression-like symptoms in mice, a widely used model for studying depression associated with inflammation. N-acetylcysteine (NAC) exhibits anti-inflammatory and ameliorative effects on depressive symptoms. This study sought to determine whether NAC use could mitigate inflammatory depressive behavior through the enhancement of synaptic transmission, synaptic plasticity, and increasing levels of brain-derived neurotrophic factor (BDNF). In this study, we discovered that in mice modeled with depression-like symptoms, the expression levels of dendrites, BDNF, and miniature excitatory postsynaptic potential (mEPSC) in glutamatergic neurons, as well as the α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid glutamate receptors (AMPARs) GluA1 and GluA2 subunits, were significantly decreased. These findings suggest an impairment in the synaptic transmission of glutamatergic neurons. Following treatment with NAC, the previously mentioned levels improved, indicating an enhancement in both synaptic transmission and synaptic plasticity. Our results suggest that NAC exerts a protective effect on mouse models of inflammatory depression, potentially through the enhancement of synaptic transmission and plasticity, as well as the restoration of neurotrophic factor expression. These findings offer vital animal experimental evidence supporting NAC's role in mitigating inflammatory depressive behaviors.

Pineapple (Ananas comosus) Ameliorates Depressant-like Behaviors in Rats Induced by Lipopolysaccharide

Background: Lipopolysaccharide (LPS) injection can lead to depression and mood disorders by reducing tryptophan availability through increased activity of the enzyme indoleamine 2,3-dioxygenase. Tryptophan, sourced from fruits such as pineapple (Ananas cosmosus), is vital for the body, especially the serotonergic system. Aim: This study aims to assess how pineapple pulp (PP) counters LPS-induced depressive behaviors in male Wistar rats. Methods: The experiment involved force-feeding PP for 28 days before LPS injection (0.5 mg/kg intraperitoneal [i.p.]) in 30 male Wistar rats, divided into five groups. Groups I (normal) and II (LPS control) received 15 ml aquadest/kg/day. Test Groups III, IV, and V were given varied doses of PP; low dose (3.75 ml/kg/day), medium dose (7.5 ml/kg/day), and high dose (15 ml/kg/day). At the study’s end, rats underwent the open field test (OFT) and the tail suspension test (TST). In addition, blood and brain samples were analyzed for neuroendocrine markers related to depression. Results: LPS triggers depressive symptoms, as evidenced by increased immobility time in the TST and altered behaviors indicative of anxiety in the OFT, especially in groups not receiving PP. This is followed by decreased serotonin levels in both plasma and brain when compared to groups given PP. In addition, higher corticosterone levels were observed in the LPS group than in the PP-treated group. Administering PP at 7.5 ml/kg/day for 28 days can alleviate the depressive effects induced by LPS injection. Conclusion: PP may have antidepressant properties, potentially by mitigating behaviors leading to depressive symptoms.

Ginsenoside Rh2 Reduced Neurogenesis Dysfunction to Alleviate Depression-like Behaviour in CSDS-induced Mice

Background: Depression is a mental health disorder with high morbidity and disability rates that has harmful effects on public health worldwide. Despite many hypotheses about its mechanism have been put forward, its deeper mechanism is still unclear. Nowadays, there are many antidepressants developed by pharmaceutical companies, such as fluoxetine, ketamine, and paroxetine used in clinical practice, but the therapeutic effects are not satisfactory, with serious adverse reactions and drug addiction. Objective: Ginsenoside Rh2 (G-Rh2) is one of the major bioactive ginsenosides extracted from Panax ginseng that has been conducted for the treatment of many inflammatory diseases. However, the possible mechanisms of G-Rh2 involved in these neuroprotective effects on neuroinflammation are currently unclear. Methods: We established a CSDS depression model in normal mice, and then the depressive symptoms of mice were evaluated by a series of behavioral testing. Finally, molecular biology experiments were conducted to demonstrate that G-Rh2 had anti-inflammatory and antidepressant effects. Results: We showed that G-Rh2 (30 mg/kg) significantly relieved depressive behavior in mice via attenuating oxidative stress injury and release of proinflammatory cytokines. Moreover, G-Rh2 reduced impaired neurogenesis in the hippocampus of CSDS-induced mice. Conclusion: We demonstrated the anti-inflammatory and antioxidative effects of G-Rh2 to alleviate depression through improved neurogenesis in depressive mice for the first time. What's more, we aimed to verify the protective effects of G-Rh2 on neuroinflammation and provide novel insights for understanding the roles of G-Rh2 in the treatment of depression

Metagenome of Tibetan kefir grains and its alleviating effect on dysfunction of gut microbiome and depressive colorectal cancer comorbidity induced by chronic stress and AOM/DSS

The prevalence of major depression in cancer patients ranges from 5% to 26%. The research on the screening of neurotrophic and anticancer psychoprobiotics is way of important. The aim of this work was to demonstrate the interventional effect of Tibetan kefir fermented goat milk on colorectal cancer and a co-morbidity model established by chronic unpredictable stress (CUMS). The results showed that the Tibetan kefir fermented milk significantly alleviated the manifestations of depressive behavior and altered the level of corticotropin-releasing factor (CRF), serum corticosterone, and inflammatory factors (IL-6, IL-17, TNF-α and IL-1β) in serum, hippocampus and colon Moreover, the Tibetan kefir fermented milk could alleviate the inflammatory response and the hyperactivity of the HPA axis and inhibite the disturbance of 5-hydroxytryptamine system caused by colorectal cancer and CUMS to prevent the progress of depressive colorectal cancer. These results interpreted the potential mechanism of Tibetan kefir on antidepressant and anticancer. It provided a theoretical basis for the exploitation of psychotropic probiotic dairy products and enriched patients' dietary supplement.

Hippocampal excitation-inhibition balance underlies the 5-HT2C receptor in modulating depressive behaviours.

The implication of 5-hydroxytryptamine 2C receptor (5-HT2CR) in depression is a topic of debate, and the underlying mechanisms remain largely unclear. We now elucidate hippocampal excitation-inhibition (E/I) balance underlies the regulatory effects of 5-HT2CR in depression. Molecular biological analyses showed that chronic mild stress (CMS) reduced the expression of 5-HT2CR in hippocampus. We revealed that inhibition of 5-HT2CR induced depressive-like behaviors, reduced GABA release and shifted the E/I balance towards excitation in CA3 pyramidal neurons by using behavioral analyses, microdialysis coupled with mass spectrum, and electrophysiological recording. Moreover, 5-HT2CR modulated neuronal nitric oxide synthase (nNOS)-carboxy-terminal PDZ ligand of nNOS (CAPON) interaction through influencing intracellular Ca2+ release, as determined by fiber photometry and coimmunoprecipitation. Notably, disruption of nNOS-CAPON by specific small molecule compound ZLc-002 or AAV-CMV-CAPON-125C-GFP, abolished 5-HT2CR inhibition-induced depressive-like behaviors, as well as the impairment in soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex assembly-mediated GABA vesicle release and a consequent E/I imbalance. Importantly, optogenetic inhibition of CA3 GABAergic neurons prevented the effects of AAV-CMV-CAPON-125C-GFP on depressive behaviors in the presence of 5-HT2CR antagonist. Conclusively, our findings disclose the regulatory role of 5-HT2CR in depressive-like behaviors and highlight the hippocampal nNOS-CAPON coupling-triggered E/I imbalance as a pivotal cellular event underpinning the behavioral consequences of 5-HT2CR inhibition.

Deleterious effect of sustained neuroinflammation in pediatric traumatic brain injury

IntroductionDespite improved management of traumatic brain injury (TBI), it still leads to lifelong sequelae and disability, particularly in children. Chronic neuroinflammation (the so-called tertiary phase), in particular, microglia/macrophage and astrocyte reactivity, is among the main mechanisms suspected of playing a role in the generation of lesions associated with TBI. The role of acute neuroinflammation is now well understood, but its persistent effect and impact on the brain, particularly during development, are not. Here, we investigated the long-term effects of pediatric TBI on the brain in a mouse model. MethodsPediatric TBI was induced in mice on postnatal day (P) 7 by weight-drop trauma. The time course of neuroinflammation and myelination was examined in the TBI mice. They were also assessed by magnetic resonance, functional ultrasound, and behavioral tests at P45. ResultsTBI induced robust neuroinflammation, characterized by acute microglia/macrophage and astrocyte reactivity. The long-term consequences of pediatric TBI studied on P45 involved localized scarring astrogliosis, persistent microgliosis associated with a specific transcriptomic signature, and a long-lasting myelination defect consisting of the loss of myelinated axons, a decreased level of myelin binding protein, and severe thinning of the corpus callosum. These results were confirmed by reduced fractional anisotropy, measured by diffusion tensor imaging, and altered inter- and intra-hemispheric connectivity, measured by functional ultrasound imaging. In addition, adolescent mice with pediatric TBI showed persistent social interaction deficits and signs of anxiety and depressive behaviors. ConclusionsWe show that pediatric TBI induces tertiary neuroinflammatory processes associated with white matter lesions and altered behavior. These results support our model as a model for preclinical studies for tertiary lesions following TBI.

Dynamics of somatostatin 4 receptor expression during chronic-stress loading and its potential as a chronic-stress marker

Chronic stress has been implicated in mental illnesses and depressive behaviors. Somatostatin 4 receptor (SSTR4) has been shown to mediate anxiolytic and depression-like effects. Here, we aimed to explore the potential of SSTR4 as a diagnostic marker for chronic stress in mice. The mice were divided into single stress, chronic restraint stress, and control groups, and Sstr4 mRNA expression in the pituitary, lungs, and thymus, its protein expression in the thymus, were analyzed. Compared to controls, Sstr4 mRNA expression decreased significantly in the pituitary gland of the chronic and single-stress groups (P = 0.0181 and 0.0022, respectively) and lungs of the single-stress group (P = 0.0124), whereas it significantly increased in the thymus of the chronic-stress group (P = 0.0313). Thymic SSTR4 expression did not decrease significantly in stress groups compared to that in the control group (P = 0.0963). These results suggest that SSTR4 expression fluctuates in response to stress. Furthermore, Sstr4 mRNA expression dynamics in each organ differed based on single or chronic restraint stress-loading periods. In conclusion, this study suggests that investigating SSTR4 expression in each organ could allow for its use as a stress marker to estimate the stress-loading period and aid in diagnosing chronic stress.

The antioxidant and neuroprotective effects of melatonin on glyphosate-based herbicide-induced affective and cognitive impairments in rats

ABSTRACT Several studies have found that exposure to glyphosate-based herbicides (GBH) can lead to memory impairment and affective disorders. Oxidative stress (OS) is one of the mechanisms that can explain the neurotoxicity of GBH. Consequently, molecules with an antioxidant effect may have neuroprotective potential against GBH-related brain damage. In this work, we aim to evaluate the neuroprotective effect of melatonin (MEL) against affective and cognitive disorders caused by GBH. For this experiment, male Wistar rats received, during the peripubertal period, a daily administration of GBH (75 mg/kg) or GBH + MEL (4 mg/kg). At the end of the treatment, the open field, elevated plus maze, and forced swimming tests were used to explore anxiety levels and depression-like symptoms. While the Y-Maze and Morris Water Maze have been used to detect cognitive deficits, we also measured markers of OS, specifically catalase, nitric oxide, and lipid peroxidation, in the hippocampus and prefrontal cortex. Our results revealed that MEL reduces anxiety and depressive behavior, as well as the cognitive deficits caused by GBH. In addition, co-administration of MEL and GBH induced an improvement in the various markers of OS. The positive action of MEL against OS is therefore one of the mechanisms explaining its neuroprotective power against GBH.

Changes in Cerebral Mitochondrial Function in Postpartum Dams Exposed to a Low-resource Environment during Weaning

Background. Postpartum depression is a serious mental-health condition, affecting over 14% of all mothers in the U.S. Poverty, a lack of educational and economic resources, is a major determinant of adult mental health. Within the U.S., poverty impacts 11% of adults, with a greater incidence in women of childbearing age (roughly 16%) and postpartum women (roughly 14%). While pregnancy and poverty separately increase risks of developing depression, few studies have combined these conditions to determine their role in the development of depression. Further, no studies have explored mechanisms contributing to depression following pregnancy and poverty. However, cerebral mitochondrial dysfunction (C-mtDys) may be one mechanism. The aim of this study is to examine C-mtDys in postpartum (PP) dams exposed to the limited-bedding-nesting (LBN) model in rats, which reduces their nesting material to simulate a low-resource environment. We hypothesize that PP dams exposed to the LBN model will exhibit C-mtDys and elevated oxidative stress. Methods. Pregnant Sprague-Dawley rats gave birth naturally and were divided randomly into LBN (n =2) or control (n = 2) groups. LBN dams were exposed to the LBN model from PD 2 through PD 9. To validate the success of the LBN model, entropy scores, which are a measure of behavior unpredictability, were recorded for each dam. At 17 weeks PP, equivalent to 8 years PP in humans, brains were collected and used to isolate mitochondria through differential centrifugation. Mitochondrial respiratory states were evaluated via respiration (mtRes) to determine function. Oxidative stress in the whole brain was examined through H2O2 and total antioxidant capacity colorimetric biochemical assays. Results. LBN PP dams displayed higher entropy scores (1.10 ± 0.04 v. 0.79 ± 0.04, p < 0.05), as expected based on prior literature, serving as validation of the model. At 17 weeks, PP LBN dams had reduced mtRes in all states, including the basal state (176.09 ± 5.90 v. 360.70 ± 7.73 pmol/s/mg, ns), State 2 (1044.72 ± 14.00 v. 1703.00 ± 18.10 pmol/s/mg, ns), State 3 (3843.27 ± 31.86 v. 6705.72 ± 37.54 pmol/s/mg, ns) and State 4 (776.83 ± 13.65 v. 1533.54 ± 16.46 pmol/s/mg, ns). PP LBN dams demonstrated reduced total antioxidant capacity by roughly 20% (54.10 ± 1.24 v. 63.04 ± 0.99 mM Trolox, ns) and elevated H2O2 by roughly 50% (2.12 ± 0.52 v. 1.35 ± 0.28 nM/mg, ns). Summary. In summary, preliminary data shows C-mtDys via reduced mtRes in PP dams exposed to an impoverished environment during weaning. Furthermore, this study suggests that decreased mtRes could contribute to increased oxidative stress in the brain. Elevated oxidative stress may cause damage at the cellular and circuitry levels in the brain that could facilitate the development of depression later in life. Future studies will further examine C-mtDys, oxidative stress, and depressive behaviors in PP dams exposed to LBN. This study is significant because it identifies C-mtDys as a possible mechanism causing depression after exposure to both pregnancy and poverty. This project was funded by the American Heart Association Early Career Development Award [AHA 18CDA34110264 (Cunningham)]. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

A narrative review of advances in pharmacotherapy for depression and suicidal behavior in youth within the era of heightened social media

A narrative review of advances in pharmacotherapy for depression and suicidal behavior in youth within the era of heightened social media

Prolonged Blue Light Exposure Does Not Elicit Adverse Changes to Physical Activity in Male Mice

Color plays a role in human and animal circadian rhythm patterns, behaviors, and emotional responses. Environments containing blue colors improve information storage in humans and reproductive success in animals; however, environments containing blue light influence behavioral and emotional responses in rodents and humans in adverse ways. Exposure to blue light alters sleeping patterns, induces the stress response, and elicits depressive behaviors. These initial responses then affect awake time functionality and productivity. Under normal physiological conditions, mice, when provided access to an in-cage running wheel, exhibit high levels of nocturnal physical activity behavior. It is unknown if this nocturnal behavior changes after prolonged blue light exposure. Therefore, this project's hypothesis is wheel running utilization decreases after exposure to blue light during the diurnal restful period in the normally nocturnal mouse. The purpose of this study was to expose mice to overhead blue LED lights during the daytime rest period and to examine nighttime physical activity patterns. Daily wheel running distance, duration, and speed monitoring in C57BL/6j male mice (n=12) occurred for 21 days. During the second week of the study, an experimental group (n=6) underwent blue light-emitting diode (LED) light exposure, and a control group (n=6) experienced white LED light exposure at the same intensity. The lights were on a 12-hour light/dark cycle at full brightness during the exposure period. Differences in wheel running distance, duration, and speed following exposure to blue LED light were assessed via individual two-way (group by phase of study) ANOVAs. Blue LED light exposure did not appear to affect average daily wheel running distance [F=0.42, p=0.57], duration [F=0.79, p=0.42], or speed [F=0.08, p=0.87]. Following exposure to blue LED light during the restful diurnal period, wheel running remained stable. This lack of effect indicates that mechanisms may exist to protect mice from the adverse effects associated with blue light exposure, especially as it pertains to participating in routine physical activity. These postulated mechanisms may allow robust participation in physical activity-related behaviors in these animals and represent a potential biological regulator that could aid in mitigating the adverse effects of blue light exposure experienced in humans. All funding for this research was provided by the Union University Department of Biology. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

HUBUNGAN DEPRESI DAN PERILAKU KONFORMITAS DENGAN KEJADIAN INTERNET GAMING DISORDER PADA REMAJA

Internet gaming disorder is a phenomenon that causes quite a bad impact. Several influencing factors are internal factors, situational factors, external factors, and social factors. Regarding situational factors, a person often uses online games to make himself comfortable when his psychology is bad. While regarding social factors in adolescence, a person wants to be liked and tends to change his opinion or behavior to be accepted by his group. The purpose of this research is to find out the relationship between depression and conformity behavior toward internet gaming disorder in adolescents. The study was conducted with a population of students from the Faculty of Medicine, the University of Muhammadiyah Semarang with a sample of 85. The study was conducted using the IGDS9-SF, PHQ-9, and Conformity Questionnaires. From the data obtained, a correlation test was carried out. The study's results found a significant relationship between depression and conformity behavior with internet gaming disorder. The depressive state has moderate or strong strength and is positive linear. Meanwhile, conformity behavior has a low or relatively weak relationship strength and is negatively linear. The results of this study can help identify factors related to internet gaming disorder so that this can be minimized.

Impact of Abl2/Arg deficiency on anxiety and depressive behaviors in mice

Abl2/Arg (ABL-related gene) is a member of the Abelson family of nonreceptor tyrosine kinases, known for its role in tumor progression, metastasis, tissue injury responses, inflammation, neural degeneration, and other diseases. In this study, we developed Abl2/Arg knockout (abl2-/-) mice to explore its impact on sensory/motor functions and emotion-related behaviors. Our findings show that abl2-/- mice exhibit normal growth and phenotypic characteristics, closely resembling their wild-type (WT) counterparts. Behavioral tests, including the elevated plus maze, marble-burying behavior test, and open field test, indicated pronounced anxiety-like behaviors in abl2-/- mice compared to WT mice. Furthermore, in the tail suspension test, abl2-/- mice showed a significant decrease in mobility time, suggesting depressive-like behavior. Conversely, in the Y-maze and cliff avoidance reaction tests, no notable differences were observed between abl2-/- and WT mice, suggesting the absence of working memory deficits and impulsivity in abl2-/- mice. Proteomic analysis of the hippocampus in abl2-/- mice highlighted significant alterations in proteins related to anxiety and depression, especially those associated with the GABAergic synapse in inhibitory neurotransmission. The expression of Gabbr2 was significantly reduced in the hippocampus of abl2-/- compared to WT mice, and intraperitoneal treatment of GABA receptor agonist Gaboxadol normalized anxiety/depression-related behaviors of abl2-/- mice. These findings underscore the potential role of Abl2/Arg in influencing anxiety and depressive-like behaviors, thereby contributing valuable insights into its broader physiological and pathological functions.

Latent Profile Analysis of Eating Disorders and Emotional Well-being in College Students

Abstract Background: University students face a unique combination of academic pressures, transitional life stages, and potential social isolation, which can contribute to the development of unhealthy eating patterns and emotional problems. Objectives: To explore the association between quality of life, emotional problems, and eating disorders (ED) among university students, using Latent Profile Analysis (LPA) to identify distinct eating profiles. Methods: This cross-sectional exploratory study involved a total of 1,798 university students from Brazil and Canada (mean age= 21.2; women = 78.4%). The instruments used included the Addiction-like Eating Behaviour Scale (AEBS), Depression, Anxiety, and Stress Scale (DASS-21), WHOQOL-bref, Yale Food Addiction Scale 2.0 (YFAS), Difficulties in Emotion Regulation Scale (DERS), and Impulsive Behavior Scale (UPPS-P). Results: The LPA, conducted based on the AEBS raw scores due to the absence of diagnostic criteria, identified three eating behavior profiles: Profile 1 with lower scores in AEBS and YFAS, indicating a healthy eating pattern; Profile 2 with high scores, reflecting eating compulsion; and Profile 3 with intermediate characteristics. Profile 2, associated with higher levels of anxiety, depression, and stress, showed a significantly reduced quality of life. No differences were detected regarding nationality, gender, type of university, or housing. Conclusion: The results highlight the complex relationships between eating behavior, mental health, and quality of life in university students, underscoring the need for targeted interventions to improve their well-being. Thus, ED and their consequent impact on mental health and quality of life are increasingly recognized as critical issues among university students, a group uniquely vulnerable to such challenges due to transitional life stages and academic pressures. Keywords: Latent Profile Analysis, Eating Disorders, University Students, Mental Health, Cross-Sectional Study.