Electroretinography (ERG) in the wild giant panda (Ailuropoda melanoleuca).

PURPOSE: Using a quick electroretinography (ERG) protocol for rapid assessment of the retinal function of wild giant pandas (Ailuropoda melanoleuca) performed in field conditions to demonstrate the range of ERG recordings in giant pandas of unknown retinal status. ANIMALS STUDIED: Nine free range giant pandas. PROCEDURE: All the giant pandas were anesthetized using an intramuscular dexMTZ injection, which is a combination of dexmedetomidine and tiletamine-zolazepam. After 20 mins of dark adaptation, scotopic ERGs were obtained by using three flash intensities: -25 dB (0.0087 cd·s/m2 ), 0 dB (2.75 cd·s/m2 ), and +5 dB (8.7 cd·s/m2 ). Next, photopic ERGs were acquired using a single flash protocol with a flash intensity of 3.0 cd·s/m2 after 10 minutes of light adaptation. RESULTS: In scotopic ERG at 0.0087 cd·s/m2 , mean b-wave amplitude and peak time were 82.26 µV (SD ± 16.65 and 95% CI 68.33-96.18) and 66.97 ms (SD ± 10.86 and 95% CI 57.90-76.05), respectively. This flash intensity was below a-wave threshold and resulted in b waves with greater peak times compared to those with higher intensities. At 2.75 cd·s/m2 , the mean a-wave amplitude and peak time were 53.95 µV (SD ± 11.63 and 95% CI 44.23-63.67) and 16.13 ms (SD ± 2.62 and 95% CI 13.94-18.31), and mean b-wave amplitude and peak time were 119.57 µV (SD ± 15.54 and 95% CI 106.57-132.56) and 32.00 ms (SD ± 6.47 and 95% CI 26.59-37.41). At 8.7 cd·s/m2 , the mean a-wave amplitude and peak time were 58.85 µV (SD ± 14.90 and 95% CI 46.39-71.31) and 15.59 ms (SD ± 2.63 and 95% CI 13.40-17.79), and the mean b-wave amplitude and peak time were 132.97 µV (SD ± 22.11 and 95% CI 114.48-151.46) and 32.66 ms (SD ± 6.87 and 95% CI 26.91-38.40). In photopic ERG at 2.75 cd·s/m2 , the mean a-wave amplitude and peak time were 62.08 µV (SD ± 16.61 and 95% CI 48.19-75.97) and 16.28 ms (SD ± 0.90 and 95% CI 15.53-17.03), and the mean b-wave amplitude and peak time were 214.93 µV (SD ± 70.41 and 95% CI 156.07-273.80) and 33.09 ms (SD ± 1.27 and 95% CI 32.03-34.15). CONCLUSION: Using a portable ERG system with a brief ERG protocol to perform electroretinographies in wild giant pandas is a practical, useful, and reliable method for the rapid assessment of their retinal function.

ß3-adrenoceptor mediates metabolic protein remodeling in a rabbit model of tachypacing-induced atrial fibrillation.

BACKGROUND: The beta 3-adrenoceptor (ß3-AR) is closely associated with energy metabolism. This study aimed to explore the role of ß3-AR in energy remodeling in a rabbit model of pacing-induced atrial fibrillation (AF). METHODS: Rabbits with a sham-operation or pacing-induced AF were used for this study, and the latter group was further divided into three subgroups: 1) the pacing group, 2) the ß3-AR agonist (BRL37344)-treated group, and 3) the ß3-AR antagonist (SR59230A)-treated group. Atrial electrogram morphology and surface ECG were used to monitor the induction of AF and atrial effective refractory period (AERP). RT-PCR and western blot (WB) were used to show alterations in ß3-AR and metabolic-related protein. RESULTS: RT-PCR and WB results showed that ß3-AR was significantly upregulated in the pacing group, and that it corresponded with high AF inducibility and significantly decreased AERP200 and ATP production in this group. Inhibition of ß3-AR decreased the AF induction rate, reversed AERP200 reduction, and restored ATP levels in the AF rabbits. Further activation of ß3-AR using agonist BRL37344 exacerbated AF-induced metabolic disruption. Periodic acid Schiff (PAS) and Oil Red O staining showed ß3-AR-dependent glycogen and lipid droplet accumulation in cardiac myocytes with AF. Glucose transporter-4 (GLUT-4) and CD36, key transporters of glucose and fatty acids, were downregulated in the pacing group. Expression of carnitine-palmitoyltransferase I (CPT-1), a key regulator in fatty acid metabolism, was also significantly downregulated in the pacing group. Reduced glucose transportation and fatty acid oxidation could be restored by inhibition of ß3-AR. Furthermore, key regulators of metabolism, peroxisome proliferator-activated receptor-α (PPARα) and PPAR co-activator (PGC-1α) can be regulated by pharmacological intervention of the ß3-AR. CONCLUSIONS: ß3-AR is involved in metabolic protein remodeling in AF. PPARα/PGC-1α signaling pathway might be the relevant down-stream molecular machinery in response to AF-induced activation of ß3-AR. ß3-AR might be a novel target in AF treatment.

Metabolomics Analysis of Electroacupuncture Pretreatment Induced Neuroprotection on Mice with Ischemic Stroke.

The brain metabolic changes caused by the interruption of blood supply are the initial factors of brain injury in ischemic stroke. Electroacupuncture (EA) pretreatment has been shown to protect against ischemic stroke, but whether its neuroprotective mechanism involves metabolic regulation remains unclear. Based on our finding that EA pretreatment significantly alleviated ischemic brain injury in mice by reducing neuronal injury and death, we performed a gas chromatography-time of flight mass spectrometry (GC-TOF/MS) to investigate the metabolic changes in the ischemic brain and whether EA pretreatment influenced these changes. First, we found that some glycolytic metabolites in the normal brain tissues were reduced by EA pretreatment, which may lay the foundation of neuroprotection for EA pretreatment against ischemic stroke. Then, 6[Formula: see text]h of cerebral ischemia-induced brain metabolic changes, especially the enhanced glycolysis, were partially reversed by EA pretreatment, which was manifested by the brain levels of 11 of 35 up-regulated metabolites and 18 of 27 down-regulated metabolites caused by cerebral ischemia significantly decreasing and increasing, respectively, due to EA pretreatment. A further pathway analysis showed that these 11 and 18 markedly changed metabolites were mainly involved in starch and sucrose metabolism, purine metabolism, aspartate metabolism, and the citric acid cycle. Additionally, we found that EA pretreatment raised the levels of neuroprotective metabolites in both normal and ischemic brain tissues. In conclusion, our study revealed that EA pretreatment may attenuate the ischemic brain injury by inhibiting glycolysis and increasing the levels of some neuroprotective metabolites.