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On the functions of astrocyte-mediated neuronal slow inward currents

Neural Regeneration Research 2024年第12期19卷 2602-2612页

作者： Balázs Pál department of physiology Faculty of MedicineUniversity of DebrecenDebrecenHungary

Slow inward currents are known as neuronal excitatory currents mediated by glutamate release and activation of neuronal extra synaptic N-met hyl-D-aspartate receptors with the contribution of astrocytes.These events are significantly slower than the excitatory postsynaptic currents.Parameters of slow inward currents are determined by seve ral factors including the mechanisms of astrocytic activation and glutamate release,as well as the diffusion pathways from the release site towards the extra synaptic recepto rs.Astrocytes are stimulated by neuronal network activity,which in turn excite neurons,forming an astrocyte-neuron feedback loop.Mostly as a consequence of brain edema,astrocytic swelling can also induce slow inward currents under pathological conditions.There is a growing body of evidence on the roles of slow inward currents on a single neuron or local network level.These events often occur in synchro ny on neurons located in the same astrocytic domain.Besides synchronization of neuronal excitability,slow inward currents also set synaptic strength via eliciting timing-dependent synaptic plasticity.In addition,slow inward currents are also subject to non-synaptic plasticity triggered by long-la sting stimulation of the excitatory inputs.Of note,there might be important regionspecific differences in the roles and actions triggering slow inward currents.In greater networks,the pathophysiological roles of slow inward currents can be better understood than physiological ones.Slow inward currents are identified in the pathophysiological background of autism,as slow inward currents drive early hypersynchrony of the neural networks.Slow inward currents are significant contributors to paroxysmal depolarizational shifts/interictal spikes.These events are related to epilepsy,but also found in Alzheimer's disease,Parkinson's disease,and stroke,leading to the decline of cognitive functions.Events with features overlapping with slow inward currents(excitatory,N-methyl-Daspartate-receptor mediated currents with astrocyti

关键词： astrocyte cortical spreading depolarization gliotransmission glutamate neural synchronization NMDA receptor paroxysmal depolarizational shift slow inward current

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Regenerative medicine strategies for chronic complete spinal cord injury

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Neural Regeneration Research 2024年第4期19卷 818-824页

作者： Shogo Hashimoto Narihito Nagoshi Masaya Nakamura Hideyuki Okano department of Orthopedic Surgery Keio University School of Medicine department of physiology Keio University School of Medicine

Spinal cord injury is a condition in which the parenchyma of the spinal cord is damaged by trauma or various diseases.While rapid progress has been made in regenerative medicine for spinal cord injury that was previously untreatable,most research in this field has focused on the early phase of incomplete injury.However,the majority of patients have chronic severe injuries;therefore,treatments for these situations are of fundamental importance.The reason why the treatment of complete spinal cord injury has not been studied is that,unlike in the early stage of incomplete spinal cord injury,there are various inhibitors of neural regeneration.Thus,we assumed that it is difficult to address all conditions with a single treatment in chronic complete spinal cord injury and that a combination of several treatments is essential to target severe pathologies.First,we established a combination therapy of cell transplantation and drug-releasing scaffolds,which contributes to functional recovery after chronic complete transection spinal cord injury,but we found that functional recovery was limited and still needs further investigation.Here,for the further development of the treatment of chronic complete spinal cord injury,we review the necessary approaches to the different pathologies based on our findings and the many studies that have been accumulated to date and discuss,with reference to the literature,which combination of treatments is most effective in achieving functional recovery.

关键词： cell transplantation chronic phase complete transection regenerative medicine spinal cord injury

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Mechanism of Cu entry into the brain:many unanswered questions

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Neural Regeneration Research 2024年第11期19卷 2421-2429页

作者： Shubhrajit Roy Svetlana Lutsenko department of physiology Johns Hopkins University School of MedicineBaltimoreMDUSA

Brain tissue requires high amounts of copper(Cu)for its key physiological processes,such as energy production,neurotransmitter synthesis,maturation of neuropeptides,myelination,synaptic plasticity,and radical scavenging.The requirements for Cu in the brain vary depending on specific brain regions,cell types,organism age,and nutritional status.Cu imbalances cause or contribute to several life-threatening neurologic disorders including Menkes disease,Wilson disease,Alzheimer’s disease,Parkinson’s disease,and others.Despite the well-established role of Cu homeostasis in brain development and function,the mechanisms that govern Cu delivery to the brain are not well defined.This review summarizes available information on Cu transfer through the brain barriers and discusses issues that require further research.

关键词： ATOX1 ATP7A ATP7B blood-brain barrier brain choroid plexus copper SLC31A1

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K^(+) channel-mediated retarded maturation of interneurons and its role in neurodevelopmental disorders

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Neural Regeneration Research 2024年第7期19卷 1403-1404页

作者： Kaizhen Li Daria Savitska Olga Garaschuk Laboratory of Systems Neuroscience Department of PhysiologyUniversity of BernBernSwitzerland Institute of physiology Department of NeurophysiologyEberhard Karls University of TübingenTübingenGermany

De novo mutations in genes encoding K^(+)channels are implicated in many severe neurodevelopmental disorders.Specifically,mutations in KCNA2,encoding the Shaker-type voltage-gated K^(+)channel Kv1.2,and KCNJ2,encoding the inwardly rectifying K^(+)channel Kir2.1,associate with focal and generalized epilepsies,brain atrophy,autism,ataxia and hereditary spastic paraplegia(Syrbe et al.,2015;Masnada et al.,2017;Cheng et al.,2021).

关键词： disorders atrophy

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Short neuropeptide F in integrated insect physiology

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Journal of Zhejiang University-Science B(Biomedicine & Biotechnology) 2024年第5期25卷 389-409页

作者： Marcin CHOLEWINSKI Szymon CHOWANSKI Jan LUBAWY Arkadiusz URBANSKI Karolina WALKOWIAK-NOWICKA Pawet MARCINIAK department of Animal physiology and Developmental Biology Addm Mickiewicz UniversityPoznan 61-614Poland

The short neuropeptide F(sNPF)family of peptides is a multifunctional group of neurohormones involved in the regulation of various physiological processes in insects.They have been found in a broad spectrum of species,but the number of isoforms in the precursor molecule varies from one to four.The receptor for sNPF(sNPFR),which belongs to the G protein-coupled receptor family,has been characterized in various insect orders and was shown to be an ortholog of the mammalian prolactin-releasing peptide receptor(PrPR).The sNPF signaling pathway interacts with other neurohormones such as insulin-like peptides,SIFamide,and pigment-dispersing factors(PDFs)to regulate various processes.The main physiological function of sNPF seems to be involved in the regulation of feeding,but the observed effects are species-specific.sNPF is also connected with the regulation of foraging behavior and the olfactory system.The influence of sNPF on feeding and thus energy metabolism may also indirectly affect other vital processes,such as reproduction and development.In addition,these neurohormones are involved in the regulation of locomotor activity and circadian rhythm in insects.This review summarizes the current state of knowledge about the sNPF system in insects.

关键词： Insect neuropeptide Invertebrate neurobiology Short neuropeptide F(sNPF) Feeding Neurohormone

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TonEBP expression is essential in the IL-1β–induced migration and invasion of human A549 lung cancer cells

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Oncology Research 2024年第1期32卷 151-161页

作者： HEE JU SONG TAEHEE KIM HAN NA CHOI SOO JIN KIM SANG DO LEE department of physiology School of MedicineChungnam National UniversityDaejeon35015Korea

Lung cancer has the highest mortality rate among all cancers,in part because it readily metastasizes.The tumor microenvironment,comprising blood vessels,fibroblasts,immune cells,and macrophages[including tumor-associated macrophages(TAMs)],is closely related to cancer cell growth,migration,and invasion.TAMs secrete several cytokines,including interleukin(IL)-1β,which participate in cancer migration and invasion.p21-activated kinase 1(PAK1),an important signaling molecule,induces cell migration and invasion in several carcinomas.Tonicityresponsive enhancer-binding protein(TonEBP)is also known to participate in cancer cell growth,migration,and invasion.However,the mechanisms by which it increases lung cancer migration remain unclear.Therefore,in this study,we aimed to elucidate the mechanisms by which IL-1βand TonEBP affect lung cancer cell migration and invasion.We found that A549 cocultured-MΦ-secreted IL-1βinduced A549 cell migration and invasion via the PAK1 pathway.TonEBP deficiency reduced A549 cell migration and invasion and increased responsiveness to IL-1β–induced migration and invasion.PAK1 phosphorylation,which was promoted by IL-1β,was reduced when TonEBP was depleted.These results suggest that TonEBP plays an important role in IL-1βinduction and invasiveness of A549 cells via the PAK1 pathway.These findings could be valuable in identifying potential targets for lung cancer treatment.

关键词： Lung cancer TonEBP Tumor microenvironment Tumor-associated macrophage IL-1β

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New pharmacological tools:the use of diterpenes to promote adult hippocampal neurogenesis

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Neural Regeneration Research 2024年第8期19卷 1629-1630页

作者： Ricardo Gomez-Oliva Pedro Nunez-Abades Carmen Castro department of Biomedicine Biotechnology and Public HealthDivision of PhysiologyUniversity of CadizCadizSpain Biomedical Research and Innovation Institute of Cadiz(INiBICA) CadizSpain department of physiology University of SevilleSevilleSpain

Tissue regeneration maintains homeostasis and preserves the functional features of each tissue.However,not all tissues show a strong repairing capacity.This is the case of the central nervous system.It is now well established that the generation of new functional neurons from stem cells in the adult brain occurs in specific regions of the brain of different species such as rodents,birds,primates,and humans(Eriksson et al.,1998).

关键词： capacity maintain preserve

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Role of N-formyl peptide receptor 2 in germinal matrix hemorrhage:an intrinsic review of a hematoma resolving pathway

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Neural Regeneration Research 2024年第2期19卷 350-354页

作者： Jerry Flores Jiping Tang department of physiology&Pharmacology Loma Linda University School of MedicineLoma LindaCAUSA

Germinal matrix hemorrhage is one of the leading causes of morbidity,mortality,and acquired infantile hydrocephalus in preterm infants in the United States,with little progress made in its clinical management.Blood clots have been shown to elicit secondary brain injury after germinal matrix hemorrhage,by disrupting normal cerebrospinal fluid circulation and absorption after germinal matrix hemorrhage causing post-hemorrhagic hydrocephalus development.Current evidence suggests that rapid hematoma resolution is necessary to improve neurological outcomes after hemorrhagic stroke.Various articles have demonstrated the beneficial effects of stimulating the polarization of microglia cells into the M2 phenotype,as it has been suggested that they play an essential role in the rapid phagocytosis of the blood clot after hemorrhagic models of stroke.N-formyl peptide receptor 2(FPR2),a G-protein-coupled receptor,has been shown to be neuroprotective after stroke.FPR2 activation has been associated with the upregulation of phagocytic macrophage clearance,yet its mechanism has not been fully explored.Recent literature suggests that FPR2 may play a role in the stimulation of scavenger receptor CD36.Scavenger receptor CD36 plays a vital role in microglia phagocytic blood clot clearance after germinal matrix hemorrhage.FPR2 has been shown to phosphorylate extracellular-signal-regulated kinase 1/2(ERK1/2),which then promotes the transcription of the dual-specificity protein phosphatase 1(DUSP1)gene.In this review,we present an intrinsic outline of the main components involved in FPR2 stimulation and hematoma resolution after germinal matrix hemorrhage.

关键词： AnxA1 FPR2 GMH hematoma resolution hemorrhagic stroke M1 M2 microglia polarization microglia phagocytosis

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Pleiotropic attenuating effect of Ginkgo biloba against isoprenalineinduced myocardial infarction via improving Bcl-2/mTOR/ERK1/2/Na^(+) , K^(+) -ATPase activities

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Chinese Herbal Medicines 2024年第2期16卷 282-292页

作者： Jerome Ndudi Asiwe Abodunrin Adebayo Ojetola Nwoke Enekabokom Ekene Esthinsheen Osirim Anthony Chibuzor Nnamudi Benjamin Oritsemuelebi Jackson Erozueme Onuelu Nicholas Asiwe Harrison Ogheneochuko Eruotor Saviour Inegbenehi department of physiology Delta State UniversityAbraka 1Nigeria department of physiology University of IbadanIbadan 3017Nigeria department of physiology Adeleke UniversityEde 250Nigeria department of Pharmacology Rivers State UniversityNkpolu-Oroworukwo 5080Nigeria department of physiology Redeemer’s UniversityEde 230Nigeria department of Biochemistry PAMO University of Medical SciencesPort Harcourt 500211Nigeria department of Pharmacology Delta State UniversityAbraka 1Nigeria department of Anatomy University of Port HarcourtChoba 5323Nigeria department of Medical Laboratory Sciences University of Port HarcourtChoba 5323Nigeria

Objective:Myocardial infarction(MI)is linked to an imbalance in the supply and demand of blood oxygen in the heart muscles.Beta-blockers and calcium antagonists are just two of the common medications used to treat MI.However,these have reportedly been shown to be either ineffective or to have undesirable side effects.Extract of Ginkgo biloba leaves(GBE),a Chinese herbal product offers special compatibility benefits in therapeutic settings relating to inflammatory diseases and oxidative stress.In order to better understand how GBE affects MI in rats insulted by isoprenaline(ISO),the current study was designed.Methods:The heart weight index,serum lipid profile,cardiac marker enzymes,endogenous antioxidants[catalase(CAT),superoxide dismutase(SOD),glutathione(GSH),nitrites and malondialdehyde(MDA)],inflammatory mediators[tumour necrosis factor alpha(TNF-a)and interleukin-6(IL-6)],immunohistochemical expressions of B-cell lymphoma factor-2(Bcl-2),extracellular signal-regulated kinase(ERK1/2),and mammalian target of rapamycin(mTOR)and histopathological analysis were used to assess the cardioprotective properties of GBE.Results:The findings showed that GBE effectively attenuated myocardial infarction by boosting the body’s natural antioxidant defense system and reducing the release of inflammatory cytokines as well as heart injury marker enzymes.The expression of Bcl-2,ERK1/2 and mTOR was increased while the histomorphological alterations were reversed.Conclusion:The cardioprotective effects of GBE may be due to a mechanism involving increased Bcl-2/mTOR/ERK1/2/Na^(+),K^(+)-ATPase activity.

关键词： antioxidants extracellular signal-regulated kinase Ginkgo biloba extract isoprenaline mammalian target of rapamycin myocardial infarction Na^(+),K^(+)-ATPase

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Irisin/BDNF signaling in the muscle-brain axis and circadian system: A review

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The Journal of Biomedical Research 2024年第1期38卷 1-16页

作者： Alexey N.Inyushkin Vitalii S.Poletaev Elena M.Inyushkina Igor S.Kalberdin Andrey A.Inyushkin department of Human&Animal physiology Samara National Research UniversitySamara 443011Russia.

In mammals,the timing of physiological,biochemical and behavioral processes over a 24-h period is controlled by circadian rhythms.To entrain the master clock located in the suprachiasmatic nucleus of the hypothalamus to a precise 24-h rhythm,environmental zeitgebers are used by the circadian system.This is done primarily by signals from the retina via the retinohypothalamic tract,but other cues like exercise,feeding,temperature,anxiety,and social events have also been shown to act as non-photic zeitgebers.The recently identified myokine irisin is proposed to serve as an entraining non-photic signal of exercise.Irisin is a product of cleavage and modification from its precursor membrane fibronectin typeⅢdomain-containing protein 5(FNDC5)in response to exercise.Apart from well-known peripheral effects,such as inducing the"browning"of white adipocytes,irisin can penetrate the blood-brain barrier and display the effects on the brain.Experimental data suggest that FNDC5/irisin mediates the positive effects of physical activity on brain functions.In several brain areas,irisin induces the production of brain-derived neurotrophic factor(BDNF).In the master clock,a significant role in gating photic stimuli in the retinohypothalamic synapse for BDNF is suggested.However,the brain receptor for irisin remains unknown.In the current review,the interactions of physical activity and the irisin/BDNF axis with the circadian system are reconceptualized.

关键词： irisin brain-derived neurotrophic factor peroxisome proliferator-activated receptorγcoactivator 1α circadian rhythm circadian system muscle-brain axis

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