Acta neurobiologiae experimentalis最新文献_第2页

Different faces of autism: Patients with mutations in PTEN and FMR1 genes. 自闭症的不同面孔：PTEN和FMR1基因突变的患者。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2025-01-14 DOI: 10.55782/ane-2024-2664

Adam Gorlewicz, Ewelina Kanpska

{"title":"Different faces of autism: Patients with mutations in PTEN and FMR1 genes.","authors":"Adam Gorlewicz, Ewelina Kanpska","doi":"10.55782/ane-2024-2664","DOIUrl":"10.55782/ane-2024-2664","url":null,"abstract":"Autism spectrum disorder (ASD) is among the most common neurodevelopmental conditions in humans. While public awareness of the challenges faced by individuals with autism is steadily increasing, the underlying causes of abnormalities observed in ASD remains incompletely understood. The autism spectrum is notably broad, with symptoms that can manifest in various forms and degrees of severity. Core features of ASD, such as communication difficulties, impaired social interactions, and restricted patterns of behavior, interests, and activities, are often accompanied by other co‑occurring conditions, such as anxiety. ASD affects individuals regardless of gender, race, or ethnicity. Although we are currently unable to pinpoint a single definitive cause of autism, it is clear that genetics play a crucial role in its development. The first genes associated with an increased risk for ASD were discovered in rare monogenic disorders, such as fragile X syndrome (FXS), caused by mutations in the fragile X messenger ribonucleoprotein 1 (FMR1) gene, and macrocephaly, linked to mutations in the phosphatase and tensin homolog (PTEN) gene. This review aims to summarize the current knowledge of ASD in patients with mutations in the FMR1 and PTEN genes.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"84 4","pages":"352-358"},"PeriodicalIF":1.4,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982330","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}

引用次数: 0

Understanding the neurobiological mechanisms of LPS‑induced memory impairment. 了解LPS诱导的记忆障碍的神经生物学机制。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2025-01-14 DOI: 10.55782/ane-2024-2629

Ahmad Golkar, Mohammad Dalfardi, Mahdiyeh Hedayati-Moghadam, Hedyeh Askarpour, Mahmoud Hosseini, Yousef Baghcheghi

{"title":"Understanding the neurobiological mechanisms of LPS‑induced memory impairment.","authors":"Ahmad Golkar, Mohammad Dalfardi, Mahdiyeh Hedayati-Moghadam, Hedyeh Askarpour, Mahmoud Hosseini, Yousef Baghcheghi","doi":"10.55782/ane-2024-2629","DOIUrl":"10.55782/ane-2024-2629","url":null,"abstract":"In recent years, growing evidence suggests that lipopolysaccharide (LPS), a bacterial endotoxin found in the outer membrane of gram‑negative bacteria, can influence cognitive functions, particularly memory formation and retrieval. However, the underlying mechanisms through which LPS exerts its effects on memory remain incompletely understood. This review used various electronic databases, including PubMed, Scopus, and Web of Science, to identify relevant studies published between 2000 and 2024. Articles were selected based on their focus on LPS‑induced memory impairments, including experimental models, molecular pathways, and neurochemical alterations. LPS administration has been consistently shown to disrupt memory processes in both animals and humans, although the magnitude and duration of memory impairments might vary depending on factors such as dose, timing, and context of LPS exposure. Several potential mechanisms have been proposed to explain LPS‑induced memory deficits, including neuroinflammation, alterations in synaptic plasticity, disruption of neurotransmitter systems, and dysfunction of the blood‑brain barrier. Moreover, LPS has been found to activate immune signaling pathways, such as toll‑like receptors, interleukins, and microglia, which can further contribute to cognitive impairments. Such insights may pave the way for the development of targeted therapeutic interventions aimed at ameliorating memory deficits associated with conditions involving LPS exposure, including bacterial infections, sepsis, and neuroinflammatory disorders.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"84 4","pages":"371-394"},"PeriodicalIF":1.4,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982375","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}

引用次数: 0

Response of miRNA to treatment with Hypericum perforatum L. oil in multiple sclerosis. 贯叶连翘油治疗多发性硬化症的miRNA反应。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2025-01-14 DOI: 10.55782/ane-2024-2571

Huri Dedeakayogullari, Zozan Guleken, Sahabettin Selek, Nur Dogan, Busra Yuce, Emine Seyda Teloglu, Gulreyhan Sonuc, Cagla Yildiz, Esra Tiftik, Aysu Kilic, Beren Yildizbas, Zeynep Ece Bulut

{"title":"Response of miRNA to treatment with Hypericum perforatum L. oil in multiple sclerosis.","authors":"Huri Dedeakayogullari, Zozan Guleken, Sahabettin Selek, Nur Dogan, Busra Yuce, Emine Seyda Teloglu, Gulreyhan Sonuc, Cagla Yildiz, Esra Tiftik, Aysu Kilic, Beren Yildizbas, Zeynep Ece Bulut","doi":"10.55782/ane-2024-2571","DOIUrl":"10.55782/ane-2024-2571","url":null,"abstract":"MicroRNA‑regulated gene expression plays an important role in autoimmune diseases, such as multiple sclerosis (MS). This study investigated the expression patterns of microRNAs (miRNAs) in MS in brain tissues using an animal experimental autoimmune encephalomyelitis (EAE) model treated with Hypericum perforatum (HP) oil. C57BL/6 J mice were divided into two groups: MS and control. The MS group was subdivided into sham (MS) and MS+HP. After the EAE induction treatment protocol, the patterns of miRNA expression profiles were determined in brain samples of the groups. The array data identified eleven miRNAs and candidate miRNA validation was performed by RT‑qPCR. A literature review of the validated miRNAs found that six of the eleven miRNAs (miR‑200a‑3p, miR‑200b‑3p, miR‑200c‑3p, miR‑182‑5p, miR‑183‑5p, and miR‑1298‑5p) were directly associated with MS. These miRNAs have been suggested as biomarkers of MS because they are highly correlated with the pathology of the disease. Furthermore, miRNA array analysis identified five candidate miRNAs (miR‑299a‑5p, miR‑206‑3p, miR‑325‑5p, miR‑10b‑5p, miR‑429‑3p) that are highly likely to be associated with MS pathogenesis, which could be helpful in the diagnosis and treatment of MS disease. This research offers vital insights that could be utilized in creating biomarkers and advancing treatments for MS.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"84 4","pages":"341-351"},"PeriodicalIF":1.4,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982360","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}

引用次数: 0

Long‑term effects of vitexin against development of pentylenetetrazole‑induced kindling in rats. 牡荆素对戊四唑诱发的大鼠肢体瘫痪的长期影响

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2024-10-11 DOI: 10.55782/ane-2024-2575

Denise Dias De Oliveira, Cassio Prinholato da Silva, Luiz Luciano Falconi-Sobrinho, Rene Oliveira Beleboni

{"title":"Long‑term effects of vitexin against development of pentylenetetrazole‑induced kindling in rats.","authors":"Denise Dias De Oliveira, Cassio Prinholato da Silva, Luiz Luciano Falconi-Sobrinho, Rene Oliveira Beleboni","doi":"10.55782/ane-2024-2575","DOIUrl":"https://doi.org/10.55782/ane-2024-2575","url":null,"abstract":"Evidence is provided that the glycosylated flavonoid vitexin (apigenin‑8‑C‑beta‑D‑glucopyranoside) attenuates pentylenetetrazole (PTZ)‑induced acute tonic‑clonic seizures in rats. However, the effects of chronic and systemic vitexin in PTZ‑kindled rats remain unknown. The aim of this work was to investigate the effect of long‑term treatment with vitexin in the PTZ‑kindling model of epilepsy. Male Wistar rats received intraperitoneal injections of PTZ at a subconvulsive dose of 35 mg/kg every other day for 29 days. Either saline containing dimethyl sulfoxide - DMSO 1% (vehicle), diazepam (2 mg/kg; positive control) or vitexin (2.5 mg/kg) was administered intraperitoneally 30 min before each PTZ injection. The behavioral reactions were recorded by 30 min immediately after each PTZ injection. Furthermore, on the 31st day, that is, 48 h after the latter dose of PTZ, the animals were euthanized and renal and hepatic biochemical markers were evaluated in blood serum. Chronic treatment with either diazepam or vitexin attenuated the seizures provoked by PTZ injections. Neither diazepam nor vitexin caused changes in renal levels of creatinine and urea and in hepatic levels of aspartate aminotransferase and alanine aminotransferase. Our findings suggest that chronic administration of vitexin attenuates the progression of PTZ‑induced kindling without causing side effects on kidneys and liver.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"84 3","pages":"266-274"},"PeriodicalIF":1.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399059","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}

引用次数: 0

Microbiological bases of obsessive‑compulsive disorder - the role of viruses, bacteria, and parasites in the onset and progression of OCD. 强迫症的微生物学基础--病毒、细菌和寄生虫在强迫症的发生和发展中的作用。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2024-10-11 DOI: 10.55782/ane-2024-2516

Jacek Januszewski, Alicja Forma, Karolina Kłodnicka, Adam Brachet, Jacek Baj

{"title":"Microbiological bases of obsessive‑compulsive disorder - the role of viruses, bacteria, and parasites in the onset and progression of OCD.","authors":"Jacek Januszewski, Alicja Forma, Karolina Kłodnicka, Adam Brachet, Jacek Baj","doi":"10.55782/ane-2024-2516","DOIUrl":"https://doi.org/10.55782/ane-2024-2516","url":null,"abstract":"Obsessive‑compulsive disorder (OCD) is a current topic of discussion nowadays. OCD presents a variety of different etiologies including environmental, viral, cognitive, or genetic aspects. In this article, we focused on the possible correlation between various infectious diseases as well as generally the relationship between viruses, bacteria, and parasites, and an increased OCD risk. In this narrative review, we analyzed different types of articles found on PubMed, Google Scholar, and Scopus, as well as the articles of the National Institute of Mental Health. Searching criteria included articles from 1991 till the end of November, research involving human and animal patients (including monkeys and rats), and research published in English. Research showed a relationship between Herpes simplex virus, Rubella virus, Human immunodeficiency virus, Borna disease virus, Mycoplasma pneumoniae, Toxoplasma gondii, streptococcal infections, as well as gut microbiota and increased OCD risk. The possible mechanisms of this relation include neuroinflammation, brain tissue damage, autoimmune processes, and impairments in neurotransmitter levels. Infections caused by Varicella zoster virus, Measles virus, Mumps virus, Epstein‑Barr virus, Cytomegalovirus, or Borrelia Burgdorferi may also contribute to the increased risk of OCD. Reports showed an increased frequency of OCD occurrence in a group of infected people compared to a healthy group. However, there is no evidence of the influence of Influenza virus, Coxsackie virus, Poliovirus, Parvovirus B19, Enterovirus 71, West Nile virus, Treponema Pallidum, or Toxocara infections on the OCD risk. There is a significant relationship between various infectious diseases and an increased OCD risk. However, further studies are crucial to discover the exact pathomechanisms of these correlations and the potential influence of other pathogens on the onset of OCD.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"84 3","pages":"230-242"},"PeriodicalIF":1.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399060","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}

引用次数: 0

7,8‑dihydroxyflavone reduces lipid peroxidation, proinflammatory cytokines, and mediators in chemically induced‑phenylketonuria model. 7,8-二羟基黄酮可降低化学诱导的苯丙酮尿症模型的脂质过氧化、促炎细胞因子和介质。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2024-10-11 DOI: 10.55782/ane-2024-2541

Cigdem Cicek, Pelin Telkoparan-Akillilar

{"title":"7,8‑dihydroxyflavone reduces lipid peroxidation, proinflammatory cytokines, and mediators in chemically induced‑phenylketonuria model.","authors":"Cigdem Cicek, Pelin Telkoparan-Akillilar","doi":"10.55782/ane-2024-2541","DOIUrl":"https://doi.org/10.55782/ane-2024-2541","url":null,"abstract":"Phenylketonuria (PKU) stems from a rare genetic metabolic imbalance attributed to an insufficiency in the enzyme phenylalanine hydroxylase. Within the context of PKU, brain‑derived neurotrophic factor (BDNF) plays a pivotal role in brain function. 7,8‑dihydroxyflavone (7,8‑DHF) operates as a tropomyosin receptor kinase B (TrkB) agonist, mimicking the effects of BDNF. This study aimed to examine the effects of administering 7,8‑DHF in chemically‑induced rat models specifically induced to simulate PKU chemically. The rats were subcutaneously injected with phenylalanine and p‑chlorophenylalanine, a phenylalanine hydroxylase inhibitor, along with 7,8‑DHF. The injections began on the 2nd day after birth and continued until the 10th day. Levels of interleukin‑1β (IL‑1β), interleukin‑6 (IL‑6), interleukin‑33 (IL‑33), BDNF, malondialdehyde (MDA), monoamine oxidase (MAO), and superoxide dismutase (SOD) in the brain tissues were quantified using the enzyme‑linked immunosorbent assay (ELISA). Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was performed to assess the gene expressions of inducible nitric oxide synthase (iNOS), nuclear factor kappa beta (NF‑κB), caspase‑3, nuclear factor erythroid 2‑related factor 2 (Nrf2), heme oxygenase‑1 (HO‑1), and BDNF. The results showed a decrease in mRNA levels of iNOS, IL‑1β, IL‑6, and lipid peroxidation in the group that received 7,8‑DHF. These results indicate that administering 7,8‑DHF has the potential to reduce brain damage in PKU by lowering proinflammatory cytokine levels and lipid peroxidation in PKU models. Thus, 7,8‑DHF, as a small molecule, might offer a promising adjunct therapeutic approach for PKU.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"84 3","pages":"243-255"},"PeriodicalIF":1.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399055","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}

引用次数: 0

Microdialysis perfusion of COA-Cl enhances dopamine metabolism in the dorsal striatum of freely moving mice. 微透析灌注 COA-Cl 可促进自由活动小鼠背侧纹状体的多巴胺代谢。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2024-10-11 DOI: 10.55782/ane-2024-2585

Mostofa Jamal, Ikuko Tsukamoto, Sella Takei, Takanori Miki, Hiroshi Kinoshita, Murase Takehiko

{"title":"Microdialysis perfusion of COA-Cl enhances dopamine metabolism in the dorsal striatum of freely moving mice.","authors":"Mostofa Jamal, Ikuko Tsukamoto, Sella Takei, Takanori Miki, Hiroshi Kinoshita, Murase Takehiko","doi":"10.55782/ane-2024-2585","DOIUrl":"https://doi.org/10.55782/ane-2024-2585","url":null,"abstract":"We performed a microdialysis study to examine the effects of local perfusion of COA‑Cl on the extracellular levels of dopamine (DA) and its metabolites in the dorsal striatum of mice in vivo. The mice were perfused with Ringer's solution (control) and COA‑Cl (0.05, 0.1, or 0.5 mM) into the dorsal striatum. Dialysate samples were collected every 30 min and then analyzed using high‑performance liquid chromatography coupled with an electrochemical detector. We found that local perfusion of COA‑Cl (0.1 or 0.5 mM) into the dorsal striatum of living mice produced a significant and dose‑dependent increase in extracellular levels of DA, 3‑methoxytyramine (3‑MT), and homovanillic acid (HVA), where only 0.5 mM COA‑Cl increased dihydroxyphenylacetic acid (DOPAC) levels. However, 0.05 mM of COA‑Cl did not significantly affect either DA levels or its metabolites. Then, we administered the monoamine oxidase (MAO) inhibitor clorgyline alone or in combination with COA‑Cl (0.1 mM) to test whether COA‑Cl‑induced increases in DOPAC and HVA are mediated by increased MAO activity. Clorgyline alone increased 3‑MT levels and decreased DOPAC and HVA levels but not DA levels. When combined with COA‑Cl, clorgyline increased 3‑MT levels and reversed the decrease in DOPAC and HVA levels caused by clorgyline. The increase in DA metabolism induced by COA‑Cl suggests that some DA was further metabolized into DOPAC, 3‑MT, and HVA. This indicates that COA‑Cl plays a role in DA metabolism via increased DA release and/or activation of MAO, offering new insights into the effects of COA‑Cl on DA metabolism in the brain.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"84 3","pages":"256-265"},"PeriodicalIF":1.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399061","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}

引用次数: 0

Association between the Val66Met (rs6265) polymorphism of the brain-derived neurotrophic factor (BDNF) gene, BDNF protein level in the blood and the risk of developing early‑onset Parkinson's disease. 脑源性神经营养因子（BDNF）基因的 Val66Met (rs6265) 多态性、血液中的 BDNF 蛋白水平与早发性帕金森病发病风险之间的关系。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2024-10-11 DOI: 10.55782/ane-2024-2476

Iwona Przybylska, Jarosław Marusiak, Beata Toczyłowska, Adam Stępień, Bogdan Brodacki, Józef Langfort, Małgorzata Chalimoniuk

{"title":"Association between the Val66Met (rs6265) polymorphism of the brain-derived neurotrophic factor (BDNF) gene, BDNF protein level in the blood and the risk of developing early‑onset Parkinson's disease.","authors":"Iwona Przybylska, Jarosław Marusiak, Beata Toczyłowska, Adam Stępień, Bogdan Brodacki, Józef Langfort, Małgorzata Chalimoniuk","doi":"10.55782/ane-2024-2476","DOIUrl":"10.55782/ane-2024-2476","url":null,"abstract":"Brain-derived neurotrophic factor (BDNF) is involved in the maintenance of dopamine level and the survival of dopaminergic neurons, which may affect the functionality of brain structures responsible for motor and cognitive function. The aim of the study was to assess the association of individual and combined single nucleotide polymorphism (SNP) in the rs6265 BDNF (Val66Met), rs397595 DAT (SLC6A3), and rs4680 COMT (Val158Met) genes with early‑onset of Parkinson's disease (PD) patients. Moreover, we assessed the association between the BDNF Val66Met polymorphism and the level of BDNF protein in the serum of patients with PD and controls. The study involved 163 patients with idiopathic PD divided into early onset (<55 years) and late‑onset (>55 years) groups and 91 healthy age‑matched people (Control). The SNP were determined using the TaqMan Real‑Time PCR method. Serum BDNF levels were determined by ELISA assay. The risk of developing early PD in people with the BDNF genotype AG increases threefold in comparison with the carriers of the BDNF genotype GG. In PD patients and healthy people with the BDNF genotypes AG and AA, a lower serum BDNF level was found compared to those with the BDNF genotype GG in both groups. The results of our study indicate that the presence of the Val66Met BDNF gene polymorphism is associated with reduced blood BDNF levels and an elevated risk of developing early‑onset PD. This effect appears to be more pronounced in men.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"84 3","pages":"296-308"},"PeriodicalIF":1.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399056","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}

引用次数: 0

Changes in D₄ and GABA_A subunit α3 receptors in the thalamic reticular nucleus caused by unilateral lesion of the globus pallidus. 丘脑网状核中的D4和GABAA亚基α3受体在单侧丘脑苍白球损伤后的变化

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2024-10-11 DOI: 10.55782/ane-2024-2544

Lizette Montoya-Gress, Lizbeth Juárez-Rojas, Julio Almanza-Pérez, Eunice Farfán-García, Luis Gómez-Quiroz, Mohammad Mehdi Ommati, Reza Heidari, Enrique Querejeta-Villagómez, Alberto Alatorre-Pérez, Socorro Retana-Márquez

{"title":"Changes in D4 and GABAA subunit α3 receptors in the thalamic reticular nucleus caused by unilateral lesion of the globus pallidus.","authors":"Lizette Montoya-Gress, Lizbeth Juárez-Rojas, Julio Almanza-Pérez, Eunice Farfán-García, Luis Gómez-Quiroz, Mohammad Mehdi Ommati, Reza Heidari, Enrique Querejeta-Villagómez, Alberto Alatorre-Pérez, Socorro Retana-Márquez","doi":"10.55782/ane-2024-2544","DOIUrl":"10.55782/ane-2024-2544","url":null,"abstract":"The thalamic reticular nucleus controls information processing in thalamocortical neurons. GABAergic neurons present in this nucleus express the α3 subunit of post‑synaptic GABAA receptors, which bind GABA from globus pallidus neurons. Pallidal neurons, in turn, have dopaminergic D4 receptors in their axon terminals. The thalamic reticular nucleus connects reciprocally with the thalamus, and it receives afferents from the brain cortex, as well as from other brain structures that have an important role in the modulation of the thalamic network. Based on the above, the purpose of this study was to assess the electrophysiological and molecular effects of unilateral lesion of the globus pallidus on the electric activity of the thalamic reticular nucleus. Two‑month‑old male rats were used. The right globus pallidus was lesioned with quinolinic acid. Seven days after the lesion, ipsilateral turning was registered, confirming the lesion. Afterward, electrophysiological evaluation of the right thalamic reticular nucleus' electrical activity was performed. Subsequently, mRNA expression for D4 receptors and subunit α3, as well as protein content were assessed in the right reticular nucleus. Pallidum lesion caused an increase in firing frequency and decreased firing bursts of reticular neurons. In addition, dopaminergic D4 mRNA, as well as protein increased. In contrast, GABAergic GABAA subunit α3 expression was suppressed, but protein content increased. These results show that the globus pallidus regulates firing in reticular neurons through D4 receptors and subunit α3 of GABAA receptor in the reticular nucleus of the thalamus.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"84 3","pages":"275-287"},"PeriodicalIF":1.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399057","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}

引用次数: 0

Investigation of amyloid‑β peptide production and clearance pathways in different stages of Alzheimer's disease. 研究阿尔茨海默病不同阶段淀粉样β肽的产生和清除途径。

IF 1.4 4区医学

Acta neurobiologiae experimentalis Pub Date : 2024-10-11 DOI: 10.55782/ane-2024-2486

Sinan Yousif Saleh, Leila Sadeghi, Gholamreza Dehghan

{"title":"Investigation of amyloid‑β peptide production and clearance pathways in different stages of Alzheimer's disease.","authors":"Sinan Yousif Saleh, Leila Sadeghi, Gholamreza Dehghan","doi":"10.55782/ane-2024-2486","DOIUrl":"10.55782/ane-2024-2486","url":null,"abstract":"Alzheimer's disease (AD) is an age‑related, progressive decline in cognitive ability. Accumulation and deposition of amyloid‑β (Aβ) is still the best‑known cause of AD that worsens over time. It is unclear whether the increase in Aβ production or the inefficiency of the degradation system causes the accumulation of β‑fibrils during AD development. This research investigated Aβ‑producing and clearance pathways in different stages of AD. For this purpose, patients were categorized into four experimental groups: patients with mild cognitive impairment, patients with moderate cognitive decline, patients with very severe cognitive decline, and healthy patients as control. Levels of Aβ‑40, soluble amyloid precursor protein beta (sAPPβ), matrix metalloproteinase‑9 (MMP‑9), matrix metalloproteinase‑3 (MMP‑3), neprilysin (NEP), angiotensin‑converting enzyme (ACE), and insulin‑degrading enzyme (IDE) were determined by ELISA kits and immunoblotting in serum samples. According to the results, the levels of Aβ‑40 and sAPPβ increased in AD patients from an early stage, and levels were maintained in progressive AD stages. MMP‑9 also increased in the early stage, but its content decreased with disease development. MMP‑3 was significantly higher in the three stages of AD compared to the control patients. However, IDE, NEP, and ACE enzymes as clearing systems decreased in all studied AD samples, with their reductions more remarkable in the middle and late stages. The results showed that multiple Aβ‑degrading enzymes such as NEP and IDE in AD patients decline as AD progresses, while Aβ‑40 and sAPPβ increased from the early stage of the disease. Therefore, it could be concluded that detection of the dementia phase is a critical step for therapeutic strategies.","PeriodicalId":7032,"journal":{"name":"Acta neurobiologiae experimentalis","volume":"84 3","pages":"288-295"},"PeriodicalIF":1.4,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399058","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}

引用次数: 0