Glucocorticoid-Dependent Retinal Degeneration and Vision Impairment in Mice Susceptible to Prenatal Stress-Induced Behavioral Abnormalities DOI Creative Commons
Morin Ryu, Ju‐Young Jung,

Han Na Suh

и другие.

Cellular and Molecular Neurobiology, Год журнала: 2024, Номер 45(1)

Опубликована: Дек. 23, 2024

Chronic exposure to prenatal stress can impair neurogenesis and lead irreversible cognitive neuropsychiatric abnormalities in offspring. The retina is part of the nervous system; however, impacts on retinal visual function remain unclear. This study examined how elevated glucocorticoid levels differentially affect development offspring pregnant mice exposed chronic unpredictable mild (CUMS). Offspring were classified into control, stress-resilient, stress-susceptible groups based behavioral tests assessing spatial memory depression-like behaviors. group exhibited significantly altered synaptogenesis, reduced ganglion cell development, decreased thickness, visiual impairment. These also showed a pervasive transformation astrocytes proinflammatory A1-like reactive state, evidenced by increased GFAP STAT3 expression levels. astrocyte phenotype shift coincided with disruptions synaptic formation. Furthermore, exogenous corticosterone confirmed that effects are mediated glucocorticoid-induced neurodegeneration. Our findings suggest trigger series neurodevelopmental disturbances leading neurodegeneration vision research highlights impact health, suggesting new avenues for understanding potentially mitigating negative early-life neurodevelopment.

Язык: Английский

Sex specific gut-microbiota signatures of resilient and comorbid gut-brain phenotypes induced by early life stress DOI Creative Commons
Lars Wilmes, Valentina Caputi, Thomaz F. S. Bastiaanssen

и другие.

Neurobiology of Stress, Год журнала: 2024, Номер 33, С. 100686 - 100686

Опубликована: Ноя. 1, 2024

Alterations in gut-brain axis communication pathways and the gut microbiota ecosystem caused by early life stress have been extensively described as critical players pathophysiology of stress-induced disorders. However, extent to which alterations manifest contribute sex-specific susceptibility distinct phenotypes adulthood has yet be defined.

Язык: Английский

Процитировано

4
Prenatal maternal stress induces increased avoidance behavior in adolescent mice offspring DOI
Xueyong Yin, Rui Jiang, Xiaoyu Liu

и другие.

Pharmacology Biochemistry and Behavior, Год журнала: 2025, Номер unknown, С. 174029 - 174029

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

0
Prenatal stress increases learning and memory deficits in offspring: A toxicological study on hippocampal neuronal damage in rats DOI Creative Commons

Ruixue Huang,

Huijuan Li,

Jiani Xiao

и другие.

Ecotoxicology and Environmental Safety, Год журнала: 2025, Номер 295, С. 118167 - 118167

Опубликована: Апрель 1, 2025

Recent epidemiological studies have observed that prenatal stress induced learning and memory deficits in children, but the toxicological mechanisms remain unclear. We conducted a systematic study to explore of on offspring. established model by corticosterone (CORT) administration at different dose levels (0, 10, 40 mg/kg) from gestational days 14-21. First we assessed hippocampal damage offspring neuronal damage, synaptic neurotransmitter levels. then detected ability Morris water maze test, finally analyzed biomarkers oxidative apoptosis potential mechanism. Prenatal CORT was indicated decreased body weight, increased serum reduced food consumption (p < 0.05). With increasing, worsened, characterized damaged neurons, proteins, neurotransmitters. Learning were observed, including long escape latency travel distance find platform test 0.05).The underlying impairments biomarkers: antioxidant enzymes (SOD T-AOC), pro-inflammatory cytokines (IL-6) leads hippocampus-dependent neuron loss, injury, Our implies improving maternal well-being is helpful for development next generation.

Язык: Английский

Процитировано

0
Early life adversities, psychopathologies and novel pharmacological strategies DOI Creative Commons
Annamaria Cattaneo, Veronica Begni, Valentina Zonca

и другие.

Pharmacology & Therapeutics, Год журнала: 2024, Номер 260, С. 108686 - 108686

Опубликована: Июль 3, 2024

Exposure to adversities during early life stages (early - ELA), ranging from pregnancy adolescence, represents a major risk factor for the vulnerability mental disorders. Hence, it is important understand molecular and functional underpinning of such relationship, in order develop strategies aimed at reducing psychopathologic burden associated with ELA, which may eventually lead significant improvement clinical practice. In this review, we will initially recapitulate preclinical evidence supporting link between ELA psychopathology primarily discuss main biological mechanisms that have been described as potential mediators effects on risk, including role genetic factors well sex differences. The knowledge emerging these studies be instrumental development novel therapeutic not only correcting deficits emerge exposure, but also preventing manifestation full-blown condition. With respect, specifically focus adolescence key time frame disease onset intervention. We believe incorporating research data context can elucidate contributing or promote resilience. This ultimately allow identification 'at risk' individuals who benefit specific forms interventions that, by interfering trajectories, could result more benign outcomes.

Язык: Английский

Процитировано

1
Chronic treatment with the antipsychotic lurasidone modulates the neuroinflammatory changes associated with the vulnerability to chronic mild stress exposure in female rats DOI Creative Commons
Veronica Begni, Diana Morena Silipo, Chiara Bottanelli

и другие.

Brain Behavior and Immunity, Год журнала: 2024, Номер 123, С. 586 - 596

Опубликована: Окт. 9, 2024

Stress exposure is a key risk factor for the developmentof depressive-like conditions. However, despite higher incidence of Major Depressive Disorder in female population, classical stress-based experimental paradigms have primarily focused on males. In present study, we used well-established chronic mild stress (CMS) paradigm to investigate development anhedonia, cardinal symptom affective disorders, animals and also studied potential effect antipsychotic drug lurasidone normalizing alterations brought about by exposure. We found that three weeks CMS produced significant reduction sucrose intake 50% (vulnerable, CMS-V), whereas others were resilient (CMS-R). The an anhedonic phenotype CMS-V was associated with elevation different immune markers, such as Complement C3 C4, inflammatory cytokines, including INFß Il1ß dorsal ventral hippocampus. Interestingly, sub-chronic treatment able revert while most molecular rats vulnerable This study extends ability normalize females. Moreover, provide novel evidence lurasidone's effectiveness treating mental disorders characterized immune-inflammatory dysfunction.

Язык: Английский

Процитировано

1
Perinatal stress modulates glutamatergic functional connectivity: A post-synaptic density immediate early gene-based network analysis DOI Creative Commons
Licia Vellucci, Giuseppe De Simone, Sara Morley‐Fletcher

и другие.

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Год журнала: 2024, Номер 133, С. 111032 - 111032

Опубликована: Май 16, 2024

Early life stress may induce synaptic changes within brain regions associated with behavioral disorders. Here, we investigated glutamatergic functional connectivity by a postsynaptic density immediate-early gene-based network analysis. Pregnant female Sprague-Dawley rats were randomly divided into two experimental groups: one exposed to sessions and the other serving as stress-free control group. Homer1 expression was evaluated in situ hybridization technique eighty-eight of interest male rat offspring. Differences between perinatal group (PRS) (n = 5) (CTR) assessed performing Student's t-test via SPSS 28.0.1.0 Bonferroni correction. Additionally, all possible pairwise Spearman's correlations computed well correlation matrices networks for each generated RStudio Cytoscape. Perinatal exposure Homer1a reduction several cortical, thalamic, striatal regions. Furthermore, it found affect between: lateral septal nucleus, central medial thalamic anterior part paraventricular both retrosplenial granular b cortex hippocampal regions; orbitofrontal cortex, amygdaloid nuclei, lastly, among involved limbic system. Finally, PRS showed significant multiple connections ventrolateral anteroventral nucleus after exposure, decrease centrality ventral nuclei suggestive putative reduced cortical over these Within present preclinical setting, is modifier early neuronal circuits behaviors relevant model neurodevelopmental

Язык: Английский

Процитировано

0
Emotional dysregulation following prenatal stress is associated with altered prefrontal cortex responsiveness to an acute challenge in adolescence DOI Creative Commons
Rodrigo Orso, Kerstin Camile Creutzberg, Veronica Begni

и другие.

Progress in Neuro-Psychopharmacology and Biological Psychiatry, Год журнала: 2024, Номер 136, С. 111162 - 111162

Опубликована: Окт. 9, 2024

Exposure to prenatal stress (PNS) has the potential elicit multiple neurobiological alterations and increase susceptibility psychiatric disorders. Moreover, gestational may sensitize brain toward an altered response subsequent challenges. Here, we investigated effects of PNS in rats assessed whether these animals exhibit responsiveness acute (AS) during adolescence. From day 14 until delivery, Sprague Dawley dams were exposed or left undisturbed. During adolescence (PND38 PND41), offspring tested social interaction splash test. At PND44 half 5 min forced swim stress. Males Females showed reduced sociability increased anhedonic-like behavior. molecular level, exposure adolescent AS produced activation amygdala ventral dorsal hippocampus. Regarding prefrontal cortex (PFC), observed a pronounced males AS. Cell-type specific transcriptional analyses revealed significant imbalance PFC excitatory inhibitory neurons females Furthermore, stressed exhibited disrupted HPA-axis function, while impairments modulation antioxidant genes. Our study shows that induces emotional dysregulation alters stressor. disruption balance could influence ability respond challenging events contribute precipitate full-blown pathologic condition.

Язык: Английский

Процитировано

0
Glucocorticoid-Dependent Retinal Degeneration and Vision Impairment in Mice Susceptible to Prenatal Stress-Induced Behavioral Abnormalities DOI Creative Commons
Morin Ryu, Ju‐Young Jung,

Han Na Suh

и другие.

Cellular and Molecular Neurobiology, Год журнала: 2024, Номер 45(1)

Опубликована: Дек. 23, 2024

Chronic exposure to prenatal stress can impair neurogenesis and lead irreversible cognitive neuropsychiatric abnormalities in offspring. The retina is part of the nervous system; however, impacts on retinal visual function remain unclear. This study examined how elevated glucocorticoid levels differentially affect development offspring pregnant mice exposed chronic unpredictable mild (CUMS). Offspring were classified into control, stress-resilient, stress-susceptible groups based behavioral tests assessing spatial memory depression-like behaviors. group exhibited significantly altered synaptogenesis, reduced ganglion cell development, decreased thickness, visiual impairment. These also showed a pervasive transformation astrocytes proinflammatory A1-like reactive state, evidenced by increased GFAP STAT3 expression levels. astrocyte phenotype shift coincided with disruptions synaptic formation. Furthermore, exogenous corticosterone confirmed that effects are mediated glucocorticoid-induced neurodegeneration. Our findings suggest trigger series neurodevelopmental disturbances leading neurodegeneration vision research highlights impact health, suggesting new avenues for understanding potentially mitigating negative early-life neurodevelopment.

Язык: Английский

Процитировано

0