scholarly journals EXCLUSIVE PREFERENCE DEVELOPS LESS READILY ON CONCURRENT RATIO SCHEDULES WITH WHEEL-RUNNING THAN WITH SUCROSE REINFORCEMENT

2010 ◽  
Vol 94 (2) ◽  
pp. 135-158 ◽  
Author(s):  
Terry W. Belke
Keyword(s):  
Wheel Running ◽  
Sucrose Reinforcement

scholarly journals Reinforcement of a reinforcing behaviour: Effect of sucrose concentration on wheel-running rate

2017 ◽  
Author(s):  
Terry Belke ◽  
W. David Pierce ◽  
Alexandra C. Fisher ◽  
Mandy R. LeCocq
Keyword(s):  
Operant Behavior ◽  
Wheel Running ◽  
Sucrose Solution ◽  
Sucrose Concentration ◽  
Deprivation Level ◽  
Automatic Reinforcement ◽  
Sucrose Reinforcement ◽  
Lever Pressing ◽  
Long Evans ◽  
Extrinsic Reinforcement

Wheel running, unlike typical operant behavior, generates its own automatic reinforcement that alters the control exerted by extrinsic reinforcement on wheel running. The current study investigated the implications of the automatic reinforcement of wheel running by arranging different sucrose concentrations as extrinsic reinforcement for operant wheel running in ad-lib fed and food-deprived rats. Eleven female Long Evans rats ran on fixed revolution 30 schedules that delivered a drop of sucrose solution as reinforcement. Sucrose concentration varied across values of 0%, 2.5%, 5%, 10%, and 15% sucrose (w/v). Results showed that under ad-lib feeding, only the highest concentrations increased operant wheel-running rate. By contrast, under deprivation, all concentrations of sucrose increased the rate of wheel running. Despite the differences in sucrose-reinforced operant wheel-running rates by deprivation level (ad lib vs. deprived), wheel-running rates did not differ at the highest concentrations. Prior research on operant lever pressing, a response generating low (or no) automatic reinforcement, has shown considerably higher lever-pressing rates as a function of increasing amounts of sucrose reinforcement when rats are food deprived. Together, these previous observations and the current study suggest that automatic reinforcement generated by an operant decreases the control exerted by extrinsic reinforcement. Additionally, the regulation by extrinsic reinforcement on automatically reinforcing behavior depends on the organism’s motivation or deprivation level (ad lib vs. deprived).

scholarly journals Voluntary exercise and cardiac remodeling in a myocardial infarction model

Open Medicine ◽  
2020 ◽  
Vol 15 (1) ◽  
pp. 545-555
Author(s):  
Hamad Al Shahi ◽  
Tomoyasu Kadoguchi ◽  
Kazunori Shimada ◽  
Kosuke Fukao ◽  
Satoshi Matsushita ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Cardiac Remodeling ◽  
Skeletal Muscles ◽  
Wheel Running ◽  
Voluntary Exercise ◽  
Fibroblast Growth Factor 21 ◽  
Expression Levels ◽  
Factor Α ◽  
Necrosis Factor

AbstractWe investigated the effects of voluntary exercise after myocardial infarction (MI) on cardiac function, remodeling, and inflammation. Male C57BL/6J mice were divided into the following four groups: sedentary + sham (Sed-Sh), sedentary + MI (Sed-MI), exercise + sham (Ex-Sh), and exercise + MI (Ex-MI). MI induction was performed by ligation of the left coronary artery. Exercise consisting of voluntary wheel running started after the operation and continued for 4 weeks. The Ex-MI mice had significantly increased cardiac function compared with the Sed-MI mice. The Ex-MI mice showed significantly reduced expression levels of tumor necrosis factor-α, interleukin (IL)-1β, IL-6, and IL-10 in the infarcted area of the left ventricle compared with the Sed-MI mice. In the Ex-MI mice, the expression levels of fibrosis-related genes including collagen I and III were decreased compared to the Sed-MI mice, and the expression levels of IL-1β, IL-6, follistatin-like 1, fibroblast growth factor 21, and mitochondrial function-related genes were significantly elevated in skeletal muscle compared with the Sed mice. The plasma levels of IL-6 were also significantly elevated in the Ex-MI group compared with the Sed-MI groups. These findings suggest that voluntary exercise after MI may improve in cardiac remodeling associated with anti-inflammatory effects in the myocardium and myokine production in the skeletal muscles.

scholarly journals General Anaesthesia Shifts the Murine Circadian Clock in a Time-Dependant Fashion

2021 ◽  
Vol 3 (1) ◽  
pp. 87-97
Author(s):  
Nicola M. Ludin ◽  
Alma Orts-Sebastian ◽  
James F. Cheeseman ◽  
Janelle Chong ◽  
Alan F. Merry ◽  
...  
Keyword(s):  
Circadian Clock ◽  
General Anaesthesia ◽  
Wheel Running ◽  
Phase Shifts ◽  
Time Dependent ◽  
Suprachiasmatic Nuclei ◽  
Response Curves ◽  
Inhalational Anaesthetic ◽  
Locomotor Rhythms ◽  
Time Dependent Analysis

Following general anaesthesia (GA), patients frequently experience sleep disruption and fatigue, which has been hypothesized to result at least in part by GA affecting the circadian clock. Here, we provide the first comprehensive time-dependent analysis of the effects of the commonly administered inhalational anaesthetic, isoflurane, on the murine circadian clock, by analysing its effects on (a) behavioural locomotor rhythms and (b) PER2::LUC expression in the suprachiasmatic nuclei (SCN) of the mouse brain. Behavioural phase shifts elicited by exposure of mice (n = 80) to six hours of GA (2% isoflurane) were determined by recording wheel-running rhythms in constant conditions (DD). Phase shifts in PER2::LUC expression were determined by recording bioluminescence in organotypic SCN slices (n = 38) prior to and following GA exposure (2% isoflurane). Full phase response curves for the effects of GA on behaviour and PER2::LUC rhythms were constructed, which show that the effects of GA are highly time-dependent. Shifts in SCN PER2 expression were much larger than those of behaviour (c. 0.7 h behaviour vs. 7.5 h PER2::LUC). We discuss the implications of this work for understanding how GA affects the clock, and how it may inform the development of chronotherapeutic strategies to reduce GA-induced phase-shifting in patients.

Chronic enhancement of neuromuscular activity increases acetylcholinesterase gene expression in skeletal muscle

1995 ◽  
Vol 269 (4) ◽  
pp. C856-C862 ◽  
Author(s):  
H. Sveistrup ◽  
R. Y. Chan ◽  
B. J. Jasmin
Keyword(s):  
Ache Activity ◽  
Wheel Running ◽  
Compensatory Hypertrophy ◽  
Molecular Forms ◽  
Plantaris Muscle ◽  
Neuromuscular Activation ◽  
Neuromuscular Activity ◽  
Acetylcholinesterase Gene ◽  
Voluntary Wheel

We determined levels of mRNA encoding acetylcholinesterase (AChE) in muscles of rats subjected to chronic enhancement of neuromuscular activation. After 8 wk of voluntary wheel running, extensor digitorum longus (EDL) muscles displayed a 72% increase in total AChE activity as a result of a selective threefold increase in the G4 content. Soleus muscles, on the other hand, exhibited a 30% decrease in A12 while displaying a small (33%) increase in total AChE activity. These enzymatic adaptations were paralleled by increases in the levels of AChE mRNAs in both EDL (32%; P < 0.03) and soleus (42%; P < 0.02) muscles. In addition, compensatory hypertrophy of the plantaris muscle increased total AChE activity by 75%. This change was reflected by an elevation in all AChE molecular forms with A12 (89%) and A8 (179%) showing the most prominent increases. Similar to exercise-trained muscles, hypertrophied plantaris muscles displayed an increase in AChE transcripts (25%; P < 0.04). These results indicate that increases in neuromuscular activity modulate expression of the AChE gene in vivo and suggest the involvement of pretranslational regulatory mechanisms in the adaptive response of AChE to enhanced neuromuscular activation.

scholarly journals Paternal High Fat Diet and Exercise Differentially Regulate Placental Development and Inflammation in a Sex-Specific Manner in C57BL6/J Mice (P19-003-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Kate Larson ◽  
Amy Bundy ◽  
Travis Alvine ◽  
James Roemmich
Keyword(s):  
Skeletal Muscle ◽  
Agricultural Research ◽  
Wheel Running ◽  
Fetal Weight ◽  
High Fat ◽  
Placental Development ◽  
Funding Sources ◽  
Service Project ◽  
Diet And Exercise ◽  
Placental Inflammation

Abstract Objectives We have shown that increases in T2D risk in male offspring when the father consumes a high-fat (HF) diet can be normalized when the father also exercises during preconception, and that this protection may occur by epigenetic increases in insulin signaling within offspring skeletal muscle. In our current study, we investigated to determine how paternal HF diet and exercise conditions alter sperm miRNA, fetal weight and placental inflammation. Methods Three-week old male C57BL/6 mice were fed a normal-fat (NF) diet (16% fat) or a HF diet (45% fat) and assigned to either voluntary wheel running exercise or cage activity for 3 months prior to mating with NF diet fed dams. Sperm samples were collected to determine changes in miRNA that may account for the enhanced offspring skeletal muscle responses that helped normalize paternal HF-induced glucose intolerance. Placentae were collected to determine whether changes in sperm miRNA expression differed by amount of placental inflammation. Results Sperm expression of miRNA 193b increased with paternal HF and exercise. In F1 males, placental and fetal weight decreased with HF diet while, in F1 female, paternal HF and exercise had no effect on placental and fetal weights. Paternal HF diet decreased placental IL-6 and TNF-alpha mRNA expression in F1 females, while no effects were observed in F1 male placenta. Conclusions Taken together these data suggest that paternal HF diet has a greater impact on placental development of male fetuses while paternal exercise has greater impact on placental inflammation of female fetuses. For both female and male fetuses, these paternal influences are mediated via sperm miRNA 193b. miR-193b is involved in regulation of the cell cycle and adipogenesis but may have additional functions. Thus, the exact role of sperm miRNA 193b in sex-specific epigenetic transmission of paternal HF diet and exercise on placental and fetal development needs further evaluation. Funding Sources USDA Agricultural Research Service Project #3062-51000-052-00D.

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