Neurotoxicology最新文献

{"title":"The interaction between plasma polymetals and lifestyle on cognitive dysfunction in occupational aluminum exposed workers: A cross-sectional study in China","authors":"Tianshu Wang ,&nbsp;Lingshan Xue ,&nbsp;Chenyang Li ,&nbsp;Dan Zhao ,&nbsp;Jiaping Huan ,&nbsp;Xiao Han ,&nbsp;Jing Song ,&nbsp;Linping Wang ,&nbsp;Huifang Zhang ,&nbsp;Qiao Niu ,&nbsp;Baolong Pan ,&nbsp;Jinzhu Yin ,&nbsp;Xiaoting Lu","doi":"10.1016/j.neuro.2024.11.002","DOIUrl":"10.1016/j.neuro.2024.11.002","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the interaction between plasma polymetallic exposure and lifestyle factors on cognitive function abnormalities in occupational aluminum workers. The aim is to develop a new occupational health management model that integrates lifestyle behaviors with occupational activities to comprehensively protect the health of these workers.</div></div><div><h3>Method</h3><div>476 Participants were recruited from an aluminum factory in Shanxi, China. Cognitive functioning was assessed using the Montreal Cognitive Assessment Scale (MoCA). Plasma polymetallic levels were measured using ICP-MS. Logistic regression analyzed the relationship between nine plasma metals, lifestyle factors, and cognitive abnormalities. A 3D model validated the interaction between metals and analyzed the combined effects of plasma metals and lifestyle on MoCA scores. The Chi-squared Automatic Interaction Detector (CHAID) decision tree was used to identify factors influencing cognitive dysfunction.</div></div><div><h3>Results</h3><div>High blood aluminum concentration (&gt;47.85 μg/L), high blood lithium concentration(&gt;3.15 μg/L), as well as sleep time(≤7 h and &gt; 8 h), smoking, alcohol consumption, and length of mobile phone use(≥2 h) were risk factors for abnormal cognitive functioning. In addition aluminum and lithium have a multiplicative interaction on cognitive function(OR=1.86,95 %<em>CI</em>:1.14,3.050). There was an interaction between high plasma levels of aluminum and lithium and smoking on cognitive function in workers, and an interaction between high plasma levels of aluminum and lithium and sleep duration ≤7 or &gt;8 h on cognitive function in workers.</div></div><div><h3>Conclusion</h3><div>The levels of blood metal elements aluminum and lithium, as well as sleep time, smoking, drinking, and length of mobile phone use, are risk factors for cognitive dysfunction in occupational aluminum workers. There are the synergetic effect to increase the risk of cognitive dysfunction between blood aluminum concentration ≥50.59μg/L and blood lithium concentration ≥3.44μg/L, sleep duration ≤7h&amp; &gt;8 h, smoking, drinking, mobile phone use ≥2 h.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 313-322"},"PeriodicalIF":3.4,"publicationDate":"2024-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142693204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Developmental exposure of zebrafish to saxitoxin causes altered expression of genes associated with axonal growth","authors":"Neelakanteswar Aluru ,&nbsp;Daniel P. Chapman ,&nbsp;Kevin W. Becker ,&nbsp;Benjamin A.S. Van Mooy ,&nbsp;Sibel I. Karchner ,&nbsp;John J. Stegeman ,&nbsp;Mark E. Hahn","doi":"10.1016/j.neuro.2024.11.003","DOIUrl":"10.1016/j.neuro.2024.11.003","url":null,"abstract":"<div><div>Saxitoxin (STX) is a potent neurotoxin naturally produced by dinoflagellates and cyanobacteria. STX inhibits voltage-gated sodium channels (VGSCs), affecting the propagation of action potentials. Consumption of seafood contaminated with STX is responsible for paralytic shellfish poisoning (PSP). Humans are among the species most sensitive to PSP; neurological symptoms of exposure range from tingling of the extremities to severe paralysis. The objective of this study was to determine the effects of STX exposure on developmental processes during early embryogenesis. This study was designed to test the hypothesis that early developmental exposure to STX would disrupt key processes, particularly those related to neural development. Zebrafish embryos were exposed to STX (24 or 48 pg) or vehicle (0.3 mM HCl) at 6 h post fertilization (hpf) via microinjection. There was no overt toxicity but starting at 36 hpf there was a temporary lack of pigmentation in STX-injected embryos, which resolved by 72 hpf. Using high performance liquid chromatography, we found that STX was retained in embryos up to 72 hpf in a dose-dependent manner. Temporal transcriptional profiling of embryos exposed to 48 pg STX per embryo revealed no differentially expressed genes (DEGs) at 24 hpf, but at 36 and 48 hpf, there were 3547 and 3356 DEGs, respectively. KEGG pathway analysis revealed significant enrichment of genes related to focal adhesion, adherens junction and regulation of actin cytoskeleton, suggesting that cell-cell and cell-extracellular matrix interactions were affected by STX. Genes affected are critical for axonal growth and the development of functional neural networks. We confirmed these findings by visualizing axonal defects in transgenic zebrafish with fluorescently labeled sensory neurons. In addition, our gene expression results suggest that STX exposure affects both canonical and noncanonical functions of VGSCs. Given the fundamental role of VGSCs in both physiology and development, these findings offer valuable insights into effects of exposure to neurotoxins.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 303-312"},"PeriodicalIF":3.4,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142686952","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATF5-mediated mitochondrial unfolded protein response protects against Pb-induced mitochondria damage in SH-SY5Y cell","authors":"Yihan Xu ,&nbsp;Min Liu ,&nbsp;Sikang Gao ,&nbsp;Xiaoyi Li ,&nbsp;Jun Chen ,&nbsp;Fang Ye","doi":"10.1016/j.neuro.2024.11.001","DOIUrl":"10.1016/j.neuro.2024.11.001","url":null,"abstract":"<div><div>Mitochondria is the primary target of lead (Pb) in neural cells, and Pb exposure can cause impairment to mitochondrial function and morphology. Recent studies have reported that a conserved cellular stress response, called mitochondrial unfolded protein response (mtUPR), is activated in response to mitochondrial dysfunction and protein misfolding and play protective roles in aging and neurodegeneration, but it’s unknown whether mtUPR could protect against Pb-induced neurotoxicity. In this study, we found that sublethal level exposure of PbAc (2.5 μM) could cause mitochondria damage and then activate mtUPR by promoting the expression of mitochondrial proteases (LonP1 and ClpP), molecular chaperone (HSPA1A). ATF5 mediated mtUPR activation as knocking out ATF5 significantly inhibited Pb-induced LonP1 and ClpP expression. Moreover, ATF5 deficiency exacerbated Pb-induced mitochondrial morphological and oxidative phosphorylation (OXPHOS) functional damage, resulting in oxidative stress and ultimately promoting cell death. Conversely, overexpression of ATF5 confers protection against Pb-induced oxidative stress and cell death. Collectively, thess results highlight that mtUPR mediated by ATF5 safeguards against mitochondria damage caused by Pb exposure, providing insights into the development of new strategies for mitigating the Pb neurotoxicity.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 293-302"},"PeriodicalIF":3.4,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vilazodone exposure during pregnancy: Effects on embryo-fetal development, pregnancy outcomes and fetal neurotoxicity by BDNF/Bax-Bcl2/5-HT mediated mechanisms","authors":"Priyanka Agrawal ,&nbsp;Pallavi Singh ,&nbsp;K.P. Singh","doi":"10.1016/j.neuro.2024.10.012","DOIUrl":"10.1016/j.neuro.2024.10.012","url":null,"abstract":"<div><div>The high prevalence of major depressive disorder (MDD) among women of childbearing age necessitates careful consideration of antidepressant use during pregnancy. Although newer antidepressants, such as Vilazodone (VLZ), are preferred for their enhanced therapeutic profiles; however, their safety during pregnancy and long-term effects on offspring brains remain inadequately addressed. Therefore, this study aimed to investigate the reproductive and developmental neurotoxicity of VLZ given at equivalent therapeutic doses during gestation in a rat model. Pregnant Wistar dams were orally administered either with 1 mg/day or 2 mg/day of VLZ from gestation day (GD) 6–21. The dams were sacrificed at GD 21, and the placentas and fetuses were collected. Fetal brains were then subjected to neurohistopathological, neurochemical, and biochemical analysis. Prenatal exposure to VLZ at 2 mg/day resulted in significant maternal, reproductive, and embryo-fetal toxicity, characterized by reduced food intake, diminished weight gain in pregnant dams, and smaller litter sizes, along with decreased fetal and placental weights. These effects were associated with developmental neurotoxicity, which manifested as decreased fetal brain size and weight, a substantial reduction in neocortical layer thickness, brain-derived neurotrophic factor (BDNF) expression, serotonin, dopamine, and norepinephrine neurotransmitter levels (5-HT, DA, and NE), and increased apoptotic activity (Bax and Bcl-2 ratio) and acetylcholinesterase levels in the developing brain. Our findings indicate that prenatal VLZ exposure interfere with crucial brain development processes involving the BDNF/Bax-Bcl2/5-HT signalling pathways, leading to long-lasting neurodevelopmental impairments. This study is the first to document the adverse effects of VLZ on fetal brain development, highlighting the need for further research to assess the safety of VLZ use during pregnancy.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 280-292"},"PeriodicalIF":3.4,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The relationship between lead levels and reading acquisition in Spanish speakers, evidence from Uruguayan schoolers","authors":"Natalia Agudelo ,&nbsp;Ariel Cuadro ,&nbsp;Gabriel Barg ,&nbsp;Elena I. Queirolo ,&nbsp;Nelly Mañay ,&nbsp;Katarzyna Kordas","doi":"10.1016/j.neuro.2024.10.011","DOIUrl":"10.1016/j.neuro.2024.10.011","url":null,"abstract":"<div><div>Lead is a well-known neurotoxicant that continues to affect children´s cognition and behavior. Nevertheless, we still have little evidence on the consequences of lead exposure on reading abilities, particularly in languages other than English.</div></div><div><h3>Objective</h3><div>To investigate the cross-sectional association between blood lead levels (BLL), and pre-reading and reading abilities in first-grade children from Montevideo, Uruguay.</div></div><div><h3>Method</h3><div>Of 357 school children (age 67–105 months) enrolled into the study, 287(43 % girls) had a BLL measure and an assessment of pre-reading and reading abilities based on five tests (Verbal comprehension, Sound blending, Letter word identification, Sentence reading fluency, and Passage comprehension) from the Batería III Woodcock-Muñoz. Separate generalized linear models (GLM) were conducted on the relationship between BLL and each test score separately, adjusting for sex, maternal education, household assets, Home Observation for Measurement of the Environment Inventory score, season, test administrator, blood lead testing method, and school clusters.</div></div><div><h3>Results</h3><div>The mean BLL was 4.0 ± 2.2 µg/dL, with no differences between the sexes. BLL was associated with a poorer vocabulary knowledge (β [95 % CI]): −0.20 [-0.39, 0.01]. For all the tests, children with BLLs ≥5 µg/dL tended to exhibit poorer performance than children with lower BLLs, but these associations were not statistically significant. When stratified by sex, some evidence of differential associations between BLLs and reading abilities emerged: BLLs were associated with higher phonological awareness in girls (0.32 [0.15, 0.48]) but not boys, and with lower reading comprehension in boys (-0.54 [-1.20, 0.13]) but not girls. Also, lead exposure (BLL ≥ 5 µg/dL) was more strongly and negatively associated with phonological awareness (-1.22 [-1.57, −0.86]) in boys than girls.</div></div><div><h3>Conclusion</h3><div>In this study of first-grade children learning to read in Spanish, we found an inverse association between lead exposure and vocabulary scores, as well as tendency toward lower performance on pre-reading and reading measures among children with BLLs ≥5 µg/dL. Pre-reading and reading abilities are relevant to literacy acquisition; further research is required to confirm these links in larger studies, and to investigate differences between boys and girls, and according to key sociodemographic characteristics.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 272-279"},"PeriodicalIF":3.4,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142624722","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The impact of electronic cigarette aerosol exposure on spatial memory formation: Modulation by orally administered vitamin E","authors":"Aiman A. Yaseen ,&nbsp;Karem H. Alzoubi ,&nbsp;Nour Al-Sawalha ,&nbsp;Omar F. Khabour ,&nbsp;Anan Jarab ,&nbsp;Shirin Ali ,&nbsp;Samina Salim ,&nbsp;Thomas Eissenberg","doi":"10.1016/j.neuro.2024.10.014","DOIUrl":"10.1016/j.neuro.2024.10.014","url":null,"abstract":"<div><div>The use of electronic cigarettes (ECIGs) has grown exponentially among young adolescents. Tobacco smoking, in general and ECIG use in particular, has been linked to disruption of the oxidative system, resulting in organ damage. The current investigation intends to evaluate if orally administered Vitamin E (VitE) can protect from learning and cognitive impairment induced by ECIG aerosol exposure in a rat model. This effect was determined by studying behavioral and molecular targets for potential learning and memory impairment. Adult Wistar rats were assigned to the following groups (N= 12/group): Control, ECIG, VitE, and VitE+ECIG. The animals in the groups ECIG and VitE+ECIG were exposed to ECIG aerosol (1 hr/day, 6 days/week) for four weeks. The control group and VitE group were exposed to fresh air. At the same time, the VitE group and VitE+ECIG group were given Vitamin E 100 mg/kg/ day via gavage for the same period as the exposure. The control group and ECIG group were given the vehicle via gavage. Behavioral assessment was performed using the Radial Arm Water Maze. In addition, molecular measures (BDNF, SOD, GPx, GSH, and GSSG), were measured in rats’ hippocampal tissues. The results showed that VitE prevented ECIG aerosol exposure-induced impairment of spatial short-term and long-term memory formation (p&lt;0.05), decreased BDNF, and activities/levels of GPx, SOD, and GSH (p&lt;0.05). Moreover, VitE protected against GSSG levels increases (p&lt;0.05) associated with ECIG aerosol exposure. In summary, exposure to ECIGs resulted in spatial memory impairments, which could be mitigated by orally administered vitamin E.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 263-271"},"PeriodicalIF":3.4,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142564808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In memoriam: Bernard Jortner, professor emeritus of biomedical sciences and pathobiology.","authors":"","doi":"10.1016/j.neuro.2024.10.013","DOIUrl":"https://doi.org/10.1016/j.neuro.2024.10.013","url":null,"abstract":"","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"106 ","pages":"46-47"},"PeriodicalIF":3.4,"publicationDate":"2024-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex differences in β-N-Methylamino-L-alanine effects on zebrafish behavioral response","authors":"Nicoli R. do Amaral ,&nbsp;Murilo S. de Abreu ,&nbsp;Alexander Zanella ,&nbsp;Júlia P. Poletto ,&nbsp;Gabriel P. de Mello ,&nbsp;Marco A. da Croce ,&nbsp;Larissa B. Garbelotto ,&nbsp;Manuela G. Bernardon ,&nbsp;Ana C.V.V. Giacomini","doi":"10.1016/j.neuro.2024.10.010","DOIUrl":"10.1016/j.neuro.2024.10.010","url":null,"abstract":"<div><div>The β-N-methylamino-L-alanine (BMAA) is a neurotoxin produced by cyanobacteria and diatoms and related by triggered neurodegeneration. The exposure to neurotoxins has also been reported by causing emotional and neuroendocrine effects and these effects may be sex-specific. However, the effects of BMAA on emotions and pain, as well as neuroendocrine modulations remain poorly understood. Here, we evaluate potential sex differences in zebrafish behavioral responses to BMAA acute exposure on their anxiety and pain phenotypical behavioral repertoire and their neuroendocrine (cortisol) effects. Overall, sex differences in behavioral responses of adult zebrafish to BMAA exposure were demonstrated, as female fish reacted to it more strongly than males by altering their behavioral phenotype in both the novel tank and writhing -like behavior tests. In addition, sex differences were demonstrated in relation to time response, as male increased the writhing-like behavioral responses immediately after injection of BMAA, while female only 24-h after injection, reinforcing the painful stimulus caused by BMAA. However, the exposure to BMAA elevated the whole-body cortisol levels in both male and female zebrafish. Collectively, these findings emphasize the growing importance of studying sex differences in zebrafish, including the evaluation of neurotoxins effects on emotions and pain in this aquatic experimental model.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 257-262"},"PeriodicalIF":3.4,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exposure to an environmentally representative mixture of polybrominated diphenyl ethers (PBDEs) alters zebrafish neuromuscular development","authors":"Alec McDermott,&nbsp;Cécilia Bernier,&nbsp;Vanessa Piché,&nbsp;Isabelle Plante ,&nbsp;Shunmoogum A. Patten","doi":"10.1016/j.neuro.2024.10.009","DOIUrl":"10.1016/j.neuro.2024.10.009","url":null,"abstract":"<div><div>Polybrominated diphenyl ethers (PBDEs) are a prevalent group of brominated flame retardants (BFRs) added to several products such as electronics, plastics, and textiles to reduce their flammability. They are reported as endocrine disruptors and neurodevelopmental toxicants that can accumulate in human and wildlife tissues, thus making their ability to leach out of products into the environment a great cause for concern. In this study, zebrafish (<em>Danio rerio</em>) embryos and larvae were exposed to a wide concentration range (1.5, 15, 150 and 300 pM) of a PBDE mixture from one to six days post-fertilization (dpf). Hatching rates, mortality and general morphology were assessed during the exposure period. A delay in hatching was observed at the two highest PBDEs concentrations and mortality rate increased at 6 dpf. By 4 dpf, larvae exposed to 150 pM and 300 pM PBDEs developed an upcurved phenotype. Analysis of motor behavior at 6 dpf revealed that PBDE exposure acutely reduced locomotion. To further analyze these motor deficits, we assessed the neural network density and motor neuron and neuromuscular junctions (NMJ) development by immunostaining and imaging. Acetylated α-tubulin staining revealed a significant loss of neurons in a dose-dependent manner. Synaptic vesicle protein 2 (SV2) and ⍺-bungarotoxin (⍺-BTX) staining revealed a similar pattern, with a significant loss of SV2 and nicotinic acetylcholine receptors, thus preventing the colocalization of presynaptic neurons with postsynaptic neurons. Consistent with these results, the presence of cleaved caspase-3 and acridine orange positive cells showed increased cell death in zebrafish larvae exposed to PBDEs. Our results suggest that exposure to PBDEs leads to deficits in the zebrafish neuromuscular system through neuron death, inducing morphological and motor deficiencies throughout their development. They provide valuable insight into the neurotoxic effects of PBDEs, further highlighting the relevance of the zebrafish model in toxicological studies.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 247-256"},"PeriodicalIF":3.4,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142555036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Manifestation of polystyrene microplastic accumulation in brain with emphasis on morphometric and histopathological changes in limbic areas of Swiss albino mice","authors":"Manjyot Kaur,&nbsp;Anju Sharma,&nbsp;Placheril John,&nbsp;Pradeep Bhatnagar","doi":"10.1016/j.neuro.2024.10.008","DOIUrl":"10.1016/j.neuro.2024.10.008","url":null,"abstract":"<div><div>The widespread problem of microplastic (MP) contamination is becoming a major threat to the globe. Although most of the research to date has concentrated on the physiological impacts of MPs exposure, a relatively new field of study is beginning to examine its effects on the behaviour and limbic regions of the brain. In this study, exposure to polystyrene MPs (PS-MPs) for acute and sub-chronic durations negatively affected cognition and induced anxiety-like behaviour in mice. PS-MPs were detected in vital organs of mice, including the brain, which induced neurobehavioural and pathological changes in the limbic system. Furthermore, morphometric analysis revealed a significant decrease in the total cell count in the Dentate Gyrus (DG) and Cornu Ammonis (CA) regions of the hippocampus. Signs of neuronal injury and dystrophic changes were observed in the cortex, amygdala, and hypothalamus, potentially affecting anxiety and fear responses. Our study thus provides insight into the effect of PS-MPs on the neurobiology of the brain’s limbic system and related behavioural alterations.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"105 ","pages":"Pages 231-246"},"PeriodicalIF":3.4,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142470943","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}