Neuroinflammation as a possible link between cannabinoids and addiction

2013 ◽  
Vol 26 (6) ◽  
pp. 334-346 ◽  
Author(s):  
Livia C.M. Rodrigues ◽  
Pedro H. Gobira ◽  
Antonio Carlos de Oliveira ◽  
Renan Pelição ◽  
Antonio Lucio Teixeira ◽  
...  
Keyword(s):  
Drug Addiction ◽  
Microglial Activation ◽  
Cell Activation ◽  
Microglial Cell ◽  
Substance Dependence ◽  
Present Review ◽  
Therapeutic Effects ◽  
Neuroprotective Effects ◽  
The Past

ObjectiveSubstance dependence disorder is a chronically relapsing condition characterised by neurobiological changes leading to loss of control in restricting a substance intake, compulsion and withdrawal syndrome. In the past few years, (endo)cannabinoids have been raised as a possible target in the aetiology of drug addiction. On the other hand, although the exact mechanisms of the genesis of addiction remain poorly understood, it is possible that neuroinflammation might also play a role in the pathophysiology of this condition. Studies demonstrated that (endo)cannabinoids act as immunomodulators by inhibiting cytokines production and microglial cell activation. Thus, in the present review, we explore the possible role of neuroinflammation on the therapeutic effects of cannabinoids on drug addiction.MethodsWe conducted an evidence-based review of the literature in order to assess the role of cannabinoids on the neuroinflammatory hypothesis of addiction (terms: addiction, cannabinoids and inflammation). We searched PubMed and BioMedCentral databases up to April 2014 with no date restrictions.ResultsIn all, 165 eligible articles were included in the present review. Existing evidence suggests that disruption in cannabinoid signalling during the drug addiction process leads to microglial activation and neuroinflammation.ConclusionThe literature showed that inflammation and changes in endocannabinod signalling occur in drug abuse; however, it remains uncertain whether these changes are causally or coincidentally associated with addiction. Additional studies, therefore, are needed to elucidate the contribution of neuroinflammation on the behavioural and neuroprotective effects of cannabinoids on drug addiction.

scholarly journals (GTG)5-PCR Mediated Molecular Typing of Zoonotic Bacteria

2021 ◽  
Vol 11 (2) ◽  
pp. 279-283
Author(s):  
Daryoush Babazadeh ◽  
Reza Ranjbar
Keyword(s):  
Molecular Typing ◽  
Cost Effective ◽  
Present Review ◽  
Published Data ◽  
Bacterial Isolates ◽  
The Past ◽  
Virulent Strains ◽  
Pcr Method ◽  
Zoonotic Bacteria

The present review aimed to reveal the role of (GTG)5-PCR microbial typing in indicating the routes and source of infections, investigate the outbreaks and genotypes of clinical strains, as well as finding virulent strains and epidemiology of bacterial isolates. All available and published data in Google scholar, PubMed, ResearchGate, and Science Direct during the past two decades that used the (GTG)5-PCR method for genotyping the bacterial isolates were included in the current study. The findings have indicated that (GTG)5-PCR can be recommended as a possible, cost-effective, fast, and easy tool for molecular typing of bacterial isolates.

scholarly journals Drug addiction: a general review of new concepts and future challenges

2000 ◽  
Vol 6 (4) ◽  
pp. 723-733
Author(s):  
N. A. Qureshi ◽  
Y. S. Al Ghamdy ◽  
T. A. Al Habeeb
Keyword(s):  
Drug Addiction ◽  
Substance Dependence ◽  
Public Health Problem ◽  
The Past ◽  
New Concepts ◽  
Future Challenges ◽  
Compulsive Behaviour ◽  
Pertinent Information ◽  
Genetic Techniques ◽  
Reward Mechanism

Relevant papers published in peer reviewed journals in the past 2 decades were identified and screened to abstract pertinent information. Substance dependence/addiction, involving both a common brain reward mechanism and longer-lasting molecular and cellular changes, is a preventable chronic, relapsing brain disease and as such a public health problem. Physical and psychological dependence, characterized by withdrawal syndrome, are now given less weight compared with compulsive behaviour and uncontrolled use of drugs in the comprehension of addiction. The challenging components of drug addictions, including counteradaptation, sensitization, abstinence, craving and relapse need further neurobiological and non-neurobiological exploration and understanding, which may be possible through the use of advanced imaging and genetic techniques and animal models of drug addiction together with relevant human studies

scholarly journals PD-1 Knockout Aggravates Motor Dysfunction In The MPTP Model of Parkinson's Disease By Inducing Microglial Activation And Neuroinflammation In Mice

2021 ◽  
Author(s):  
Ying-Ying Cheng ◽  
Bei-Yu Chen ◽  
Gan-Lan Bian ◽  
Yin-Xiu Ding ◽  
Liang-Wei CHEN
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Microglial Activation ◽  
Cell Activation ◽  
Microglial Cell ◽  
Motor Dysfunction ◽  
Glial Cell Activation ◽  
Tnf Α ◽  
Regulation Mechanisms ◽  
Mptp Model

Abstract Background: Abundant microglial reaction and neuroinflammation are typical pathogenetic hallmark of brains in Parkinson’s disease (PD) patients, but regulation mechanisms are poorly understood. In this study, the promoting effects of PD-1-difficiency on microglial activation, neuroinflammation and motor dysfunction were identified using PD animal model.Methods: Using C57 wild-type (WT), PD-1 knockout (KO) and MPTP model, we designed WT-control, KO-control, WT-MPTP and KO-MPTP groups. Motor dysfunction of animal, distribution of PD-1-positive cells, dopaminergic neuronal survival, glial cell activation and generation of inflammatory cytokines in midbrains were observed by behavior detection, immunohistochemistry and western blot methods. Results: Microglial cells showing PD-1/Iba1 double-positivity were numerously distributed in the substantia nigra of control whereas they decreased in MPTP model. Compared with WT-MPTP, KO-MPTP mice exacerbated in their motor dysfunction, decreased level of TH expression and decreased TH-positive neuronal protrusions. Microglial cell activation and expression of proinflammatory cytokine iNOS, TNF-α, IL-1β and IL-6 significantly increased, and levels and phosphorylation of AKT and ERK1/2 were also elevated in KO-MPTP mice. Conclusions: PD-1 knockout could aggravate motor dysfunction of MPTP mouse model by promoting microglial activation and neuroinflammation in midbrains, suggesting that PD-1 signaling abnormality might be involved in PD pathogenesis or progression.

scholarly journals The Role of Toll-Like Receptor 4 Mediates Microglial Activation during Remifentanil-Induced Hyperalgesia in Rats

2018 ◽  
Author(s):  
Xiang Xiang Chen ◽  
Xin Wei
Keyword(s):  
Mechanical Allodynia ◽  
Microglial Activation ◽  
Cell Activation ◽  
Thermal Hyperalgesia ◽  
Toll Like Receptor ◽  
Sprague Dawley ◽  
Toll Like Receptor 4 ◽  
Withdrawal Threshold ◽  
Incisional Pain

Abstract Background: Opioids can induce a state of nociceptive sensitization, also known as opioid-induced hyperalgesia. Nevertheless, the exact mechanism is still unclear. The following study investigates the role of Toll-like receptor 4 (TLR4) in the microglial activation during remifentanil—induced hyperalgesia in rats’ model of incisional pain. Methods: Mechanical allodynia induced by remifentanil was established in adult male Sprague–Dawley rats with incisional pain. Paw withdrawal threshold (PWT) and paw withdrawal thermal latency (PWTL) were performed to evaluate mechanical and thermal hyperalgesia. The 32-G catheter intrathecal placement was used to deliver a specific TLR4 antagonist (LPS-RS).Western blot analysis was performed to measure the expression of the TLR4 and iba-1, while Immunofluorescence staining was used to investigate the cell type and cell activation. Results：Incisionalpain-remifentanil decreased the PWT and PWTL, upregulated the expression of TLR4 and microglial activation in the spinal cord. On the contrary, the intrathecal delivery of LPS-RS at the dose of 25 μg significantly decreased mechanical allodynia and prevented the upregulation of TLR4 induced by incisional pain-remifentanil Conclusion: These findings suggest that TLR4 signaling pathway has an important role in incisional pain-remifentanil hyperalgesia, and that it could serve as the therapeutic target for persistent postsurgical pain

scholarly journals Therapeutic Effects of Melatonin on Ocular Diseases: Knowledge Map and Perspective

2021 ◽  
Vol 12 ◽  
Author(s):  
Haozhe Yu ◽  
Qicong Wang ◽  
Wenyu Wu ◽  
Weizhen Zeng ◽  
Yun Feng
Keyword(s):  
Clinical Evidence ◽  
Critical Role ◽  
Knowledge Map ◽  
Therapeutic Effects ◽  
Ocular Diseases ◽  
Ocular Tissues ◽  
The Past ◽  
Clinical Transformation ◽  
And Oxidative Stress

Melatonin plays a critical role in the pathophysiological process including circadian rhythm, apoptosis, and oxidative stress. It can be synthesized in ocular tissues, and its receptors are also found in the eye, triggering more investigations concentrated on the role of melatonin in the eye. In the past decades, the protective and therapeutic potentials of melatonin for ocular diseases have been widely revealed in animal models. Herein, we construct a knowledge map of melatonin in treating ocular diseases through bibliometric analysis and review its current understanding and clinical evidence. The overall field could be divided into twelve topics through keywords co-occurrence analysis, in which the glaucoma, myopia, and retinal diseases were of greatest research interests according to the keywords burst detection. The existing clinical trials of melatonin in ocular diseases mainly focused on the glaucoma, and more research should be promoted, especially for various diseases and drug administration. We also discuss its bioavailability and further research topics including developing melatonin sensors for personalized medication, acting as stem cell therapy assistant drug, and consuming food-derived melatonin for facilitating its clinical transformation.

scholarly journals mTORC1 Activation in Chx10-Specific Tsc1 Knockout Mice Accelerates Retina Aging and Degeneration

2021 ◽  
Vol 2021 ◽  
pp. 1-21
Author(s):  
Yu-Qing Rao ◽  
Yu-Tong Zhou ◽  
Wenchuan Zhou ◽  
Jia-Kai Li ◽  
Baojie Li ◽  
...  
Keyword(s):  
Bipolar Cell ◽  
Cell Activation ◽  
Molecular Mechanisms ◽  
Microglial Cell ◽  
Photoreceptor Cell ◽  
Ganglion Cells ◽  
Amacrine Cells ◽  
Mtorc1 Signaling ◽  
Mtorc1 Activation

Age-associated decline in retina function is largely responsible for the irreversible vision deterioration in the elderly population. It is also an important risk factor for the development of degenerative and angiogenic diseases. However, the molecular mechanisms involved in the process of aging in the retina remain largely elusive. This study investigated the role of mTORC1 signaling in aging of the retina. We showed that mTORC1 was activated in old-aged retina, particularly in the ganglion cells. The role of mTORC1 activation was further investigated in Chx10-Cre;Tsc1fx/fx mouse (Tsc1-cKO). Activation of mTORC1 was found in bipolar and some of the ganglion and amacrine cells in the adult Tsc1-cKO retina. Bipolar cell hypertrophy and Müller gliosis were observed in Tsc1-cKO since 6 weeks of age. The abnormal endings of bipolar cell dendritic tips at the outer nuclear layer resembled that of the old-aged mice. Microglial cell activation became evident in 6-week-old Tsc1-cKO. At 5 months, the Tsc1-cKO mice exhibited advanced features of old-aged retina, including the expression of p16Ink4a and p21, expression of SA-β-gal in ganglion cells, decreased photoreceptor cell numbers, decreased electroretinogram responses, increased oxidative stress, microglial cell activation, and increased expression of immune and inflammatory genes. Inhibition of microglial cells by minocycline partially prevented photoreceptor cell loss and restored the electroretinogram responses. Collectively, our study showed that the activation of mTORC1 signaling accelerated aging of the retina by both cell autonomous and nonautonomous mechanisms. Our study also highlighted the role of microglia cells in driving the decline in retina function.

Evidence for a protective role of the CX3CL1/CX3CR1 axis in a model of amyotrophic lateral sclerosis

2019 ◽  
Vol 400 (5) ◽  
pp. 651-661 ◽  
Author(s):  
Chang Liu ◽  
Kun Hong ◽  
Huifang Chen ◽  
Yanping Niu ◽  
Weisong Duan ◽  
...  
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Communication System ◽  
Microglial Activation ◽  
Neuronal Cell ◽  
Cell Loss ◽  
Degradation Pathway ◽  
Neuroprotective Effects ◽  
End Stage ◽  
Lateral Sclerosis

Abstract Aberrant microglial activation and neuroinflammation is a pathological hallmark of amyotrophic lateral sclerosis (ALS). Fractalkine (CX3CL1) is mostly expressed on neuronal cells. The fractalkine receptor (CX3CR1) is predominantly expressed on microglia. Many progressive neuroinflammatory disorders show disruption of the CX3CL1/CX3CR1 communication system. But the exact role of the CX3CL1/CX3CR1 in ALS pathology remains unknown. F1 nontransgenic/CX3CR1+/− females were bred with SOD1G93A/CX3CR1+/− males to produce F2 SOD1G93A/CX3CR1−/−, SOD1G93A/CX3CR1+/+. We analyzed end-stage (ES) SOD1G93A/CX3CR1−/− mice and progression-matched SOD1G93A/CX3CR1+/+ mice. Our study showed that the male SOD1G93A/CX3CR1−/− mice died sooner than male SOD1G93A/CX3CR1+/+ mice. In SOD1G93A/CX3CR1−/− mice demonstrated more neuronal cell loss, more microglial activation and exacerbated SOD1 aggregation at the end-stage of ALS. The NF-κB pathway was activated; the autophagy-lysosome degradation pathway and the autophagosome maturation were impaired. Our results indicated that the absence of CX3CR1/CX3CL1 signaling in the central nervous system (CNS) may worsen neurodegeneration. The CX3CL1/CX3CR1 communication system has anti-inflammatory and neuroprotective effects and plays an important role in maintaining autophagy activity. This effort may lead to new therapeutic strategies for neuroprotection and provide a therapeutic target for ALS patients.

Isolation Process and Bioactive Activity of Bioactive Polysaccharides from Fungal Mycelium

2013 ◽  
Vol 726-731 ◽  
pp. 401-405 ◽  
Author(s):  
Xiang Yu Cao ◽  
Wei Yang ◽  
Jian Li Lui ◽  
Hai Xin Ai
Keyword(s):  
Present Review ◽  
Current Status ◽  
Fungal Mycelium ◽  
Bioactive Substances ◽  
The Past ◽  
Research Areas ◽  
Future Direction ◽  
Available Information ◽  
Intense Debate

Fungus has been valued as one of edible and medicinal resources, and bioactive substances have been identified in many fungus species. In all of them, polysaccharides are the most famous and potent fungus-derived substances with antioxidant, antitumor, immunoregulation and so on. Although the isolation process and bioactive activity of fungal mycelium polysaccharides have been investigated in the past decade, the new bioactive activity and the mechanism of fungal mycelium polysaccharides are not systematic studied. These studies are still in progress and the role of polysaccharides as bioactive activity is especially under intense debate. The purpose of the present review is to summarize the available information of isolation process and bioactive activity, and to reflect the current status of these research areas with a view for future direction.

scholarly journals Neuroinflammation: A Potential Risk for Dementia

2022 ◽  
Vol 23 (2) ◽  
pp. 616
Author(s):  
Md Afroz Ahmad ◽  
Ozaifa Kareem ◽  
Mohammad Khushtar ◽  
Md Akbar ◽  
Md Rafiul Haque ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Cell Activation ◽  
Microglial Cell ◽  
Oxygen Species ◽  
Independent Function ◽  
Published Evidence ◽  
Inflammatory Processes ◽  
The Central Nervous System ◽  
The Brain

Dementia is a neurodegenerative condition that is considered a major factor contributing to cognitive decline that reduces independent function. Pathophysiological pathways are not well defined for neurodegenerative diseases such as dementia; however, published evidence has shown the role of numerous inflammatory processes in the brain contributing toward their pathology. Microglia of the central nervous system (CNS) are the principal components of the brain’s immune defence system and can detect harmful or external pathogens. When stimulated, the cells trigger neuroinflammatory responses by releasing proinflammatory chemokines, cytokines, reactive oxygen species, and nitrogen species in order to preserve the cell’s microenvironment. These proinflammatory markers include cytokines such as IL-1, IL-6, and TNFα chemokines such as CCR3 and CCL2 and CCR5. Microglial cells may produce a prolonged inflammatory response that, in some circumstances, is indicated in the promotion of neurodegenerative diseases. The present review is focused on the involvement of microglial cell activation throughout neurodegenerative conditions and the link between neuroinflammatory processes and dementia.

Neuroprotective effects of nitidine in Parkinson's disease models through inhibiting microglia activation: role of the Jak2–Stat3 pathway

RSC Advances ◽  
2016 ◽  
Vol 6 (75) ◽  
pp. 71328-71337 ◽  
Author(s):  
Bao Wang ◽  
Xing-qin Wang ◽  
Shao-song Yang ◽  
Xi Liu ◽  
Da-yun Feng ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Animal Models ◽  
Microglial Activation ◽  
Microglia Activation ◽  
Disease Models ◽  
Neuroprotective Effects ◽  
Stat3 Pathway ◽  
Behavioural Function

In this work we found that nitidine could significantly suppress microglial activationviathe Jak2–Stat3 pathway and obviously improve behavioural function in Parkinson's disease (PD) animal models, which sheds light on PD treatment.

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