scholarly journals Role of standardized grape polyphenol preparation as a novel treatment to improve synaptic plasticity through attenuation of features of metabolic syndrome in a mouse model

2013 ◽  
Vol 57 (12) ◽  
pp. 2091-2102 ◽  
Author(s):  
Jun Wang ◽  
Cheuk Tang ◽  
Mario G. Ferruzzi ◽  
Bing Gong ◽  
Brian J. Song ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Novel Treatment

scholarly journals Loss of Non-Apoptotic Role of Caspase-3 in the PINK1 Mouse Model of Parkinson’s Disease

2019 ◽  
Vol 20 (14) ◽  
pp. 3407 ◽  
Author(s):  
Paola Imbriani ◽  
Annalisa Tassone ◽  
Maria Meringolo ◽  
Giulia Ponterio ◽  
Graziella Madeo ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Synaptic Plasticity ◽  
Mouse Model ◽  
Caspase 3 ◽  
Cysteine Proteases ◽  
Synaptic Function ◽  
Adult Brain ◽  
Striatal Slices

Caspases are a family of conserved cysteine proteases that play key roles in multiple cellular processes, including programmed cell death and inflammation. Recent evidence shows that caspases are also involved in crucial non-apoptotic functions, such as dendrite development, axon pruning, and synaptic plasticity mechanisms underlying learning and memory processes. The activated form of caspase-3, which is known to trigger widespread damage and degeneration, can also modulate synaptic function in the adult brain. Thus, in the present study, we tested the hypothesis that caspase-3 modulates synaptic plasticity at corticostriatal synapses in the phosphatase and tensin homolog (PTEN) induced kinase 1 (PINK1) mouse model of Parkinson’s disease (PD). Loss of PINK1 has been previously associated with an impairment of corticostriatal long-term depression (LTD), rescued by amphetamine-induced dopamine release. Here, we show that caspase-3 activity, measured after LTD induction, is significantly decreased in the PINK1 knockout model compared with wild-type mice. Accordingly, pretreatment of striatal slices with the caspase-3 activator α-(Trichloromethyl)-4-pyridineethanol (PETCM) rescues a physiological LTD in PINK1 knockout mice. Furthermore, the inhibition of caspase-3 prevents the amphetamine-induced rescue of LTD in the same model. Our data support a hormesis-based double role of caspase-3; when massively activated, it induces apoptosis, while at lower level of activation, it modulates physiological phenomena, like the expression of corticostriatal LTD. Exploring the non-apoptotic activation of caspase-3 may contribute to clarify the mechanisms involved in synaptic failure in PD, as well as in view of new potential pharmacological targets.

scholarly journals Critical role of chemokine (C-C motif) receptor 2 (CCR2) in the KKAy + Apoe −/− mouse model of the metabolic syndrome

Diabetologia ◽  
2011 ◽  
Vol 54 (10) ◽  
pp. 2660-2668 ◽  
Author(s):  
H. G. Martinez ◽  
M. P. Quinones ◽  
F. Jimenez ◽  
C. A. Estrada ◽  
K. Clark ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Mouse Model ◽  
Critical Role ◽  
The Metabolic Syndrome ◽  
Apoe Mouse

scholarly journals Impairment of bidirectional synaptic plasticity in the striatum of a mouse model of DYT1 dystonia: role of endogenous acetylcholine

Brain ◽  
2009 ◽  
Vol 132 (9) ◽  
pp. 2336-2349 ◽  
Author(s):  
Giuseppina Martella ◽  
Annalisa Tassone ◽  
Giuseppe Sciamanna ◽  
Paola Platania ◽  
Dario Cuomo ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Mouse Model ◽  
Dyt1 Dystonia

Extrasynaptic CaMKIIα is involved in the antidepressant effects of ketamine by downregulating GluN2B receptors in an LPS-induced depression model

2020 ◽  
Author(s):  
Xiao-Hui Tang ◽  
Guang-Fen Zhang ◽  
Ning Xu ◽  
Gui-Fang Duan ◽  
Min Jia ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Mouse Model ◽  
Cellular Mechanism ◽  
Antidepressant Effect ◽  
Immunoprecipitation Assay ◽  
Antidepressant Effects ◽  
High Level ◽  
Induced Changes ◽  
The Relationship

Abstract Background A subanesthetic dose of ketamine provides rapid and effective antidepressant effects, but the molecular mechanism of this treatment remains elusive. Methods In this study, we investigated the role of CaMKIIα in the antidepressant effects of ketamine using an LPS-induced mouse model of depression, explored the different changes of CaMKIIα in the synaptic and extrasynaptic regions of the hippocampus, and clarified the relationship between CaMKIIα and GluN2B from extrasynaptic perspective. Results Ketamine (10 mg/kg, i.p.) administration attenuated the LPS-induced increase in extrasynaptic CaMKIIα activity (p-CaMKIIα) and extrasynaptic GluN2B localization and phosphorylation and that ketamine exerted antidepressant effects. Immunoprecipitation assay revealed that in the extrasynaptic region of the hippocampus, p-CaMKIIα bound to GluN2B, and ketamine administration attenuated the enhanced interaction between p-CaMKIIα and GluN2B induced by LPS. KN93, a CaMKIIα inhibitor, could also reverse the high level of extrasynaptic p-CaMKIIα, reduce hippocampal extrasynaptic GluN2B localization and phosphorylation, and exert antidepressant effects. Additional changes downstream of the ketamine-induced changes in extrasynaptic GluN2B included rescuing the downregulated expression of p-CREB, BDNF, and GluR1 and reversing the impaired induction of LTP in the hippocampus induced by LPS. Conclusion These results indicate that extrasynaptic CaMKIIα plays a key role in the cellular mechanism of ketamine's antidepressant effect and is related to the down-regulation of extrasynaptic GluN2B localization and phosphorylation and further affects synaptic plasticity.

scholarly journals Neuroimmune Mechanisms as Novel Treatment Targets for Substance Use Disorders and Associated Comorbidities

2021 ◽  
Vol 15 ◽  
Author(s):  
Mark D. Namba ◽  
Jonna M. Leyrer-Jackson ◽  
Erin K. Nagy ◽  
M. Foster Olive ◽  
Janet L. Neisewander
Keyword(s):  
Substance Abuse ◽  
Substance Use ◽  
Nervous System ◽  
Synaptic Plasticity ◽  
Substance Use Disorders ◽  
Immune Signaling ◽  
Treatment Targets ◽  
Novel Treatment ◽  
The Brain

Recent studies examining the neurobiology of substance abuse have revealed a significant role of neuroimmune signaling as a mechanism through which drugs of abuse induce aberrant changes in synaptic plasticity and contribute to substance abuse-related behaviors. Immune signaling within the brain and the periphery critically regulates homeostasis of the nervous system. Perturbations in immune signaling can induce neuroinflammation or immunosuppression, which dysregulate nervous system function including neural processes associated with substance use disorders (SUDs). In this review, we discuss the literature that demonstrates a role of neuroimmune signaling in regulating learning, memory, and synaptic plasticity, emphasizing specific cytokine signaling within the central nervous system. We then highlight recent preclinical studies, within the last 5 years when possible, that have identified immune mechanisms within the brain and the periphery associated with addiction-related behaviors. Findings thus far underscore the need for future investigations into the clinical potential of immunopharmacology as a novel approach toward treating SUDs. Considering the high prevalence rate of comorbidities among those with SUDs, we also discuss neuroimmune mechanisms of common comorbidities associated with SUDs and highlight potentially novel treatment targets for these comorbid conditions. We argue that immunopharmacology represents a novel frontier in the development of new pharmacotherapies that promote long-term abstinence from drug use and minimize the detrimental impact of SUD comorbidities on patient health and treatment outcomes.

The role of tachykinin 1 in a mouse model of trait anxiety

2007 ◽  
Vol 40 (05) ◽  
Author(s):  
L Czibere ◽  
LA Baur-Jaronowski ◽  
P Weber ◽  
B Pütz ◽  
M Panhuysen ◽  
...  
Keyword(s):  
Mouse Model ◽  
Trait Anxiety

Glucocorticoid-induced metabolic syndrome: establishing the role of AgRP

2018 ◽  
Author(s):  
Charlotte Sefton ◽  
Erika Harno ◽  
Alison Davies ◽  
Tiffany-Jayne Allen ◽  
Jonathan R Wray ◽  
...  
Keyword(s):  
Metabolic Syndrome
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