Functional Status of Somatodendritic Serotonin 1A Autoreceptor after Long-Term Treatment with Fluoxetine in a Mouse Model of Anxiety/Depression Based on Repeated Corticosterone Administration

2011 ◽  
Vol 81 (2) ◽  
pp. 106-112 ◽  
Author(s):  
Quentin Rainer ◽  
Hai T. Nguyen ◽  
Gaël Quesseveur ◽  
Alain M. Gardier ◽  
Denis J. David ◽  
...  
Keyword(s):  
Mouse Model ◽  
Functional Status ◽  
Term Treatment ◽  
Long Term Treatment ◽  
Anxiety Depression

scholarly journals Neuropharmacology of the Neuropsychiatric Symptoms of Dementia and Role of Pain: Essential Oil of Bergamot as a Novel Therapeutic Approach

2019 ◽  
Vol 20 (13) ◽  
pp. 3327 ◽  
Author(s):  
Damiana Scuteri ◽  
Laura Rombolà ◽  
Luigi Antonio Morrone ◽  
Giacinto Bagetta ◽  
Shinobu Sakurada ◽  
...  
Keyword(s):  
Essential Oil ◽  
Psychological Symptoms ◽  
Neuropsychiatric Symptoms ◽  
Term Treatment ◽  
Long Term Treatment ◽  
Anxiety Depression ◽  
Cognitive Disturbance

Aging of the population makes of dementia a challenge for health systems worldwide. The cognitive disturbance is a serious but not the only issue in dementia; behavioral and psychological syndromes known as neuropsychiatric symptoms of dementia remarkably reduce the quality of life. The cluster of symptoms includes anxiety, depression, wandering, delusions, hallucinations, misidentifications, agitation and aggression. The pathophysiology of these symptoms implicates all the neurotransmitter systems, with a pivotal role for the glutamatergic neurotransmission. Imbalanced glutamatergic and GABAergic neurotransmissions, over-activation of the extrasynaptic N-methyl-D-aspartate (NMDA) receptors and alterations of the latter have been linked to the development of neuropsychiatric symptoms experienced by almost the entire demented population. Drugs with efficacy and safety for prevention or long term treatment of these disorders are not available yet. Aromatherapy provides the best evidence for positive outcomes in the control of agitation, the most resistant symptom. Demented patients often cannot verbalize pain, resulting in unrelieved symptoms and contributing to agitation. Bergamot essential oil provides extensive preclinical evidence of analgesic properties. Incidentally, the essential oil of bergamot induces anxyolitic-like effects devoid of sedation, typical of benzodiazepines, with a noteworthy advantage for demented patients. These data, together with the reported safety profile, form the rational basis for bergamot as a neurotherapeutic to be trialed for the control of behavioral and psychological symptoms of dementia.

P.11.3 Long term treatment with naproxcinod significantly improves skeletal and cardiac function in mdx mouse model of dystrophy

2013 ◽  
Vol 23 (9-10) ◽  
pp. 799
Author(s):  
K. Nagaraju ◽  
K. Uaesoontrachoon ◽  
J. Quinn ◽  
K. Tatem ◽  
B. Creeden ◽  
...  
Keyword(s):  
Mouse Model ◽  
Cardiac Function ◽  
Term Treatment ◽  
Mdx Mouse ◽  
Long Term Treatment

scholarly journals Comparison of folate-conjugated rapamycin versus unconjugated rapamycin in an orthologous mouse model of polycystic kidney disease

2018 ◽  
Vol 315 (2) ◽  
pp. F395-F405 ◽  
Author(s):  
Kevin R. Kipp ◽  
Samantha L. Kruger ◽  
Margaret F. Schimmel ◽  
Nikki Parker ◽  
Jonathan M. Shillingford ◽  
...  
Keyword(s):  
Mouse Model ◽  
Small Molecule ◽  
Drug Targets ◽  
Renal Cyst ◽  
Term Treatment ◽  
Rodent Models ◽  
Polycystic Kidney ◽  
Long Term Treatment ◽  
Cyst Growth

Autosomal-dominant polycystic kidney disease (ADPKD) is a very common genetic disease leading to renal failure. Numerous aberrantly regulated signaling pathways have been identified as promising molecular drug targets for ADPKD therapy. In rodent models, many small-molecule drugs against such targets have proven effective in reducing renal cyst growth. For example, mammalian target of rapamycin (mTOR) inhibition with rapamycin greatly ameliorates renal cystic disease in several rodent models. However, clinical trials with mTOR inhibitors were disappointing largely due to the intolerable extrarenal side effects during long-term treatment with these drugs. Most other potential drug targets in ADPKD are also widely expressed in extrarenal tissues, which makes it likely that untargeted therapies with small-molecule inhibitors against such targets will lead to systemic adverse effects during the necessary long-term treatment of years and decades in ADPKD patients. To overcome this problem, we previously demonstrated that folate-conjugated rapamycin (FC-rapa) targets polycystic kidneys due to the high expression of the folate receptor (FRα) and that treatment of a nonortholgous PKD mouse model leads to inhibition of renal cyst growth. Here we show, in a head-to-head comparison with unconjugated rapamycin, that FCrapa inhibits renal cyst growth, mTOR activation, cell cycling, and fibrosis in an orthologous Pkd1 mouse model. Both unconjugated rapamycin and FC-rapa are similarly effective on polycystic kidneys in this model. However, FC-rapa lacks the extrarenal effects of unconjugated rapamycin, in particular immunosuppressive effects. We conclude that folate-conjugation is a promising avenue for increasing the tissue specificity of small-molecule compounds to facilitate very long-term treatment in ADPKD.

Long-term treatment with EGFR inhibitor erlotinib attenuates renal inflammatory cytokines but not nephropathy in Alport syndrome mouse model

2017 ◽  
Vol 21 (6) ◽  
pp. 952-960 ◽  
Author(s):  
Kohei Omachi ◽  
Rui Miyakita ◽  
Ryosuke Fukuda ◽  
Yukari Kai ◽  
Mary Ann Suico ◽  
...  
Keyword(s):  
Mouse Model ◽  
Inflammatory Cytokines ◽  
Alport Syndrome ◽  
Term Treatment ◽  
Egfr Inhibitor ◽  
Long Term Treatment

scholarly journals YDJC Induces Epithelial-Mesenchymal Transition via Escaping from Interaction with CDC16 through Ubiquitination of PP2A

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Eun Ji Kim ◽  
Mi Kyung Park ◽  
Gyeoung-Jin Kang ◽  
Hyun Jung Byun ◽  
Hyun Ji Kim ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Mouse Model ◽  
Cancer Progression ◽  
Epithelial Mesenchymal Transition ◽  
Term Treatment ◽  
Orthotopic Mouse Model ◽  
Mesenchymal Transition ◽  
Long Term Treatment ◽  
Phosphatase 2A

Lung cancer is the number 1 cause of cancer-related casualties in the world. Appropriate diagnostic markers and novel targets for lung cancer are needed. Chitooligosaccharide deacetylase homolog (YDJC) catalyzes the deacetylation of acetylated carbohydrates; however, the role of YDJC in lung cancer progression has yet to be studied. A549 lung cancer orthotopic mouse model was used for mice experiments. We found that YDJC overexpression contributes to lung cancer progression in an orthotopic mouse model. Long-term treatment (48 h) induces YDJC expression in sphingosylphosphorylcholine (SPC)-induced epithelial-mesenchymal transition (EMT). Gene silencing of YDJC (siYDJC) reduced N-cadherin expression and increased E-cadherin expression in SPC-induced EMT. Overexpression of YDJC reverses them but overexpression of the deacetylase deficient mutant YDJCD13A could not. Interestingly, overexpression of CDC16, a YDJC binding partner, suppressed EMT. ERK2 is activated in siCDC16-induced EMT. YDJC overexpression reduces expression of protein phosphatase 2A (PP2A), whereas CDC16 overexpression induces PP2A expression. YDJC overexpression induced ubiquitination of PP2A but YDJCD13A could not. CDC16 overexpression increased the ubiquitination of YDJC. These results suggest that YDJC contributes to the progression of lung cancer via enhancing EMT by inducing the ubiquitination of PP2A. Therefore, YDJC might be a new target for antitumor therapy against lung cancer.

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