Kidney International (2009) 76, 1040-1048; doi:10.1038/ki.2009.318; published online 26 August 2009″
“We present the photochemically induced olfactory bulbectomy (P-bulbectomy) as a novel method to ablate the

olfactory bulb thus inducing an animal model of depression. The photosensitizer Rose Bengal was injected through the tail vein and then the cool halogen light illuminated the skull region overlying of the FG-4592 mouse olfactory bulb for 10 min. Two weeks after surgery, P-bulbectomy had completely removed olfactory bulb uniformly in all animals. P-bulbectomy induced typical depression-related behaviors such as hyperactivity in the open field test and an enhancement of immobility time and in the forced swimming test. Depression-related neurohistological phenomenon was also seen;

reduction of choline-acetyltransferase-positive cell numbers in the medial septum and a decline in cell proliferation in the dentate gyrus of hippocampus. This study shows that P-bulbectomy may be a convenient and reproducible experimental method to produce an animal model of depression. NeuroReport 21:179-184 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.”
“Our previous studies suggest that peroxisome proliferator-activated receptor-alpha (PPAR alpha) plays a critical role in regulating fatty acid beta-oxidation in kidney tissue and this directly correlated with preservation of kidney morphology and function during acute kidney injury. To further

study this, we generated transgenic mice expressing PPAR alpha in the proximal BV-6 tubule under the control of the promoter of KAP2 (kidney androgen-regulated protein 2). Segment-specific upregulation of PPAR alpha expression by testosterone treatment of female transgenic mice improved kidney function during cisplatin or ischemia-reperfusion-induced acute kidney injury. Ischemia-reperfusion injury or treatment with cisplatin in wild-type mice caused inhibition of fatty-acid oxidation, reduction of mitochondrial genes of oxidative phosphorylation, mitochondrial DNA, fatty-acid metabolism, and the tricarboxylic acid cycle. Similar injury in testosterone-treated transgenic mice resulted in amelioration Morin Hydrate of these effects. Similarly, there were increases in the levels of 4-hydroxy-2-hexenal-derived lipid peroxidation products in wild-type mice, which were also reduced in the transgenic mice. Similarly, necrosis of the S3 segment was reduced in the two injury models in transgenic mice compared to wild type. Our results suggest proximal tubule PPAR alpha activity serves as a metabolic sensor. Its increased expression without the use of an exogenous PPA R alpha ligand in the transgenic mice is sufficient to protect kidney function and morphology, and to prevent abnormalities in lipid metabolism associated with acute kidney injury. Kidney International (2009) 76, 1049-1062; doi:10.1038/ki.2009.