Project description:Lead (Pb) is a potent neurotoxin with disastrous effects on cognition, memory, and sensory functions. Pb exposure during the developmental stage of life causes irreversible changes in neuronal morphology impacting the physiological functions from reduced motor skills and lowered intelligence quotient to developmental disorders and delayed puberty. To investigate the effect of developmental Pb exposure on the rodent hippocampus, we exposed rat pups to 100 ppm lead acetate via lactation and looked into the morphological and proteomic alterations in the hippocampal neurons. Our Nissl stain data revealed a significant reduction in the number of CA1 neurons in the hippocampus of the Pb-exposed rats. Further, we analyzed the dendritic tree morphology of the CA1 neurons and reported neuronal hypertrophy and a reduction in spine density in both the basal and the apical dendrites in Pb-exposed rats. Our mass spectrometric data identified a total of 6780 proteins out of which 190 proteins were p-value significant. We reported a total of 31 dysregulated proteins in the hippocampus of Pb-exposed rats. The changes seen in the protein expression profile and reduction in neuronal numbers in addition to the altered dendritic tree of Pb-exposed neurons suggest the molecular and morphological changes that could underlie the memory and cognitive deficits seen in Pb-exposed animals.
Project description:These data show differences in up- and down-regulation for protein abundances in the hippocampus of double blast vs. sham rats. Tandem mass tags (TMT)-MS results showed 136 up-regulated and 94 down-regulated proteins between the two groups. These TMT-MS findings revealed changes never described before in blast studies. In the absence of behavioral changes, these proteomic data further support the existence of an asymptomatic blast-induced molecular altered status (ABIMAS) associated with specific protein changes in the rat hippocampus.
Project description:To address the hypothesis that silencing deleterious or protective injury-induced genes in the rat hippocampus will reduce or increase the numbers of injured hippocampal neurons, alter cellular pathways essential for neuronal function and improve or worsen functional outcome after traumatic brain injury (TBI), we evaluated the effects of silencing neuronal nitric oxide synthase (nNOS) and glutathione peroxidase-1 (GPx-1) expression in the injured rat hippocampus.
Project description:Whole-genome bisulfite sequencing on the rat hippocampus identifies DMRs near genes concerning neuronal development and plasticity which are affected by an iron-deficient diet in pregnancy.
