A dual approach to self-stimulation and locomotor trace affected by chronic methamphetamine treatment for an animal model of schizophrenia

1993 ◽  
Vol 71 (5-6) ◽  
pp. 321-325 ◽  
Author(s):  
Morikuni Takigawa ◽  
Hiroshi Maeda ◽  
Kenichi Ueyama ◽  
Hidefumi Tominaga ◽  
Kei Matsumoto

The effect of long-term methamphetamine (MAP) treatment on intracranial self-stimulation of the lateral hypotholamus and locomotor traces was assessed. An attempt was made to provide a useful animal model for understanding anhedonia, stereotypy, and reoccurrence of liability, which are analogous to symptoms of schizophrenia. The frequency of intracranial self-stimulation (ICSS) as used as a measure of the animals' "hedonic–anhedonic" state. Following long-term MAP treatment (3 mg/kg), rats gradually showed stereotyped behavior, and became inactive and unresponsive to ICSS. These behavioral changes and decreased ICSS lasted several weeks after cessation of chronic MAP treatment and seemed to suggest post-MAP chronic psychosis and (or) anhedonia, two of the negative symptoms of schizophrenia. The traces of rat behavior affected by chronic MAP treatment were classified into three types, peripheral, mixed, and fixed, occurring in a dose-dependent manner. Reverse tolerance, similar to the reoccurrence of schizophrenic symptoms, was observed as a fixed stereotypy associated with loss of ICSS. These abnormal phenomena were suppressed by pretreatment with haloperidol. In the present study, the combination of ICSS and locomotor trace affected by chronic MAP treatment was proposed as an animal model of schizophrenia and as a useful technique for gauging the effect of neuroleptics.Key words: self-stimulation, anhedonia, stereotypy, reverse tolerance, animal disease model, schizophrenia, methamphetamine.

2001 ◽  
Vol 21 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Gutemberg G. Alves ◽  
Luis Maurício T. R. Lima ◽  
Maely P. Fávero-Retto ◽  
Adriana P. Lemos ◽  
Carlos E. Peres-Sampaio ◽  
...  

The plasma membrane (Ca2++Mg2+)ATPase hydrolyzes pseudo-substrates such as p-nitrophenylphosphate. Except when calmodulin is present, Ca2+ ions inhibit the p-nitrophenylphosphatase activity. In this report it is shown that, in the presence of glycerol, Ca2+ strongly stimulates phosphatase activity in a dose-dependent manner. The glycerol- and Ca2+-induced increase in activity is correlated with modifications in the spectral center of mass (average emission wavenumber) of the intrinsic fluorescence of the enzyme. It is concluded that the synergistic effect of glycerol and Ca2+ is related to opposite long-term hydration effects on the substrate binding domain and the Ca2+ binding domain.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Yun Feng ◽  
Linlin Wang ◽  
Xiaoying Ma ◽  
Xiaotong Yang ◽  
Ocholi Don ◽  
...  

Abstract Background ALI/ARDS is the major cause of acute respiratory failure in critically ill patients. As human chorionic villi-derived MSCs (hCMSCs) could attenuate ALI in the airway injury model, and liraglutide, glucagon-like peptide 1 (GLP-1) agonist, possesses anti-inflammatory and proliferation promotion functions, we proposed to probe the potential combinatory effect of hCMSCs and liraglutide on ALI. Methods We examined the time- and dose-dependent manner of GLP-1R, SPC, Ang-1, and FGF-10 with LPS via western blot and qRT-PCR. Western blot and chromatin immunoprecipitation assay detected the effects of liraglutide on GLP-1R, SPC, Ang-1, and FGF-10 through PKAc/β-catenin pathway and cAMP pathway. In the ALI animal model, we detected the effects of MSC and liraglutide combination on ALI symptoms by H&E staining, western blot, ELISA assays, calculating wet-to-dry ratio of the lung tissue, and counting neutrophils, leukocytes, and macrophages in mouse bronchoalveolar lavage fluid (BALF). Results The data demonstrated that LPS reduced hCMSC proliferation and GLP-1R, SPC, Ang-1, and FGF-10 levels in a dose- and time-dependent manner. Liraglutide significantly dampened the reduction of GLP-1R, SPC, Ang-1, and FGF-10 and reversed the effect of LPS on hCMSCs, which could be regulated by GLP-1R and its downstream cAMP/PKAc/β-catenin-TCF4 signaling. Combination of hCMSCs with liraglutide showed more therapeutic efficacy than liraglutide alone in reducing LPS-induced ALI in the animal model. Conclusions These results reveal that the combination of hCMSCs and liraglutide might be an effective strategy for ALI treatment.


Author(s):  
ELAHE KARIMI ◽  
SHAHRYAR ABBASI ◽  
ALI AIDY ◽  
HORI GHANEIALVAR ◽  
SHAHRAM MOHAMMADPOUR ◽  
...  

Objective: The aim of this study was to evaluate the effect of thymol and thymol nano polymer on the blood biochemical parameters and anti-diabetic activity in Streptozotocin (STZ)-induced diabetic rats. Methods: The synthesized nano polymer (NP) was characterized by using different spectroscopy methods, such as IR, HNMR and CNMR. Loading and releasing of thymol were investigated by HPLC. Eleven groups of the Streptozotocin-induced diabetic and normal rats (overall 110 males) were tested through various biochemical factors such as: serum glucose, insulin, liver function-related enzymes including ALT, AST, ALP and bilirubin by ELISA kit methods. Results: It has shown that thymol nano polymer is desirable for transferring drug. The amount of thymol loaded on NP estimated at 43±2.5 %. Then, 65% of the loaded drug was released. LD50 for thymol and thymol nano polymer were 435 and 583 mg/kg, respectively. thymol nano polymer at doses of 30, 60 and 90 mg/kg, in a dose-dependent manner, reduced blood glucose, increased insulin levels, and controlled liver enzymes ALT, AST, ALP and bilirubin in the STZ-induced diabetic rats. Conclusion: The use of thymol nano polymer appears to be a new aspect concerning to protect diabetes-induced damage in the animal model.


2015 ◽  
Vol 9s1 ◽  
pp. JEN.S27733 ◽  
Author(s):  
Nobue Kitanaka ◽  
Junichi Kitanaka ◽  
F. Scott Hall ◽  
Masaru Kayama ◽  
Hironobu Sugimori ◽  
...  

Aripiprazole is a third-generation atypical antipsychotic and a dopamine D2 receptor partial agonist. In the present study, we investigated whether a single administration of aripiprazole to mice, either as a pretreatment or as a posttreatment, would affect stereotypy induced by methamphetamine (METH). Pretreatment of male ICR mice with aripiprazole (1 or 10 mg/kg, i.p.) attenuated the incidence of METH-induced stereotypical behavior in a dose-dependent manner. Pretreatment of mice with 1 mg/kg aripiprazole produced an increase in the locomotor activity in mice treated with METH compared with mice treated with vehicle plus METH and with 10 mg/kg aripiprazole plus METH. This increase in locomotion is indicative of a rightward shift in the dose-response curve for METH, consistent with a shift in the type of stereotypical behavior observed from biting to sniffing. Aripiprazole posttreatment, after METH-induced stereotypical behavior, was fully expressed and also significantly attenuated overall stereotypy in an aripiprazole dose-dependent manner. These data suggest that the antagonism of METH effects by aripiprazole should be investigated as a potential treatment for acute METH overdose.


1983 ◽  
Vol 61 (12) ◽  
pp. 2698-2702 ◽  
Author(s):  
Steven R. Scadding

The objective of this experiment was to determine the effect of retinoic acid on the process of limb regeneration in the African clawed frog, Xenopus laevis. Limbs were bilaterally amputated through the radio-ulna and then treated for 15 days with retinoic acid in the aquarium water, at 3, 15, or 75 IU/mL. The retinoic acid inhibited limb regeneration in a dose-dependent manner, reduced the length of the regenerates, and produced irregularities in the morphogenesis of the cartilage rod in the regenerate. The regenerated limbs were removed after 150 days by amputation through the humerus, and the limbs were again allowed to regenerate. In the retinoic acid treated animals, despite the fact that retinoic acid treatment had been discontinued over 4 months previously, limb regeneration was still inhibited. These results suggest that retinoic acid has a long-term effect on the treated animals.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Zheng-Fei Yan ◽  
Nai-Xu Liu ◽  
Xin-Xin Mao ◽  
Yu Li ◽  
Chang-Tian Li

Flammulina velutipesmycorrhizae have increasingly been produced with increasing ofF. velutipesproduction. A mouse model was thus used to examine potential effect ofF. velutipesmycorrhizae on the immune function. Fifty female Wistar mice (5-weeks-old) weighed 15–20 g were randomly allocated into five groups. Polysaccharide ofF. velutipesmycorrhizae were treated with mice and mice spleen lymphocytes. The levels of CD3+, CD4+, and CD8+T lymphocyte, interleukin-2 (IL-2), and tumor necrosis factor-a (TNF-α) were determined. The results showed that the proportions of CD3+, and CD4+T lymphocyte, the ratio of CD4+/CD8+, and the levels of IL-2 and TNF-a were significantly increased in polysaccharide ofF. velutipesmycorrhizae, while the proportion of CD8+T lymphocyte was decreased in polysaccharide ofF. velutipesmycorrhizae-dose dependent manner. Our findings indicated that a long term exposure of polysaccharide ofF. velutipesmycorrhizae could activate the T lymphocyte immune function. Polysaccharide ofF. velutipesmycorrhizae was expected to develop into the immune health products.


2013 ◽  
Vol 781-784 ◽  
pp. 643-646
Author(s):  
Xiao Lin ◽  
Li Yu

In this study, we aim to investigate the effect of curcumin on the expression of a-synuclein in the APPswe/PS1dE9 double transgenic mice. APPswe/PS1dE9 double transgenic mice were used as AD (Alzheimer's disease) model and fed with different concentrations of curcumin every day for 6 months, then immunohistochemistry method were used to detect the expression of a-synuclein in hippocampus of mice. The expression of a-syn in hippocampal neuron was decreased significantly after treated with 0.16g/kg to 1.0g/kg curcumin, the change was apparent in dose-dependent manner (P<0.05). a-synuclein pay an important role in the genesis and development of Alzheimer's disease and decreased level of a-synuclein might contribute to the neuroprotective effect of Curcumin, which may become a new target for the prevention and treatment of Alzheimer's disease.


Blood ◽  
1994 ◽  
Vol 83 (4) ◽  
pp. 911-915 ◽  
Author(s):  
RT Jr Means ◽  
SB Krantz ◽  
J Luna ◽  
SA Marsters ◽  
A Ashkenazi

It has been previously reported that inhibition of human erythroid colony-forming units (CFU-E) in vitro by interleukin-1 (IL-1) is an indirect effect, occurring through the production of interferon gamma (IFN gamma). IFN gamma, in turn, inhibits CFU-E colony formation directly, and its inhibitory effect can be overcome by exposure to high concentrations of erythropoietin (EPO). To develop an in vitro animal model for investigating inhibition of erythropoiesis by IFN gamma, the effects of recombinant murine (rm) IFN gamma on highly purified CFU-E from the spleens of mice infected with the anemia strain of the Friend virus (FVA) were studied. rmIFN gamma inhibited CFU-E colony formation in a dose-dependent manner. This inhibition occurred with large (> or = 8 cell) colonies only; smaller colonies were not affected. The inhibitory effect was corrected to 72% of control by high EPO concentrations of 64 U/mL. Murine CFU-E were then cultured with rmIFN gamma in the presence of a soluble murine IFN gamma receptor fused to the hinge and Fc domains of the human IgG1 heavy chain (mIFN gamma R-IgG). Inhibition of CFU-E colony formation by rmIFN gamma (100 U/mL) was corrected by mIFN gamma R-IgG in a dose-dependent manner, with an approximate IC50 of 0.05 nmol/L, and complete or near complete correction at 0.5 nmol/L. Similarly, a human IFN gamma R-IgG greatly reduced the inhibitory effect of recombinant human IFN gamma on human CFU-E. These experiments provide an in vitro animal model for studying the inhibitory effects of IFN gamma on erythropoiesis and indicate that IFN gamma R-IgG may be a useful agent for reducing the toxicity of IFN gamma in vivo.


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