Journal of chemical neuroanatomy最新文献

{"title":"The effects of induced type I diabetes on developmental regulation of GDNF, NRTN, and NCAM proteins in the dentate gyrus of male rat offspring","authors":"Hamideh Mostafaee ,&nbsp;Faezeh Idoon ,&nbsp;Mina Mohasel-Roodi ,&nbsp;Fatemeh Alipour ,&nbsp;Nasim Lotfi ,&nbsp;Akram Sadeghi","doi":"10.1016/j.jchemneu.2024.102391","DOIUrl":"10.1016/j.jchemneu.2024.102391","url":null,"abstract":"<div><h3>Background</h3><p>Maternal diabetes during pregnancy can affect the neurological development of offspring. Glial cell-derived neurotrophic factor<span><span> (GDNF), neurturin<span> (NRTN), and neural cell adhesion molecules (NCAM) are three important proteins for brain development. Therefore, this study aimed to investigate the impacts of the mentioned neurotrophic factors in the hippocampal </span></span>dentate gyrus (DG) of rat offspring born to diabetic mothers.</span></p></div><div><h3>Methods</h3><p><span>Wistar female rats<span> were randomly allocated into diabetic (STZ-D) [(45 mg/kg BW, STZ<span> (Streptozotocin), i.p)], diabetic + NPH insulin (STZ-INS) [(4–6 unit/kg/day SC)], and control groups. The animals in all groups were mated by non-diabetic male rats. Two weeks after birth, male pups from each group were sacrificed and then protein contents of GDNF, NRTN, and NCAM were evaluated using </span></span></span>immunohistochemistry.</p></div><div><h3>Results</h3><p>The study found that the expression of GDNF and NRTN in the hippocampus of diabetic rat offspring was significantly higher compared to the diabetic+ insulin and control groups, respectively (P &lt; 0.01, P &lt; 0.001). Additionally, the expression of NCAM was significantly higher in the diabetic group the diabetic+ insulin and control groups (P &lt; 0.01, P &lt; 0.001).</p></div><div><h3>Conclusions</h3><p>The results of the study revealed that diabetes during pregnancy significantly impacts the distribution pattern of GDNF, NRTN, and NCAM in the hippocampus of rat neonates.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"136 ","pages":"Article 102391"},"PeriodicalIF":2.8,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139459414","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":"Tetrahydropiperine, a natural alkaloid with neuroprotective effects in ischemic stroke","authors":"Hongyan Ren ,&nbsp;Qianqian Yuan ,&nbsp;Jiayuan Lu ,&nbsp;Siyu Xi ,&nbsp;Yanbo Liu ,&nbsp;Guangyu Yang ,&nbsp;Zhixi Xie ,&nbsp;Bo Wang ,&nbsp;Li Ma ,&nbsp;Xueyan Fu ,&nbsp;Juan Liu ,&nbsp;Yiwei Zhang","doi":"10.1016/j.jchemneu.2024.102397","DOIUrl":"10.1016/j.jchemneu.2024.102397","url":null,"abstract":"<div><h3>Background</h3><p>Ischemic stroke (IS) is a life-threatening neurological disease with various pathological mechanisms. Tetrahydropiperine (THP) is a natural alkaloid with protective effects against multiple diseases, such as seizure, and pain. This study was to examine the impact of THP on IS and investigate its potential mechanism.</p></div><div><h3>Material and methods</h3><p>We employed network pharmacology and molecular docking techniques to identify the target proteins of THP for intervention in IS. Adult male Sprague-Dawley rats were used to create a permanent middle cerebral artery occlusion model. PC-12 cells were chosen to establish an oxygen–glucose deprivation (OGD) cell model. Disease modeling followed by nimodipine (NIMO); 3-methyladenine (3-MA) and rapamycin (RAP) interventions. Open field test, Longa score, balance beam test, and forelimb grip test were used to measure motor and neurological functions. The degree of neurological damage recovery was assessed through behavioral analysis, and cerebral infarction volume was determined using TTC staining. Morphological changes were examined through HE and Nissl staining, and ultrastructural changes in neurons were observed using transmission electron microscopy. The protein expression of autophagy and related pathways was analyzed through Western blot (WB). The appropriate hypoxia time and drug concentration were determined using CCK-8 assay, which also measured cell survival rate.</p></div><div><h3>Results</h3><p>The network pharmacology findings indicated that the impact of THP on IS was enhanced in the PI3K/Akt signaling pathway. THP demonstrated robust docking capability with proteins associated with the autophagy and PI3K/Akt/mTOR, as indicated by the molecular docking outcomes. THP significantly improved behavioral damage, reduced the area of cerebral infarction, ameliorated histopathological damage from ischemia, increase neuronal survival, and alleviated ultrastructural damage in neurons (P &lt; 0.05). THP enhanced the survival of PC-12 cells induced by OGD and ameliorated the morphological harm to the cells (P &lt; 0.05). THP was found to elevate the quantities of P62, LC3-Ⅰ, PI3K, P-AKt/Akt, and P-mTOR/mTOR proteins while reducing the levels of Atg7 and Beclin1 proteins. The results of transmission electron microscopy showed no autophagosomes in the THP, 3-MA, and 3-MA + THP groups.</p></div><div><h3>Conclusion</h3><p>The activation of the PI3K/Akt/mTOR signaling pathway by THP inhibits autophagy and provides relief from neurological damage in IS.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"136 ","pages":"Article 102397"},"PeriodicalIF":2.8,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0891061824000103/pdfft?md5=2c9b876e37f1774133cd75ac25809008&pid=1-s2.0-S0891061824000103-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139706897","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":"Icariin attenuates dopaminergic neural loss in haloperidol-induced Parkinsonism in rats via GSK-3β and tyrosine hydroxylase regulation mechanism","authors":"Hend A. Sabry ,&nbsp;Mai M. Zahra","doi":"10.1016/j.jchemneu.2023.102385","DOIUrl":"10.1016/j.jchemneu.2023.102385","url":null,"abstract":"<div><p><span><span><span>Parkinson’s Disease (PD) is an age-dependent, incessant, dynamic neurodegenerative illness. In animal models<span><span>, the administration of the dopaminergic </span>D2 antagonist </span></span>Haloperidol<span> (HP) affects the nigrostriatal pathway<span><span><span>, inducing catalepsy, a state of immobility like PD, </span>bradykinesia<span>, and akinesia. The present study investigated the neural effects of </span></span>Icariin (ICA), a </span></span></span>flavonoid derived from </span><em>Herba Epimedii</em><span><span>, against HP-induced PD in rats compared to a standard drug levodopa (L-DOPA). Twenty-four adult male rats were divided into 4 groups: the control group treated with vehicle, the 2nd group treated with HP intraperitoneally, the 3rd group treated with the same dose of HP+L-DOPA orally, and the 4th one, treated with the same dose of HP+ICA orally. All the groups were treated for fourteen consecutive days. Two days before the last dose, locomotor activity was assessed in open field and rotarod tasks. At the end of the experiment, the malondialdehyde, </span>nitric oxide<span><span> (NO), iron, glycogen synthase kinase-3beta (GSK-3β), and tyrosine hydroxylase (TH) contents, glutathione S-transferase, </span>catalase<span>, superoxide dismutase<span>, activities were estimated in the midbrain. Also, cortex and midbrain monoamine<span> contents (norepinephrine, dopamine, and serotonin) were determined. Moreover, the midbrain histopathology<span><span> was detected in all treated groups. The results suggested that the neuroleptic effect of HP was completely improved by ICA. This improvement occurred by decreasing the neurotoxicity via lowering midbrain </span>lipid peroxidation, NO, GSK-3β contents, increasing antioxidant biomarkers, TH, and recovering the treated groups' cortex and midbrain monoamines contents. In conclusion, this study suggests that ICA is a suitable treatment for Parkinson's induced by HP.</span></span></span></span></span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"136 ","pages":"Article 102385"},"PeriodicalIF":2.8,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139067497","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":"Chronic sub lethal nerve agent (Soman) exposure induced long-term neurobehavioral, histological, and biochemical alterations in rats","authors":"RamaRao Golime ,&nbsp;Naveen Singh ,&nbsp;Ankush Rajput ,&nbsp;Nagar DP ,&nbsp;Vinod K. Lodhi","doi":"10.1016/j.jchemneu.2024.102388","DOIUrl":"10.1016/j.jchemneu.2024.102388","url":null,"abstract":"<div><p><span><span>Organophosphorus (OP) pesticides and insecticides are used in agriculture and other industries can also cause adverse effects through environmental exposures in the people working in agricultural and pesticide industries. OP nerve agent exposures have been associated with delayed neurotoxic effects including sleep disorders, cognitive malfunctions, and </span>brain damage<span><span> in Gulf War victims, and Japanese victims of terrorist attacks with nerve agents. However, the mechanisms behind such prolonged adverse effects after chronic OP nerve agent’s exposures in survivors are not well understood. In the present study, male Wistar rats were subcutaneously exposed to nerve agent </span>soman (0.25XLD</span></span>₅₀<span><span><span><span>) for 21 consecutive days to evaluate the neurobehavioral, neuropathological and biochemical alterations (oxidative stress and antioxidants levels). Neurobehavioral studies using Elevated Plus Maze (EPM), T-Maze, and </span>rotarod tests<span> revealed that chronic soman exposure produced alterations in behavioral functions including increased anxiety and reduction in working memory and neuromuscular<span> strength. Biochemical studies showed that antioxidants enzyme (glutathione peroxidase (GPx), </span></span></span>catalase<span><span> (CAT), and superoxide dismutase (SOD) levels were reduced and </span>oxidative stress<span> (reduced glutathione (GSH) and lipid peroxidation levels (malondialdehyde (MDA)) were significantly increased in brain at 30 days in soman exposed rats as compared to control rats. Neuroselective fluorojade-c stain was used to examine the brain damage after chronic soman exposure. Results demonstrated that chronic soman exposure induced </span></span></span>neurodegeneration as brain damage was detected at 30- and 90-days post exposure. The present study results suggest that chronic nerve agent exposures even at low doses may produce long-term adverse effects like neurobehavioral deficits in rats.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"136 ","pages":"Article 102388"},"PeriodicalIF":2.8,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139092127","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":"Astrocyte response to melatonin treatment in rats under high-carbohydrate high-fat diet","authors":"Davood Dorranipour ,&nbsp;Fahimeh Pourjafari ,&nbsp;Reza Malekpour-Afshar ,&nbsp;Mohsen Basiri ,&nbsp;Mehran Hosseini","doi":"10.1016/j.jchemneu.2024.102389","DOIUrl":"10.1016/j.jchemneu.2024.102389","url":null,"abstract":"<div><p><span><span><span>The involvement of consumption of high-carbohydrate high-fat (HCHF) diet in cognitive impairment is attributed, at least in part, to the activation of astrocytes, which contributes to the development of neuroinflammation, </span>oxidative stress, and subsequent cognitive deficits. This study aimed to assess the influence of </span>melatonin<span><span> on cognitive impairment and astrogliosis induced by the HCHF diet in rats. Male </span>Wistar rats<span> were fed an HCHF diet for eight weeks to induce obesity and metabolic syndrome. Subsequently, they received oral melatonin treatment for four weeks at doses of 5 mg/kg, 10 mg/kg, and 30 mg/kg, alongside the HCHF diet. Cognitive function was evaluated using the Y-maze test, while the levels of proinflammatory cytokines<span>, oxidative stress, and the number glial fibrillary acidic protein<span> (GFAP) positive cells were assessed in the hippocampi and hypothalamus. The consumption of the HCHF diet resulted in weight gain, </span></span></span></span></span>hyperlipidemia<span><span><span>, impaired glucose tolerance, cognitive decline, neuroinflammation, oxidative stress damage, and astrogliosis in rats. Although melatonin treatment did not demonstrate beneficial effects on blood glucose and lipid metabolism, it improved the impaired working memory caused by the HCHF diet. Melatonin exhibited a dose-dependent reduction of astrogliosis, neuroinflammation, and </span>lipid peroxidation while restored </span>superoxide dismutase in the hippocampus and hypothalamus of HCHF diet-treated rats. These findings provide evidence that melatonin inhibits astrocyte activation, thereby attenuating inflammation and minimizing oxidative stress damage induced by the HCHF diet.</span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"136 ","pages":"Article 102389"},"PeriodicalIF":2.8,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139414876","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":"Electroacupuncture protects against the striatum of ischemia stroke by inhibiting the HMGB1/RAGE/p-JNK signaling pathways","authors":"Zeyin Nie,&nbsp;Chenying Hu,&nbsp;Huachun Miao,&nbsp;Feng Wu","doi":"10.1016/j.jchemneu.2023.102376","DOIUrl":"10.1016/j.jchemneu.2023.102376","url":null,"abstract":"<div><p><span>The striatum (Str) is injured 20 min after permanent ischemic stroke, leading to neurological deficits. Here, we aimed to explore the effect of electroacupuncture (EA) on ischemic stroke and elucidate the possible underlying mechanism. Rat permanent </span>middle cerebral artery<span> occlusion (pMCAO) model, EA treatment, sham-EA (SEA) treatment, beam-balance test, hematoxylin<span><span><span> and eosin (HE) </span>staining, Nissl staining, immunofluorescence staining, and </span>Western blot<span> were used to investigate the role of EA in pMCAO. The results showed that balance ability and motor coordination were obviously injured after pMCAO. EA improved balance ability and motor coordination in pMCAO rats. EA reduced striatal injury by reducing the expression of high-mobility group box 1(HMGB1)/receptor for advanced glycation end products (RAGE)/phosphorylated C-Jun N-terminal kinase (p-JNK), whereas SEA did not. Thus, EA plays a neuroprotective role during pMCAO injury, which may be related to the inhibition of HMGB1/RAGE/p-JNK expression.</span></span></span></p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"136 ","pages":"Article 102376"},"PeriodicalIF":2.8,"publicationDate":"2024-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138820424","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":"Aqueous leaf extract of Phyllanthus amarus protects against oxidative stress and misfiring of dopaminergic neurons in Paraquat-induced Parkinson’s disease-like model of adult Wistar rats","authors":"Felix U. Enemali,&nbsp;Kingsley Afoke Iteire,&nbsp;Raphael E. Uweigho,&nbsp;Ogunberi Blessing,&nbsp;Gbayisomore Tolulope Judah","doi":"10.1016/j.jchemneu.2023.102365","DOIUrl":"10.1016/j.jchemneu.2023.102365","url":null,"abstract":"<div><h3>Background of the study</h3><p><span>Phyllanthus amarus has high nutritional value and is beneficial in managing and treating diverse ailments. This study assessed the role of aqueous leaf extract of Phyllanthus amarus on Paraquat (PQ) induced </span>neurotoxicity<span> in the substantia nigra<span> of Wistar rats.</span></span></p></div><div><h3>Materials and methods</h3><p>The role of aqueous leaves extract of Phyllanthus amarus was assessed using an open field test (OFT) for motor activity, oxidative stress<span> biomarkers [Catalase (CAT), and Superoxide Dismutase<span> (SOD)], histological examination (H and E stained) for cytoarchitectural changes and immunohistochemical studies using tyrosine hydroxylase<span> (TH) as a marker for dopaminergic neurons. Forty-two (42) rats were categorized into six groups (n = 7); group 1: control was administered 0.5 ml/kg distilled water, group 2: received 10 mg/kg PQ + 10 mg/kg L-dopa as reference drug, group 3; received 10 mg/kg PQ, while group 4: received 10 mg/kg PQ + 200 mg/kg P. amarus, group 5: received 10 mg/kg PQ + 300 mg/kg P. amarus, and group 6: received 10 mg/kg PQ + 400 mg/kg P. amarus respectively, for 14 days. All administrations were done orally; a significant difference was set at p &lt; 0.05.</span></span></span></p></div><div><h3>Results and discussion</h3><p>The study's open field test (OFT) revealed no motor activity deficit with Paraquat (PQ) exposure. Also, cytoarchitectural distortions were not observed with Paraquat (PQ) only treatment group compared to the control and other groups pretreated with P. amarus and L-dopa. Moreover, the Paraquat (PQ) only treatment group showed oxidative stress by significantly decreasing the antioxidant enzyme (SOD) compared to the control and L-dopa pretreated group. A significant decrease in tyrosine hydroxylase (TH) expressing dopaminergic neurons was also observed in Paraquat (PQ) only treatment. However, P. amarus treatment showed therapeutic properties by significantly increasing tyrosine hydroxylase (TH) expressing dopaminergic neuron levels relative to control.</p></div><div><h3>Conclusion</h3><p>Aqueous leaf extract of Phyllanthus amarus possesses therapeutic properties against Paraquat (PQ) induced changes in the substantia nigra of Wistar rats.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"135 ","pages":"Article 102365"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138460159","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":"Coenzyme Q10 attenuates neurodegeneration in the cerebellum induced by chronic exposure to tramadol","authors":"Majid Keyhanifard ,&nbsp;Roghayeh Javan ,&nbsp;Reza Ataee Disfani ,&nbsp;Maryam Bahrami ,&nbsp;Mohamad Sedigh Mirzaie ,&nbsp;Saeid Taghiloo ,&nbsp;Hossein Mokhtari ,&nbsp;Davood Nasiry ,&nbsp;Zahra Sadrzadeh Aghajani ,&nbsp;Mahdi Shooraj","doi":"10.1016/j.jchemneu.2023.102367","DOIUrl":"10.1016/j.jchemneu.2023.102367","url":null,"abstract":"<div><h3>Background</h3><p><span>Chronic use of tramadol can cause neurotoxic effects and subsequently cause neurodegeneration in the </span>cerebellum<span>. The main damage mechanisms identified are oxidative stress<span> and inflammation. Currently, we investigated the effects of coenzyme Q10 (CoQ10) in attenuates of neurodegeneration in the cerebellum induced by chronic exposure to tramadol.</span></span></p></div><div><h3>Material and methods</h3><p>Seventy-two male mature albino rats were allocated into four equal groups, including; non-treated group, CoQ10 group (which received CoQ10 at 200 mg/kg/day orally for three weeks), tramadol group (which received tramadol hydrochloride at 50 mg/kg/day orally for three weeks), and tramadol+CoQ10 group (which received tramadol and CoQ10 at the same doses as the previous groups). Tissue samples were obtained for stereological, immunohistochemical, biochemical, and molecular evaluations. Also, functional tests were performed to evaluate behavioral properties.</p></div><div><h3>Results</h3><p><span>We found a significant increase in stereological parameters, antioxidant factors (catalase, glutathione, and superoxide dismutase), and behavioral function scores in the tramadol+CoQ10 group compared to the tramadol group (p &lt; 0.05). In addition, malondialdehyde levels, the density of apoptotic cells, as well as the expression of pro-inflammatory (tumor necrosis factor-alpha, </span>interleukin 1 beta<span>, and interleukin 6) and autophagy (lysosome-associated membrane protein 2, autophagy-related 5, beclin 1, and autophagy-related 12) genes were considerably reduced in the tramadol+CoQ10 group compared to the tramadol group (p &lt; 0.05).</span></p></div><div><h3>Conclusion</h3><p>We conclude that the administration of CoQ10 has neuroprotective effects in the cerebellum of rats that have chronic exposure to tramadol.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"135 ","pages":"Article 102367"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138477805","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":"Supplementation with vitamins D3 and a mitigates Parkinsonism in a haloperidol mice model","authors":"Mujittapha Umar Sirajo ,&nbsp;John C. Oyem ,&nbsp;Mohammed Ibrahim Badamasi","doi":"10.1016/j.jchemneu.2023.102366","DOIUrl":"10.1016/j.jchemneu.2023.102366","url":null,"abstract":"<div><h3>Background</h3><p><span>Earlier reports suggest that vitamin D3 (Vit D3) supplementation attenuates </span>Parkinsonism in drug-induced motor deficits. Moreover, the function of Vit D3 may be optimized by co-administration with vitamin A (Vit A). In line with the synergistic interplay between vitamins, we hypothesized that the efficacy of Vit D3 to attenuate Parkinsonism in a haloperidol-induced mouse model of motor deficits would be more potent when concomitantly administered with Vit A.</p></div><div><h3>Methods</h3><p><span>Thirty-six (36) adult male mice were randomly divided into six groups of six animals each: the control group, the PD model (haloperidol-treated only group) (-D2), and four other groups treated with </span>haloperidol<span> together with either one or two of the following vitamin supplementations: Vit D3, Vit A, Vit D3 +VA, or bromocriptine a known PD drug respectively. Motor functions were assessed using a battery of neurobehavioral tests in experimental animals, after which brain tissues were harvested and processed for biochemical and histomorphological analysis.</span></p></div><div><h3>Results</h3><p>We recorded a significant decline in motor activity in the PD mice model treated with haloperidol alone compared to other experimental groups that received vitamin supplementations. The significant decrease in motor activity observed in the PD mice model corresponded with marked neurodegenerative features in the cytoarchitecture<span> of the pyramidal cells<span><span> in the striatum and primary motor cortex (M1). Furthermore, the haloperidol-induced PD mice model treated with Vit D3 +Vit A showed significant improvement in motor activity and attenuation of </span>oxidative stress levels and neurodegenerative features compared to other groups treated with Vit A, Vit D3 and bromocriptine alone.</span></span></p></div><div><h3>Conclusion</h3><p>Altogether, our findings suggest that concomitant administration of both Vit D3 and Vit A prevents the development of Parkinsonism features in the haloperidol mouse model of motor deficit. Thus, supplementation with Vit D3 +Vit A may be a viable option for slowing the onset and progression of motor deficits.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"135 ","pages":"Article 102366"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138470341","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":"Immunoreactivity of glutamine synthetase in satellite glia around various subpopulations of lumbar dorsal root ganglia neurons in adult rats treated with monosodium glutamate","authors":"Aleksandra Krawczyk,&nbsp;Sylwia Mozel,&nbsp;Karol Rycerz,&nbsp;Jadwiga Jaworska-Adamu,&nbsp;Marcin Bartłomiej Arciszewski","doi":"10.1016/j.jchemneu.2023.102347","DOIUrl":"10.1016/j.jchemneu.2023.102347","url":null,"abstract":"<div><p>Satellite glial cells (SGCs), involved inter alia in glutamate (Glu) metabolism, form a glial sheath around sensory neurons of dorsal root ganglia (DRGs). SGCs show a presence of glutamine synthetase (GS) which transform uptaken Glu into glutamine (Gln). In DRGs, this aminoacid is used mainly by small neurons which are able to synthetize substance P (SP) that play a crucial role in nociception. The aim of the study was to define the influence of monosodium glutamate (MSG) on GS immunoreactivity in satellite glia around various subpopulations of neurons including SP immunopositive cells in DRGs of adult rats. The studies were carried out on lumbar DRGs slides in rats which received subcutaneous injection of saline solution (control group) or 4 g/kg b. w. of MSG (MSG group). Immunofluorescence reactions were conducted with use of anti-GS and anti-SP antibodies. Administration of MSG to adult rats increased the GS immunoexpression in SGCs. In rats receiving MSG, a number of small neurons with GS-immunopositive glial sheath was not altered when compared to control individuals, whereas there was a statistically significant increase of GS immunoexpression in SGCs around large and medium neurons. Moreover, in these animals, a statistically significant increase in the number of small SP-positive neurons with GS-positive glial sheath was observed. SP is responsible for transmission of pain, thus the obtained results may be useful for further research concerning the roles of glia in nociceptive pathway regulation.</p></div>","PeriodicalId":15324,"journal":{"name":"Journal of chemical neuroanatomy","volume":"134 ","pages":"Article 102347"},"PeriodicalIF":2.8,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41202161","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}