Millipore Sigma Vibrant Logo
 

ALC-0315


195 Results Gelişmiş Arama  
Showing
Products (0)
Dokümanlar (194)
Site Content (1)

Sonuçlarınızı Daraltın Use the filters below to refine your search

Aradığınızı Bulamadınız mı?
Müşteri Hizmetleri ile
İletişime Geçin

 
MilliporeSigma Documents

Doküman ararken yardıma ihtiyacınız var mı?
  • Analiz sertifikaları, Kalite Sertifikaları veya Güvenlik Bilgi Formlarını aramak için Doküman Arayıcı’yı kullanmayı deneyin.
     
  • Kullanım Kılavuzlarına erişmek için yardıma ihtiyacınız olur ise Müşteri Hizmetleri ile iletişime geçebilirsiniz.

  • Exercise-induced pain requires NMDA receptor activation in the medullary raphe nuclei. 21795998

    Pain in response to physical activity is common in people with chronic musculoskeletal pain and is likely a barrier to regular exercise, which would lead to a sedentary lifestyle. We recently developed a model of exercise-induced pain that is associated with increased activation of neurons in the medullary raphe nuclei, i.e., the nucleus raphe obscurus (NRO) and nucleus raphe pallidus (NRP). Because the NRO and NRP not only modulate motor output but also respond to noxious stimuli, we hypothesized that the NRO and NRP were key nuclei in the interaction between pain and exercise. We tested whether exercise enhances hyperalgesia through activation of N-methyl D-aspartate (NMDA) receptors in the NRO/NRP.Muscle insult was induced by two injections of pH 5.0 saline 5 d apart into one gastrocnemius muscle. We initially tested whether hyperalgesia developed in mice injected with acidic saline (pH 5.0) into the gastrocnemius muscle immediately after a 30-min or 2-h exercise task or 2 h after a 2-h exercise task. Next, we tested whether blockade of NMDA receptors in the NRO/NRP during the exercise task prevented the development of exercise-induced hyperalgesia. Finally, we evaluated changes in phosphorylation of the NR1 subunit of the NMDA receptor (pNR1) after the exercise task at times in which muscle insult was given in behavioral experiments, i.e., immediately after a 30-min or 2-h exercise task or 2 h after the 2-h exercise task.All exercise conditions enhanced nociception (hyperalgesia) after combining with two injections of pH 5.0 saline. Microinjection of AP5 (1.0-0.1 nmol; 2-amino-5-phophonopenanoate) dose-dependently prevented the development of exercise-induced hyperalgesia. All exercise conditions increased pNR1 in the NRO and NRP.Thus, exercise-induced pain in sedentary mice is associated with increased phosphorylation and activation of NMDA receptors in the NRO/NRP, suggesting that changes in central excitability mediate an interaction between unaccustomed exercise and pain.
    Document Type:
    Reference
    Product Catalog Number:
    ABN99
    Product Catalog Name:
    Anti-phospho NR1 (Ser897) Antibody

  • Changes in calpain activity, muscle structure, and function after eccentric exercise. 20010126

    PURPOSE: The aim of this study was to investigate changes in muscle function, muscle structure, and calpain activity after high-force eccentric exercise. METHODS: Eleven healthy males performed 300 maximal voluntary eccentric actions with knee extensors in one leg. Maximal force-generating capacity was measured before exercise and regularly during the next 7 d. Biopsies from musculus vastus lateralis were taken in both control and exercised legs 0.5, 4, 8, 24, 96, and 168 h after exercise for evaluation of myofibrillar structure, extracellular matrix proteins, and calpain activity. RESULTS: In the exercised leg, peak torque was reduced by 47 +/- 5% during exercise and was still 22 +/- 5% lower than baseline 4 d after the exercise. Calpain activity was three times higher in the exercised leg compared with the control leg 30 min after exercise. Myofibrillar disruptions were observed in 36 +/- 6% of all fibers in exercised muscle and in 2 +/- 1% of fibers in control muscle. The individual reductions in peak torque correlated with the proportion of fibers with myofibrillar disruptions (r = 0.89). The increase in calpain activity was not correlated to the proportion of fibers with myofibrillar disruptions. Nevertheless, the characteristics of the myofibrillar disruptions mimicked calpain-mediated degradation of myofibrils. Tenascin-C and the N-terminal propeptide of procollagen type III showed increased staining intensity on cross-sections 4-7 d after the exercise. CONCLUSIONS: Myofibrillar disruptions seem to be a main cause for the long-lasting reduction in force-generating capacity after high-force eccentric exercise. The increase in calpain activity, but the lack of a relationship between calpain activity and the amount of muscle damage, suggests multiple roles of calpain in the damage and repair process.
    Document Type:
    Reference
    Product Catalog Number:
    AB764P
    Product Catalog Name:
    Anti-Procollagen Type III PIIINP Antibody

  • Effects of exercise and obesity on UCP3 content in rat hindlimb muscles. 18685530

    Uncoupling protein 3 (UCP3) is a mitochondrial inner membrane protein, which is hypothesized to shuttle nonmetabolized fatty acids, particularly when excessive fatty acids are present. PURPOSE: Obese Zucker rats (OZR) have systematically elevated levels of fatty acids, with decreased fatty acid metabolism. We hypothesized that basal UCP3 protein expression levels would be elevated in the skeletal muscles of the OZR compared with the lean Zucker rats (LZR). In addition, because aerobic exercise training has been shown to elevate the ability of skeletal muscle to metabolize lipids, we also hypothesized that aerobic exercise training would decrease skeletal muscle UCP3 protein expression and that this would be more pronounced in the skeletal muscles of the OZR. METHODS: OZR and LZR were aerobically trained on a motorized treadmill for 55 min x d(-1), 5 d x wk(-1), for 9 wk. UCP3 and oxidative enzymes were measured in plantaris, gastrocnemius, and soleus muscles. RESULTS: Basal UCP3 protein expression was elevated approximately eightfold in the plantaris muscles and threefold in the gastrocnemius muscles of the OZR compared with the LZR (P 0.05). However, there was no difference in UCP3 protein expression in the soleus muscles of the OZR compared with the LZR (P = 0.34). Furthermore, aerobic exercise training did not significantly alter UCP3 protein expression in the soleus, plantaris, or gastrocnemius muscles of the LZR; however, UCP3 protein expression levels decreased in trained OZR soleus and gastrocnemius muscles compared with controls. CONCLUSIONS: The decrease in UCP3 with aerobic exercise training was most notable in the soleus of the OZR. These data demonstrate that the exercise-induced adaptations of UCP3 protein levels are muscle specific in obese animals compared with lean animals.
    Document Type:
    Reference
    Product Catalog Number:
    AB3046
    Product Catalog Name:
    Anti-Uncoupling Protein 3 Antibody