Mice lacking the peroxisome proliferator-activated receptor alpha gene present reduced number of dopamine neurons in the substantia nigra without altering motor behavior or dopamine neuron decline over life

High Fat Diet Suppresses Peroxisome Proliferator-Activated Receptors and Reduces Dopaminergic Neurons in the Substantia Nigra

“…PPAR-α is expressed by DA neurons of the nigrostriatal circuit [54]. PPAR-α null mice, despite normal locomotion in the OFT, had reduced numbers of DA neurons in the SN, which suggested that PPAR-α is necessary for the normal development of the SN [55]. PPAR-α agonist fenofibrate and palmitoylethanolamide could prevent DA cell death in the SNpc, attenuate the loss of TH immunoreactivity in the striatum, and reverse motor deficits by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) [56,57] or 6-hydroxydopamine (6-OHDA) [58].…”

Alteration of neuropathic and visceral pain in female C57BL/6J mice lacking the PPAR-α gene

“…Adult mice from wild-type and homozygous females were genotyped for PPAR-α deletion using DNA isolated from a small part of the tail and following the protocol from the supplier (http:// www.jax.org). Schemes of PCR assay for detection of wildtype allele (143 bp) and targeted PPAR-α deletion containing fragment from bacterial neomycin resistance gene (280 bp) have been presented by the authors elsewhere (Gonzalez-Aparicio et al 2011). Expected product sizes were obtained after the use of genomic DNA (50 ng/μl/ reaction), added as a template in a 25 ll PCR (heating up to 94°C for 3 min followed by 12 cycles of 94°C decreased in 0.5°C per cycle for 20 s, 64°C for 30 s, and 72°C for 35 s and 25 cycles of 94°C for 30 s, 58°C for 30 s, and 72°C for 35 s, with a final incubation of 72°C for 2 min before cooling to 10°C) containing BioTherm-Mix™ reagent (Genecraft GmbH) and with the following primers: IMR0013 (50-CTTGGGTGGAGAGGCTATTC-3; Tm059°C), IMR0014 (50-AGGTGAGATGACAGGAGATC-30; Tm 054°C), IMR11999 (50-CCATCCAGATGACACCTTCC-30; Tm0 60°C), IMR1200 (50-TCTCTTGCAACAGTGGGTGC-30; Tm062°C).…”

The effect of neuronal conditional knock-out of peroxisome proliferator-activated receptors in the MPTP mouse model of Parkinson’s disease

“…It was necessary to generate double knockouts of PPARγ and PPARδ as PPAR isoforms are known to be subject to functional compensation ( Patsouris et al, 2006 ). Importantly, this compensatory change is known to occur in neurons ( Gonzalez-Aparicio et al, 2011 ). Conditional knock-outs were required as a complete knock-out of either receptor is lethal.…”