Journal of chemical neuroanatomy最新文献

{"title":"To what extent are orally ingested nanoplastics toxic to the hippocampus in young adult rats?","authors":"Orhan Baş ,&nbsp;Hasan İlhan ,&nbsp;Hatice Hancı ,&nbsp;Hüseyin Çelikkan ,&nbsp;Deniz Ekinci ,&nbsp;Muhammet Değermenci ,&nbsp;Burak Oğuzhan Karapınar ,&nbsp;Aymen A. Warille ,&nbsp;Soner Çankaya ,&nbsp;Sezgin Özkasapoğlu","doi":"10.1016/j.jchemneu.2023.102314","DOIUrl":"10.1016/j.jchemneu.2023.102314","url":null,"abstract":"<div><p>As the use of plastic-containing materials in our daily lives becomes increasingly common, exposure to nanoplastics accordingly becomes inevitable. Micro and nanoplastics released from large amounts of plastic waste constitute a serious environmental problem. Therefore, this study aimed to examine the effects of polystyrene nanoplastic (PS-NP) on the hippocampus.</p></div><div><h3>Material and method</h3><p>Thirty Wistar albino rats, 15 male and 15 female, aged 6–8 weeks, were used in the research. These were randomly divided into three groups of five males and five females each. A five-minute open field test was applied to all rats on the first and last days of the study. Three groups of rats (Control, NP1 and NP2) received the standard chow and water. Additionally, rats in the first neoplastic group (NP1) received 25 mg/kg PS-NP and rats in the second nanoplastic group (NP2) received 50 mg/kg PS-NP, at the same time each day by oral gavage. The rats were sacrificed under deep anesthesia at the end of four weeks. The hippocampi were removed and subjected to histopathological and biochemical analyses.</p></div><div><h3>Results</h3><p><span>Green fluorescent dots were detected in the hippocampi of both dose groups receiving nanoplastics (NPs) administered orally to female and male rats. Histopathological examination revealed neuronal degeneration<span> in the hippocampi of male and female rats from both dose groups. However, while no significant difference was observed among the groups in terms of changes in antioxidant enzyme values and open-field test data in male rats, significant differences in </span></span>peroxidase (POD) and glutathione S-transferase (GST) values and fecal boli and grooming numbers were determined in female rats exposed to NPs.</p><p>In conclusion, exposure to NP substances extend as far as the hippocampus, causing neuronal damage and behavioral problems.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102314"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10284490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maternal diabetes decreases the expression of α2-adrenergic and M2 muscarinic receptors in the visual cortex of male rat neonates","authors":"Javad Bagheri ,&nbsp;Somaye Fallahnezhad ,&nbsp;Nasim Alipour ,&nbsp;Hamideh Babaloo ,&nbsp;Fatemeh Tahmasebi ,&nbsp;Hamed Kheradmand ,&nbsp;Ghasem Sazegar ,&nbsp;Hossein Haghir","doi":"10.1016/j.jchemneu.2023.102326","DOIUrl":"10.1016/j.jchemneu.2023.102326","url":null,"abstract":"<div><h3>Aims</h3><p><span>This study investigates the impact of maternal diabetes on the expression of α2-adrenergic and M2 muscarinic receptors in the primary </span>visual cortex of male offspring born to diabetic rats.</p></div><div><h3>Main methods</h3><p>In adult female rats, a single dose<span><span> of intraperitoneal streptozotocin (STZ) was used to induce diabetes (Diabetic group). Diabetes was controlled with insulin in the Insulin-treated group. Female rats in the control group received normal saline instead of STZ. Male newborns were euthanized at P0, P7, and P14, and the expression of α2-adrenergic and M2 muscarinic receptors in the primary visual cortex was determined using </span>immunohistochemistry (IHC).</span></p></div><div><h3>Key findings</h3><p>The study showed that α2-adrenergic and M2 muscarinic receptors were significantly suppressed in all layers of the primary visual cortex of male neonates born to diabetic rats at P0, P7, and P14 compared to the control group. The highest expression was for the Con group at P14 and the lowest one was in the Dia group at P0 for both receptors. The insulin treatment in diabetic mothers modulated the expression of these receptors to normal levels in their newborns.</p></div><div><h3>Significance</h3><p>The results demonstrate maternal diabetes decreases the expression of α2-adrenergic and M2 muscarinic receptors in the primary visual cortex of male offspring born to diabetic rats. Insulin treatment can offset these effects of diabetes.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102326"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10275301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperbaric oxygen therapy and coenzyme Q10 synergistically attenuates damage progression in spinal cord injury in a rat model","authors":"Alireza Ghaemi ,&nbsp;Mohammad Ghiasvand ,&nbsp;Melody Omraninava ,&nbsp;Mohammed Yousif Merza ,&nbsp;Adnan Taan Alkhafaji ,&nbsp;Amir Raoofi ,&nbsp;Davood Nasiry ,&nbsp;Mohammad Darvishi ,&nbsp;Reza Akhavan-Sigari","doi":"10.1016/j.jchemneu.2023.102322","DOIUrl":"10.1016/j.jchemneu.2023.102322","url":null,"abstract":"<div><h3>Background</h3><p><span>Identifying effective spinal cord injury (SCI) treatments remains a major challenge, and current approaches are still unable to effectively improve its. Currently, we investigated the combined effects of hyperbaric oxygen (HBO) along with </span>coenzyme Q10 (CoQ10) in the recovery of SCI in rats.</p></div><div><h3>Material and methods</h3><p>Ninety female mature Sprague-Dawley rats were allocated into five equal groups, including; sham group, SCI group, HBO group (underwent SCI and received HBO), CoQ10 group (underwent SCI and received CoQ10), and HBO+CoQ10 group (underwent SCI and received HBO plus CoQ10). Tissue samples at the lesion site were obtained for evaluation of stereological, immunohistochemical, biochemical, molecular. Also, functional tests were performed to evaluate of behavioral properties.</p></div><div><h3>Results</h3><p>We found that a significant increase in stereological parameters, biochemical factors (GSH, SOD and CAT), IL-10 gene expression and behavioral functions (BBB and EMG Latency) in the treatment groups, especially HBO+CoQ10 group, compared to SCI group. In addition, MDA levels, the density of apoptotic cells, as well as expression of inflammatory genes (TNF-α and IL-1β) were considerably reduced in the treatment groups, especially HBO+CoQ10 group, compared to SCI group.</p></div><div><h3>Conclusion</h3><p>We conclude that co-administration of HBO and HBO+CoQ10 has a synergistic neuroprotective effects in animals undergoing SCI.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102322"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10284039","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Protective mechanism of the EZH2/microRNA-15a-5p/CXCL10 axis in rats with depressive-like behaviors","authors":"Xuezhu Huang ,&nbsp;Chuang Yang ,&nbsp;Min Huang","doi":"10.1016/j.jchemneu.2023.102283","DOIUrl":"10.1016/j.jchemneu.2023.102283","url":null,"abstract":"<div><h3>Objective</h3><p><span>Enhancer of zeste homolog 2 (EZH2), microRNA-15a-5p (miR-15a-5p), and </span>chemokine<span> C-X-C ligand 10 (CXCL10) have been studied in many diseases. However, the investigation of the EZH2/miR-15a-5p/CXCL10 axis in depression is not sufficient. Our study aimed to investigate the regulatory functions of the EZH2/miR-15a-5p/CXCL10 axis in rats with depressive-like behaviors.</span></p></div><div><h3>Methods</h3><p><span>The rat model of depression-like behaviors was established by chronic unpredictable mild stress (CUMS), and EZH2, miR-15a-5p, and CXCL10 expression levels in rats with depression-like behaviors were detected. The silenced EZH2 or enhanced miR-15a-5p recombinant lentivirus<span> was injected into the rats with depression-like behaviors to assess the changes in behavioral tests, hippocampal pathological structure, levels of inflammatory cytokines in the hippocampus, and hippocampal </span></span>neuron apoptosis. The regulatory relationships among EZH2, miR-15a-5p, and CXCL10 were measured.</p></div><div><h3>Results</h3><p>miR-15a-5p expression was reduced, and EZH2 and CXCL10 expression levels were elevated in rats with depressive-like behaviors. Downregulation of EZH2 or elevation of miR-15a-5p improved depressive behavior, and inhibited hippocampal inflammatory response and hippocampal neuron apoptosis. EZH2 promoted histone methylation at the promoter of miR-15a-5p, and miR-15a-5p bound to CXCL10 to inhibit its expression.</p></div><div><h3>Conclusion</h3><p>Our study summarizes that EZH2 promotes the hypermethylation of the miR-15a-5p promoter, thereby promoting CXCL10 expression. Upregulation of miR-15a-5p or inhibition of EZH2 can improve the symptoms in rats with depressive-like behaviors.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102283"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10278449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosome-shuttled MYCBPAP from bone marrow mesenchymal stem cells regulates synaptic remodeling and ameliorates ischemic stroke in rats","authors":"Qiuyue Yan,&nbsp;Yong Yin,&nbsp;Xuechun Li,&nbsp;Meng Li","doi":"10.1016/j.jchemneu.2023.102309","DOIUrl":"10.1016/j.jchemneu.2023.102309","url":null,"abstract":"<div><h3>Background and purpose</h3><p><span>Mesenchymal stem cells (MSC) have been demonstrated to improve cardiac function </span><em>via</em><span> the secretion of paracrine factors rather than direct differentiation. We, therefore, investigated whether bone marrow-derived MSC (BMSC)-released exosomes (BMSC-exo) enhance neurological recovery in spontaneously hypertensive rats<span> (SHR) with ischemic stroke.</span></span></p></div><div><h3>Methods</h3><p><span>Markers of BMSC and BMSC-exo were detected to characterize BMSC and BMSC-exo. A green fluorescent PKH-67-labeled assay was conducted to ensure BMSC-exo internalization<span>. Rat neuronal cells (RNC) were induced with Ang II and oxygen-glucose deprivation. The protective effects of BMSC-exo on RNC were studied by CCK-8, LDH, and immunofluorescence assays. SHR were subjected to </span></span>middle cerebral artery<span> occlusion, and the systolic and diastolic blood pressure changes in the modeled rats were measured. The effects of BMSC-exo on SHR were investigated by mNSS scoring, foot-fault tests, immunohistochemistry<span><span>, Western blot, TTC </span>staining, TUNEL, and HE staining. The hub genes related to SHR and proteins shuttled by BMSC-exo were intersected to obtain a possible candidate, followed by rescue experiments.</span></span></p></div><div><h3>Results</h3><p>BMSC-exo significantly promoted RNC viability and repressed cell apoptosis and cytotoxicity. Moreover, SHR administrated with BMSC-exo exhibited significant improvement in functional recovery and narrowed infarct size. BMSC-exo shuttled the MYCBPAP protein. Knockdown of MYCBPAP inhibited the protective effects of BMSC-exo on RNC and exacerbated synaptic damage in SHR.</p></div><div><h3>Conclusions</h3><p>MYCBPAP shuttled by BMSC-exo facilitates synaptic remodeling in SHR, which may contribute to a therapeutic strategy for ischemic stroke treatment.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102309"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10332709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The antipsychotic olanzapine reduces memory deficits and neuronal abnormalities in a male rat model of Autism","authors":"Luis Ángel Lima-Castañeda ,&nbsp;María Elena Bringas ,&nbsp;Leonardo Aguilar-Hernandez ,&nbsp;Linda Garcés-Ramírez ,&nbsp;Julio César Morales-Medina ,&nbsp;Gonzalo Flores","doi":"10.1016/j.jchemneu.2023.102317","DOIUrl":"10.1016/j.jchemneu.2023.102317","url":null,"abstract":"<div><p><span><span><span><span>The prevalence of autism spectrum disorder (ASD), a neurodevelopmental condition that impacts </span>social interaction<span> and sensory processing, is rising. </span></span>Valproic acid<span> (VPA) exposure during pregnancy causes autistic-like traits in offspring. Olanzapine (OLZ), an atypical </span></span>antipsychotic<span><span>, is used to treat ASD. We assessed the impact of OLZ on behavior, neuromorphology, and </span>nitric oxide<span> (NO) levels in the hippocampus<span> using prenatal VPA treatment in rats. It is commonly known that ASD patients exhibit sensory abnormalities. As such, we utilized the tail flick test to validate the ASD model. In the </span></span></span></span>novel object recognition test<span> (NORT), VPA exposure reduces the discrimination index (DI) in the first introduction to the novel object. Moreover, OLZ and vehicle-treated rats perform differently in the second exposition to the DI of the novel object, suggesting that OLZ reverses VPA-induced deficits in recognition memory. The latency to find the hidden platform in the Morris water maze test of memory and learning improves in VPA-exposed rats after OLZ administration, indicating that OLZ improves spatial memory in these rats. Administration of prenatal VPA induces neuronal hypotrophy and reduces spine density in pyramidal neurons of the CA1 region of the hippocampus. Treatment with OLZ corrects the neuromorphological changes brought on by VPA. In the CA1 region of the hippocampus, VPA treatment increases the number of neurons, which normalizes with OLZ treatment. OLZ increases the NO levels in the dorsal hippocampus in control rats. In rats exposed to VPA, the second-generation antipsychotic OLZ reduces memory-related and neuroplastic alterations. The current findings support the use of OLZ in this illness and further validate the use of prenatal VPA as a model of ASD.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102317"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10283554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-dependent endozepinergic regulation of ventromedial hypothalamic nucleus glucose counter-regulatory neuron aromatase protein expression in the adult rat","authors":"A.S.M. Hasan Mahmood ,&nbsp;Sagor C. Roy ,&nbsp;Jérôme Leprince ,&nbsp;Karen P. Briski","doi":"10.1016/j.jchemneu.2023.102323","DOIUrl":"10.1016/j.jchemneu.2023.102323","url":null,"abstract":"<div><p><span><span>The hypothalamic brain cell types that produce estradiol<span> from testosterone remain unclear. Aromatase inhibition affects ventromedial hypothalamic nucleus (VMN) glucose-stimulatory </span></span>nitric oxide<span><span><span> (NO) and glucose-inhibitory γ-aminobutyric acid (GABA) transmission during insulin (INS)-induced hypoglycemia (IIH). Pure GABA and NO nerve cell samples acquired by laser-catapult-microdissection from consecutive rostro-caudal segments of the VMN were analyzed by Western blot to investigate whether regional subpopulations of each cell type contain machinery for neuro-estradiol synthesis. Astrocyte endozepinergic signaling governs brain </span>steroidogenesis. Pharmacological tools were used here to determine if the glio-peptide </span>octadecaneuropeptide (ODN) controls aromatase expression in GABA and NO neurons during eu- and/or hypoglycemia. Intracerebroventricular administration of the ODN G-protein coupled-receptor antagonist cyclo</span></span>₍₁₋₈₎[DLeu⁵<span>]OP (LV-1075) decreased (male) or enhanced (female) VMN GABAergic neuron<span> aromatase expression, but increased or reduced this profile in nitrergic neurons<span><span> in a region-specific manner in each sex. IIH suppressed aromatase levels in GABA neurons located in the middle segment of the male VMN or distributed throughout this nucleus in the female. This inhibitory response was altered by the ODN isoactive surrogate octapeptide (OP) in female, but was refractory to OP in male. NO neuron aromatase protein in hypoglycemic male (middle and caudal VMN) and female (rostral and caudal VMN) rats, but was normalized in OP- plus INS-treated rats of both sexes. Results provide novel evidence that VMN glucose-regulatory neurons may produce neuro-estradiol, and that the astrocyte </span>endozepine transmitter ODN may impose sex-specific control of baseline and/or hypoglycemic patterns of aromatase expression in distinct subsets of nitrergic and GABAergic neurons in this neural structure.</span></span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102323"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10528386/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10285045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"G protein-coupled estrogen receptor 1 deficiency impairs adult hippocampal neurogenesis in mice with schizophrenia","authors":"Chun Zhang ,&nbsp;Jian-Guo Niu ,&nbsp;Xue-Rui Kong ,&nbsp;Xiao-Juan Mi ,&nbsp;Qiang Liu ,&nbsp;Fei-Fei Chen ,&nbsp;Wei-Fang Rong ,&nbsp;Juan Liu","doi":"10.1016/j.jchemneu.2023.102319","DOIUrl":"10.1016/j.jchemneu.2023.102319","url":null,"abstract":"<div><h3>Objective</h3><p>This study aimed to confirm that G protein-coupled estrogen receptor<span><span> 1 (GPER1) deficiency affects cognitive function by reducing hippocampal neurogenesis via the PKA/ERK/IGF-I </span>signaling pathway<span> in mice with schizophrenia (SZ).</span></span></p></div><div><h3>Methods</h3><p>Mice were divided into four groups, namely, KO Con, WT Con, KO Con, and WT SZ (<em>n</em><span> = 12 in each group). All mice were accustomed to the behavioral equipment overnight in the testing service room. The experimental conditions were consistent with those in the animal house. Forced swimming test<span><span> and Y-maze test were conducted. Neuronal differentiation<span> and maturation were detected using immunofluorescence and confocal imaging. The protein in the PKA/ERK/IGF-I signaling pathway was tested using </span></span>Western blot analysis.</span></span></p></div><div><h3>Results</h3><p>GPER1 KO aggravated depression during forced swimming test and decreased cognitive ability during Y-maze test in the mouse model of dizocilpine<span> maleate (MK-801)-induced SZ. Immunofluorescence and confocal imaging results demonstrated that GPER1 knockout reduced adult hippocampal dentate gyrus neurogenesis. Furthermore, GPER1-KO aggravated the hippocampal damage induced by MK-801 in mice through the PKA/ERK/IGF-I signaling pathway.</span></p></div><div><h3>Conclusions</h3><p>GPER1 deficiency reduced adult hippocampal neurogenesis and neuron survival by regulating the PKA/ERK/IGF-I signaling pathway in the MK-801-induced mouse model of SZ.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102319"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10646471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TGN020 application against aquaporin 4 improved multiple sclerosis by inhibiting astrocytes, microglia, and NLRP3 inflammasome in a cuprizone mouse model","authors":"Yousef Mohamadi ,&nbsp;Maryam Borhani-Haghighi","doi":"10.1016/j.jchemneu.2023.102306","DOIUrl":"10.1016/j.jchemneu.2023.102306","url":null,"abstract":"<div><p><span><span><span>In multiple sclerosis<span> (MS), activation of the astrocytes and microglia induces a cascading inflammatory response. Overexpression of the </span></span>aquaporin 4<span><span> (AQP4) in the glia is a trigger for this reaction. This study aimed to block AQP4 by injecting TGN020 to alleviate the symptoms of MS. Total of 30 male mice were randomly divided into control (intact), cuprizone model of MS (fed with 0.2% cuprizone for 35 days), and TGN020-treated (received daily intraperitoneal injections of 200 mg/kg TGN020 with cuprizone intake) groups. </span>Astrogliosis<span>, M1-M2 microglia polarization, NLRP3 </span></span></span>inflammasome<span> activation, and demyelination were investigated in the corpus callosum by </span></span>immunohistochemistry<span><span><span>, real-time PCR, western blot, and luxol fast blue </span>staining<span>. The Rotarod test<span><span> was performed for a behavior<span> assessment. AQP4 inhibition caused a significant decrease in the expression of the astrocyte-specific marker, GFAP. It also changed the microglia polarization from M1 to M2 indicated by a significant downregulation of </span></span>iNOS, </span></span></span>CD86<span>, MHC-ІІ, and upregulation of arginase1, CD206, and TREM-2. In addition, western blot data showed a significant decrease in the NLRP3, caspase1, and IL-1b proteins in the treatment group, which indicated inflammasome inactivation. The molecular changes following the TGN020 injection resulted in remyelination and motor recovery enhancement in the treatment group. In conclusion, the results draw the attention to the role of AQP4 in the cuprizone model of MS.</span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102306"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10332683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The many “Neurofaces” of Prohibitins 1 and 2: Crucial for the healthy brain, dysregulated in numerous brain disorders","authors":"Hans-Gert Bernstein ,&nbsp;Karl-Heinz Smalla ,&nbsp;Gerburg Keilhoff ,&nbsp;Henrik Dobrowolny ,&nbsp;Michael R. Kreutz ,&nbsp;Johann Steiner","doi":"10.1016/j.jchemneu.2023.102321","DOIUrl":"10.1016/j.jchemneu.2023.102321","url":null,"abstract":"<div><p><span>Prohibitin<span><span> 1 (PHB1) and prohibitin 2 (PHB2) are proteins that are nearly ubiquitously expressed. They are localized in mitochondria, cytosol and cell nuclei. In the healthy CNS<span><span>, they occur in neurons and non-neuronal cells (oligodendrocytes, astrocytes, microglia, and endothelial cells) and fulfill pivotal functions in brain development and aging, the regulation of </span>brain metabolism, maintenance of structural integrity, </span></span>synapse formation<span>, aminoacidergic neurotransmission<span> and, probably, regulation of brain action of certain hypothalamic-pituitary hormones.With regard to the diseased brain there is increasing evidence that prohibitins are prominently involved in numerous major diseases of the CNS, which are summarized and discussed in the present review (brain tumors, neurotropic viruses, Alzheimer disease<span>, Down syndrome, Fronto-temporal and vascular dementia, </span></span></span></span></span>dementia with Lewy bodies<span><span>, Parkinson disease, </span>Huntington disease<span><span><span>, Multiple sclerosis, </span>Amyotrophic lateral sclerosis, stroke, alcohol use disorder, </span>schizophrenia and autism). Unfortunately, there is no PHB-targeted therapy available for any of these diseases.</span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102321"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10280550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}