Neuronal signaling最新文献_第3页

Insights into nervous system repair from the fruit fly 果蝇对神经系统修复的见解

Neuronal signaling Pub Date : 2022-03-30 DOI: 10.1042/NS20210051

D. Coupe, T. Bossing

{"title":"Insights into nervous system repair from the fruit fly","authors":"D. Coupe, T. Bossing","doi":"10.1042/NS20210051","DOIUrl":"https://doi.org/10.1042/NS20210051","url":null,"abstract":"Abstract Millions of people experience injury to the central nervous system (CNS) each year, many of whom are left permanently disabled, providing a challenging hurdle for the field of regenerative medicine. Repair of damage in the CNS occurs through a concerted effort of phagocytosis of debris, cell proliferation and differentiation to produce new neurons and glia, distal axon/dendrite degeneration, proximal axon/dendrite regeneration and axon re-enwrapment. In humans, regeneration is observed within the peripheral nervous system, while in the CNS injured axons exhibit limited ability to regenerate. This has also been described for the fruit fly Drosophila. Powerful genetic tools available in Drosophila have allowed the response to CNS insults to be probed and novel regulators with mammalian orthologs identified. The conservation of many regenerative pathways, despite considerable evolutionary separation, stresses that these signals are principal regulators and may serve as potential therapeutic targets. Here, we highlight the role of Drosophila CNS injury models in providing key insight into regenerative processes by exploring the underlying pathways that control glial and neuronal activation in response to insult, and their contribution to damage repair in the CNS.","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48917321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Cell models for Down syndrome-Alzheimer’s disease research 唐氏综合征阿尔茨海默病的细胞模型研究

Neuronal signaling Pub Date : 2022-03-22 DOI: 10.1042/NS20210054

Yixing Wu, N. West, A. Bhattacharyya, F. Wiseman

{"title":"Cell models for Down syndrome-Alzheimer’s disease research","authors":"Yixing Wu, N. West, A. Bhattacharyya, F. Wiseman","doi":"10.1042/NS20210054","DOIUrl":"https://doi.org/10.1042/NS20210054","url":null,"abstract":"Abstract Down syndrome (DS) is the most common chromosomal abnormality and leads to intellectual disability, increased risk of cardiac defects, and an altered immune response. Individuals with DS have an extra full or partial copy of chromosome 21 (trisomy 21) and are more likely to develop early-onset Alzheimer’s disease (AD) than the general population. Changes in expression of human chromosome 21 (Hsa21)-encoded genes, such as amyloid precursor protein (APP), play an important role in the pathogenesis of AD in DS (DS-AD). However, the mechanisms of DS-AD remain poorly understood. To date, several mouse models with an extra copy of genes syntenic to Hsa21 have been developed to characterise DS-AD-related phenotypes. Nonetheless, due to genetic and physiological differences between mouse and human, mouse models cannot faithfully recapitulate all features of DS-AD. Cells differentiated from human-induced pluripotent stem cells (iPSCs), isolated from individuals with genetic diseases, can be used to model disease-related cellular and molecular pathologies, including DS. In this review, we will discuss the limitations of mouse models of DS and how these can be addressed using recent advancements in modelling DS using human iPSCs and iPSC-mouse chimeras, and potential applications of iPSCs in preclinical studies for DS-AD.","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44173361","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Cholinergic blockade of neuroinflammation: from tissue to RNA regulators. 神经炎症的胆碱能阻断:从组织到RNA调节因子。

Neuronal signaling Pub Date : 2022-02-11 eCollection Date: 2022-04-01 DOI: 10.1042/NS20210035

Tamara Zorbaz, Nimrod Madrer, Hermona Soreq

{"title":"Cholinergic blockade of neuroinflammation: from tissue to RNA regulators.","authors":"Tamara Zorbaz, Nimrod Madrer, Hermona Soreq","doi":"10.1042/NS20210035","DOIUrl":"https://doi.org/10.1042/NS20210035","url":null,"abstract":"Inflammatory stimuli and consequent pro-inflammatory immune responses may facilitate neurodegeneration and threaten survival following pathogen infection or trauma, but potential controllers preventing these risks are incompletely understood. Here, we argue that small RNA regulators of acetylcholine (ACh) signaling, including microRNAs (miRs) and transfer RNA fragments (tRFs) may tilt the balance between innate and adaptive immunity, avoid chronic inflammation and prevent the neuroinflammation-mediated exacerbation of many neurological diseases. While the restrictive permeability of the blood-brain barrier (BBB) protects the brain from peripheral immune events, this barrier can be disrupted by inflammation and is weakened with age. The consequently dysregulated balance between pro- and anti-inflammatory processes may modify the immune activities of brain microglia, astrocytes, perivascular macrophages, oligodendrocytes and dendritic cells, leading to neuronal damage. Notably, the vagus nerve mediates the peripheral cholinergic anti-inflammatory reflex and underlines the consistent control of body-brain inflammation by pro-inflammatory cytokines, which affect cholinergic functions; therefore, the disruption of this reflex can exacerbate cognitive impairments such as attention deficits and delirium. RNA regulators can contribute to re-balancing the cholinergic network and avoiding its chronic deterioration, and their activities may differ between men and women and/or wear off with age. This can lead to hypersensitivity of aged patients to inflammation and higher risks of neuroinflammation-driven cholinergic impairments such as delirium and dementia following COVID-19 infection. The age- and sex-driven differences in post-transcriptional RNA regulators of cholinergic elements may hence indicate new personalized therapeutic options for neuroinflammatory diseases.","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8837817/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39959466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 9

Neuroprotection of retinal ganglion cells in vivo using the activation of the endogenous cannabinoid signaling system in mammalian eyes 利用内源性大麻素信号系统激活哺乳动物眼睛视网膜神经节细胞的体内神经保护

Neuronal signaling Pub Date : 2022-01-26 DOI: 10.1042/NS20210038

Greg Maguire, C. Eubanks, George Ayoub

{"title":"Neuroprotection of retinal ganglion cells in vivo using the activation of the endogenous cannabinoid signaling system in mammalian eyes","authors":"Greg Maguire, C. Eubanks, George Ayoub","doi":"10.1042/NS20210038","DOIUrl":"https://doi.org/10.1042/NS20210038","url":null,"abstract":"Abstract Cannabinoid and glutamatergic signaling systems in the human retina coexist and greatly influence one another. Under glaucomatous conditions, excess levels of glutamate accrete in the retinal ganglion cell (RGC) layer. The present study tests the putative neuroprotective effect mediated by cannabinoids at the CB1 and CB2 receptors. In the first experiment, mice were given intravitreal injections of 160 nmol N-methyl-d-aspartic acid (NMDA) in one eye and saline in the paired eye. In the second experiment, both eyes were given NMDA, while one of the two was additionally given the cannabinoid agonist WIN 55,212-2. Ten days later, animals were perfused and the retinae were dissected as wholemounts and stained with Cresyl Violet. Quantitative analysis revealed that 70% of the neurons in the retinal ganglion cell (RGC) layer exposed to NMDA underwent cell death. The addition of the cannabinoid CB1/CB2 agonist doubled the number of neurons surviving the NMDA treatment. These data provide evidence that cannabinoids, either exogenous or endogenous, may be harnessed to provide protection from neurodegenerative diseases, including glaucoma, and from glutamate-induced, and potentially other forms of neurotoxicity, under chronic or acute conditions.","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47518657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Sex-dependent effects of chronic exercise on cognitive flexibility but not hippocampal Bdnf in aging mice. 慢性运动对衰老小鼠认知灵活性而非海马Bdnf的性别依赖性影响。

Neuronal signaling Pub Date : 2022-01-05 eCollection Date: 2022-04-01 DOI: 10.1042/NS20210053

Annabel K Short, Viet Bui, Isabel C Zbukvic, Anthony J Hannan, Terence Y Pang, Jee Hyun Kim

{"title":"Sex-dependent effects of chronic exercise on cognitive flexibility but not hippocampal Bdnf in aging mice.","authors":"Annabel K Short, Viet Bui, Isabel C Zbukvic, Anthony J Hannan, Terence Y Pang, Jee Hyun Kim","doi":"10.1042/NS20210053","DOIUrl":"https://doi.org/10.1042/NS20210053","url":null,"abstract":"Cognitive impairments associated with advanced age involve alterations in the hippocampus that changes with experience throughout life. The hippocampus is critical for cognitive flexibility involved with extinction and reinstatement of conditioned fear. It is widely accepted that regular exercise can be beneficial for hippocampal function. Therefore, we asked whether chronic voluntary exercise in middle-aged mice can improve extinction and/or reinstatement of conditioned fear compared with standard-housing. Eight-month-old male and female C57Bl/6J mice had access to a running wheel or remained in standard-housing until 11 months of age. Alongside control standard-housed young adult (3-month-old) mice, they received tone-footshock pairings, which were subsequently extinguished with tone-alone presentations the next day. Half of the mice then received a reminder in the form of a single footshock. Male and female 11-month-old mice housed in standard conditions exhibited impaired reinstatement compared with young adult mice. However, for males that had access to a running wheel from 8 months of age, the reminder treatment rescued reinstatement ability. This was not observed in females. Additionally, exercise during middle age in both sexes increased expression of brain-derived neurotrophic factor (Bdnf) mRNA in the hippocampus, specifically exon 4 mRNA. These results show that, at least for males, physical exercise is beneficial for reducing age-related decline in cognitive abilities. Despite not affecting reinstatement, exercise also increased Bdnf gene expression in the female hippocampus, which could potentially benefit other forms of hippocampus-dependent cognition.","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8734434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39702424","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Do foetal transplant studies continue to be justified in Huntington's disease? 胎儿移植研究在亨廷顿氏病中是否仍然是合理的?

Neuronal signaling Pub Date : 2021-12-13 eCollection Date: 2021-12-01 DOI: 10.1042/NS20210019

Oliver J M Bartley, Mariah J Lelos, William P Gray, Anne E Rosser

{"title":"Do foetal transplant studies continue to be justified in Huntington's disease?","authors":"Oliver J M Bartley, Mariah J Lelos, William P Gray, Anne E Rosser","doi":"10.1042/NS20210019","DOIUrl":"https://doi.org/10.1042/NS20210019","url":null,"abstract":"Early CNS transplantation studies used foetal derived cell products to provide a foundation of evidence for functional recovery in preclinical studies and early clinical trials. However, it was soon recognised that the practical limitations of foetal tissue make it unsuitable for widespread clinical use. Considerable effort has since been directed towards producing target cell phenotypes from pluripotent stem cells (PSCs) instead, and there now exist several publications detailing the differentiation and characterisation of PSC-derived products relevant for transplantation in Huntington's disease (HD). In light of this progress, we ask if foetal tissue transplantation continues to be justified in HD research. We argue that (i) the extent to which accurately differentiated target cells can presently be produced from PSCs is still unclear, currently making them undesirable for studying wider CNS transplantation issues; (ii) foetal derived cells remain a valuable tool in preclinical research for advancing our understanding of which products produce functional striatal grafts and as a reference to further improve PSC-derived products; and (iii) until PSC-derived products are ready for human trials, it is important to continue using foetal cells to gather clinical evidence that transplantation is a viable option in HD and to use this opportunity to optimise practical parameters (such as trial design, clinical practices, and delivery strategies) to pave the way for future PSC-derived products.","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8674623/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39763624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Animal models of Parkinson's disease: a guide to selecting the optimal model for your research. 帕金森病的动物模型：为您的研究选择最佳模型的指南。

Neuronal signaling Pub Date : 2021-12-08 eCollection Date: 2021-12-01 DOI: 10.1042/NS20210026

Joana Lama, Yazead Buhidma, Edward J R Fletcher, Susan Duty

{"title":"Animal models of Parkinson's disease: a guide to selecting the optimal model for your research.","authors":"Joana Lama, Yazead Buhidma, Edward J R Fletcher, Susan Duty","doi":"10.1042/NS20210026","DOIUrl":"10.1042/NS20210026","url":null,"abstract":"Parkinson's disease (PD) is a complex, multisystem disorder characterised by α-synuclein (SNCA) pathology, degeneration of nigrostriatal dopaminergic neurons, multifactorial pathogenetic mechanisms and expression of a plethora of motor and non-motor symptoms. Animal models of PD have already been instructive in helping us unravel some of these aspects. However, much remains to be discovered, requiring continued interrogation by the research community. In contrast with the situation for many neurological disorders, PD benefits from of a wide range of available animal models (pharmacological, toxin, genetic and α-synuclein) but this makes selection of the optimal one for a given study difficult. This is especially so when a study demands a model that displays a specific combination of features. While many excellent reviews of animal models already exist, this review takes a different approach with the intention of more readily informing this decision-making process. We have considered each feature of PD in turn - aetiology, pathology, pathogenesis, motor dysfunctions and non-motor symptoms (NMS) - highlighting those animal models that replicate each. By compiling easily accessible tables and a summary figure, we aim to provide the reader with a simple, go-to resource for selecting the optimal animal model of PD to suit their research needs.","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8661507/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39764050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Identification of TGFβ signaling as a regulator of interneuron neurogenesis in a human pluripotent stem cell model. 在人多能干细胞模型中tgf - β信号作为中间神经元神经发生调节因子的鉴定。

Neuronal signaling Pub Date : 2021-12-07 eCollection Date: 2021-12-01 DOI: 10.1042/NS20210020

Maria Santos Cruz, Meng Li

{"title":"Identification of TGFβ signaling as a regulator of interneuron neurogenesis in a human pluripotent stem cell model.","authors":"Maria Santos Cruz, Meng Li","doi":"10.1042/NS20210020","DOIUrl":"https://doi.org/10.1042/NS20210020","url":null,"abstract":"Cortical interneurons are GABAergic inhibitory cells that connect locally in the neocortex and play a pivotal role in shaping cortical network activities. Dysfunction of these cells is believed to lead to runaway excitation underlying seizure-based diseases, such as epilepsy, autism and schizophrenia. There is a growing interest in using cortical interneurons derived from human pluripotent stem cells for understanding their complex development and for modeling neuropsychiatric diseases. Here, we report the identification of a novel role of transforming growth factor β (TGFβ) signaling in modulating interneuron progenitor maintenance and neuronal differentiation. TGFβ signaling inhibition suppresses terminal differentiation of interneuron progenitors, while exogenous TGFβ3 accelerates the transition of progenitors into postmitotic neurons. We provide evidence that TGFb signaling exerts this function via regulating cell cycle length of the NKX2.1+ neural progenitors. Together, the present study represents a useful platform for studying human interneuron development and interneuron-associated neurological diseases with human pluripotent stem cells.","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8661503/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39764046","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Mutations in DISC1 alter IP₃R and voltage-gated Ca²⁺ channel functioning, implications for major mental illness. DISC1突变改变IP3R和电压门控Ca2+通道功能，对主要精神疾病的影响。

Neuronal signaling Pub Date : 2021-12-07 eCollection Date: 2021-12-01 DOI: 10.1042/NS20180122

Ann R Rittenhouse, Sonia Ortiz-Miranda, Agata Jurczyk

{"title":"Mutations in DISC1 alter IP3R and voltage-gated Ca2+ channel functioning, implications for major mental illness.","authors":"Ann R Rittenhouse, Sonia Ortiz-Miranda, Agata Jurczyk","doi":"10.1042/NS20180122","DOIUrl":"https://doi.org/10.1042/NS20180122","url":null,"abstract":"Disrupted in Schizophrenia 1 (DISC1) participates in a wide variety of developmental processes of central neurons. It also serves critical roles that underlie cognitive functioning in adult central neurons. Here we summarize DISC1's general properties and discuss its use as a model system for understanding major mental illnesses (MMIs). We then discuss the cellular actions of DISC1 that involve or regulate Ca2+ signaling in adult central neurons. In particular, we focus on the tethering role DISC1 plays in transporting RNA particles containing Ca2+ channel subunit RNAs, including IP3R1, CACNA1C and CACNA2D1, and in transporting mitochondria into dendritic and axonal processes. We also review DISC1's role in modulating IP3R1 activity within mitochondria-associated ER membrane (MAM). Finally, we discuss DISC1-glycogen synthase kinase 3β (GSK3β) signaling that regulates functional expression of voltage-gated Ca2+ channels (VGCCs) at central synapses. In each case, DISC1 regulates the movement of molecules that impact Ca2+ signaling in neurons.","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-12-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8663806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39764047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Molecular mechanisms of action of stimulant novel psychoactive substances that target the high-affinity transporter for dopamine. 靶向多巴胺高亲和转运体的兴奋性新型精神活性物质的分子作用机制。

Neuronal signaling Pub Date : 2021-11-17 eCollection Date: 2021-12-01 DOI: 10.1042/NS20210006

Michelle A Sahai, Jolanta Opacka-Juffry

{"title":"Molecular mechanisms of action of stimulant novel psychoactive substances that target the high-affinity transporter for dopamine.","authors":"Michelle A Sahai, Jolanta Opacka-Juffry","doi":"10.1042/NS20210006","DOIUrl":"10.1042/NS20210006","url":null,"abstract":"Drug misuse is a significant social and public health problem worldwide. Misused substances exert their neurobehavioural effects through changing neural signalling within the brain, many of them leading to substance dependence and addiction in the longer term. Among drugs with addictive liability, there are illicit classical stimulants such as cocaine and amphetamine, and their more recently available counterparts known as novel psychoactive substances (NPS). Stimulants normally increase dopamine availability in the brain, including the pathway implicated in reward-related behaviour. This pattern is observed in both animal and human brain. The main biological target of stimulants, both classical and NPS, is the dopamine transporter (DAT) implicated in the dopamine-enhancing effects of these drugs. This article aims at reviewing research on the molecular mechanisms underpinning the interactions between stimulant NPS, such as benzofurans, cathinones or piperidine derivatives and DAT, to achieve a greater understanding of the core phenomena that decide about the addictive potential of stimulant NPS. As the methodology is essential in the process of experimental research in this area, we review the applications of in vitro, in vivo and in silico approaches. The latter, including molecular dynamics, attracts the focus of the present review as the method of choice in molecular and atomistic investigations of the mechanisms of addiction of stimulant NPS. Research of this kind is of interest to not only scientists but also health professionals as updated knowledge of NPS, their modes of action and health risks, is needed to tackle the challenges posed by NPS misuse.","PeriodicalId":74287,"journal":{"name":"Neuronal signaling","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2021-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8630395/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39710118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2