Journal of chemical neuroanatomy最新文献

{"title":"Neuroprotective effect of lansoprazole against cisplatin-induced brain toxicity: Role of Nrf2/ARE and Akt/P53 signaling pathways","authors":"Fares E.M. Ali ,&nbsp;Emad H.M. Hassanein ,&nbsp;Ali H. El-Bahrawy ,&nbsp;Mohamed S. Hemeda ,&nbsp;Ahmed M. Atwa","doi":"10.1016/j.jchemneu.2023.102299","DOIUrl":"10.1016/j.jchemneu.2023.102299","url":null,"abstract":"<div><p><span>Cisplatin<span><span> is a chemotherapeutic agent usually used in treating different patterns of malignancies. One of the significant apparent complications of cisplatin chemotherapy is brain toxicity<span>. The present study was conducted to evaluate the protective effects of lansoprazole on cisplatin-induced cortical intoxication. Thirty-two rats were allocated into four groups (8 rats/group); group I: received only a vehicle for 10 days, group II: lansoprazole was administered (50 mg/kg) via oral gavage for 10 days, group III: On 5th day of the experiment, rats were given cisplatin (10 mg/kg) i.p. once to induce cortical injury. Group IV: rats were given lansoprazole for 5 days before cisplatin and 5 days afterward. Lansoprazole administration significantly improved cisplatin-induced behavioral changes, as evidenced by decreasing the immobility time in forced swimming and open field tests. Besides, lansoprazole improved cortical histological changes, restored cortical redox balance, enhanced Nrf2/ARE expression, cisplatin-induced </span></span>neuronal apoptosis, and dampened cisplatin inflammation. In addition, lansoprazole modulated cortical Akt/p53 signal. The present work was the first to show that lansoprazole co-administration reduced cortical toxicity in cisplatin-treated rats via multiple </span></span>signaling pathways. The current findings provided crucial information for developing novel protective strategies to reduce cisplatin cortical toxicity.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102299"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10283007","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":"Caffeine alleviates anxiety-like behavior and brainstem lesions in a rotenone-induced rat model of Parkinson's disease","authors":"Timileyin Adewumi Adeyeye,&nbsp;Bamidele Richard Babatunde,&nbsp;Samuel Ehimare Ehireme,&nbsp;Philemon Dauda Shallie","doi":"10.1016/j.jchemneu.2023.102315","DOIUrl":"10.1016/j.jchemneu.2023.102315","url":null,"abstract":"&lt;div&gt;&lt;h3&gt;Background&lt;/h3&gt;&lt;p&gt;&lt;span&gt;Parkinson's disease&lt;span&gt;&lt;span&gt; (PD) is a neurodegenerative disorder&lt;span&gt; characterized by motor and non-motor symptoms. In 2016, approximately 6.1 million individuals were affected by PD, with 211,296 deaths attributed to the disease. The understanding of PD initially came from the observation of dopaminergic system alterations in a specific region of the &lt;/span&gt;&lt;/span&gt;brainstem, indicating that the core motor and non-motor features of PD are closely associated with brainstem dysfunction. The primary treatment approach for PD revolves around dopamine replacement, as many of the symptoms are responsive to this therapeutic intervention. However, long-term administration of this approach is linked to several complications, and a definitive gold-standard therapy for PD is yet to be identified. The pharmacological management of PD has been challenging and inconsistent, mainly due to the unclear underlying cause of the disease. This study aims to evaluate the effects of caffeine on the brainstem of rats with PD induced by &lt;/span&gt;&lt;/span&gt;rotenone.&lt;/p&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Methodology&lt;/h3&gt;&lt;p&gt;Fifty adult male Wistar rats weighing between 150 and 200 g were used in this study. The rats were randomly divided into five groups of ten rats each: Vehicle Group, Rotenone-only treated Group (rotenone only treated with 3 mg/kg, intraperitoneal administration [IP]), Preventive Group (caffeine 30 mg/kg + rotenone 3 mg/kg, IP), Curative Group (rotenone 3 mg/kg + caffeine 30 mg/kg, IP), and Caffeine only treated Group (caffeine only treated with 30 mg/kg, IP). The animals underwent neurobehavioral assessments, followed by sacrifice. The brains were then excised, weighed, and processed histologically. Appropriate brain sections were taken and processed. Photomicrographs were obtained, morphometric and statistical analysis was performed using an Omax LED digital&lt;/p&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Results&lt;/h3&gt;&lt;p&gt;The results demonstrated a significant (p &lt; 0.05) reduction in body weight and relative brain weight, which were increased by caffeine treatments. Rotenone administration led to histological changes similar to those observed in PD, including neuronal structural derangement, degenerated nerve fibers, loss of myelinated neurons, and Nissl substance&lt;span&gt;, as well as downregulation in the expressions of NRF2 and TH in the midbrain. However, these pathological features were counteracted or ameliorated by caffeine treatment.&lt;/span&gt;&lt;/p&gt;&lt;/div&gt;&lt;div&gt;&lt;h3&gt;Conclusion&lt;/h3&gt;&lt;p&gt;&lt;span&gt;Our study contributes additional evidence to the growing body of research supporting the therapeutic potential of caffeine in Parkinson's disease (PD). The results underscore the neuroprotective properties of caffeine and its capacity to mitigate &lt;/span&gt;oxidative stress by modulating TH (tyrosine hydroxylase) and cytoplasmic NRF2 (nuclear factor erythroid 2-related factor 2) in the mesencephalon. These findings suggest that caffeine holds promise as a viable treatment option for PD.&lt;/p&gt;","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102315"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10628973","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":"Quercetin mitigates depression-like behavior via the suppression of neuroinflammation and oxidative damage in corticosterone-induced mice","authors":"Chenjie Ge ,&nbsp;Shiliang Wang ,&nbsp;Xuqi Wu ,&nbsp;Lilei Lei","doi":"10.1016/j.jchemneu.2023.102313","DOIUrl":"10.1016/j.jchemneu.2023.102313","url":null,"abstract":"<div><p><span><span><span>Depression is a clinically common and easily overlooked mental disease. Quercetin is a </span>flavonoid<span> compound, which has anti-inflammatory and antioxidant roles. Previous reports presented the anti-depressant role of quercetin. Nevertheless, the latent mechanism of the anti-depressant function of quercetin is blurry. This research aimed to probe its effects on corticosterone<span><span> (CORT)-induced depression-like behaviors and explore the underlying mechanism. A depression model was established by subcutaneous injection of CORT (20 mg/kg). Thereafter, CORT-treated mice were given 40 mg/kg and 80 mg/kg of quercetin by gavage. This study found that quercetin mitigated depression-like behaviors, as evidenced by increased the number of line crossings, swimming time, and time spent in open arm and reduced thigmotaxis time in CORT-challenged mice in open field test and decreased immobility time as well as the swimming and climbing time in </span>forced swim test<span> and increased number of head dips, time spent and entries in open arm elevated plus maze<span> test. Also, quercetin exerted anti-inflammatory and anti-oxidation effects in hippocampus and prefrontal cortex of CORT-induced mice. Additionally, quercetin alleviated the pathological injury of the liver tissue and weakened </span></span></span></span></span>alkaline phosphatase (ALP) and </span>alanine aminotransferase<span> (ALT) concentrations of the serum in CORT-induced mice. Quercetin also suppressed Caspase-3 content but advanced vascular endothelial growth factor (VEGF) and brain derived neurotrophic factor (BDNF) contents in hippocampus of CORT-treated mice. Based on these results, quercetin mitigated CORT-induced depression-like behaviors, and the mechanism was partly related to the repression of neuroinflammation and oxidative damage.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102313"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10280050","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":"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":"Effects of e-vapour and high-fat diet on the immunohistochemical staining of nicotinic acetylcholine receptors, apoptosis, microglia and astrocytes in the adult male mouse hippocampus","authors":"Rita Chaaya ,&nbsp;Joel R. Steele ,&nbsp;Brian G. Oliver ,&nbsp;Hui Chen ,&nbsp;Rita Machaalani","doi":"10.1016/j.jchemneu.2023.102303","DOIUrl":"10.1016/j.jchemneu.2023.102303","url":null,"abstract":"<div><p><span>The use of e-cigarettes/e-vapour, and the consumption of a high-fat diet (HFD), are two popular lifestyle choices associated with alterations in the hippocampus. This study, using a mouse model, investigated the effects of exposure to e-vapour (</span><span><math><mo>±</mo></math></span> nicotine) and HFD (43% fat) consumption, on the expression of nicotinic acetylcholine receptor (nAChR) subunits <span><math><mi>α</mi></math></span>3, <span><math><mi>α</mi></math></span>4, <span><math><mi>α</mi></math></span>7 and <span><math><mi>β</mi></math></span><span><span>2, apoptosis markers caspase-3 and TUNEL, microglial marker Iba-1, and astrocyte marker </span>GFAP<span>, in hippocampal subregions of dentate gyrus (DG) and cornu ammonis (CA) 1–3. The major findings included: (1) HFD alone had minimal effect with no consistent pattern or interaction between the markers, (2) E-vapour (</span></span><span><math><mo>±</mo></math></span> nicotine) predominantly affected the CA2 subregion, decreasing α7 and β2 nAChR subunits and Iba-1, (3) Nicotine e-vapour increased TUNEL across all subregions, and (4) HFD, in the presence of nicotine-free e-vapour, decreased caspase-3 and increased TUNEL across all regions, and decreased Iba-1 in the CA subregions, while HFD and nicotine-containing e-vapour, subregion specifically affected the <span><math><mi>α</mi></math></span>3, <span><math><mi>α</mi></math></span>4 and <span><math><mi>α</mi></math></span>7 nAChR subunits, with a protective effect against change in GFAP in the DG and Iba-1 in the CA1 and CA3. These findings highlight that e-vapour itself alters nAChRs, particularly in the CA2 subregion, associated with a decrease in neuroinflammatory response (Iba-1) across the whole hippocampus, and the addition of nicotine increases cell apoptosis across the whole hippocampus. HFD alone was not detrimental in our model, but in the presence of nicotine-free e-vapour, it differentially affected apoptosis, while the addition of nicotine increased nAChR subunits.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"132 ","pages":"Article 102303"},"PeriodicalIF":2.8,"publicationDate":"2023-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10282132","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":"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":"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":"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":"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}