Home About us Contact
|
Home About us Contact | ||
|
|
||
Total Neurons (total + neuron)
Selected AbstractsTruncated tau expression levels determine life span of a rat model of tauopathy without causing neuronal loss or correlating with terminal neurofibrillary tangle loadEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 2 2008Peter Koson Abstract We have previously demonstrated in a transgenic rat model of tauopathy that human misfolded truncated tau derived from Alzheimer's disease suffices to drive neurofibrillary degeneration in vivo. We employed this model to investigate the impact of truncated tau expression levels on life span, neuronal loss and the final load of neurofibrillary tangles (NFTs) in transgenic rats. Two independent transgenic lines (SHR72, SHR318), that display different expression levels of truncated tau, were utilized in this study. We found that transgene expression levels in the brain of SHR72 rats were 44% higher than in SHR318 rats and that truncated tau protein levels determined the survival rate of transgenic rats. The line with higher expression levels of truncated tau (SHR72) showed decreased median survival (222.5 days) when compared with the line with lower expression (SHR318; 294.5 days). Interestingly, NFT loads (total NFT/total neurons) were very similar in terminal stages of disease in both transgenic lines (SHR72 , 10.9%; SHR318 , 11.6%), despite significantly different expression levels of truncated tau. Moreover, mean neuron numbers in the hippocampus (CA1,3) and brain stem (gigantocellular reticular nucleus) in the two transgenic rat strains in the terminal stages of disease were similar, and did not differ significantly from those observed in age-matched non-transgenic controls. These findings suggest that the expression levels of misfolded truncated tau determine the life span in a transgenic rat model of tauopathy without causing neuronal loss or correlating with terminal NFT load. [source] Greater hippocampal neuronal recruitment in food-storing than in non-food-storing birdsDEVELOPMENTAL NEUROBIOLOGY, Issue 4 2007Jennifer S. Hoshooley Abstract Previous research has shown heightened recruitment of new neurons to the chickadee hippocampus in the fall. The present study was conducted to determine whether heightened fall recruitment is associated with the seasonal onset of food-storing by comparing neurogenesis in chickadees and a non-food-storing species, the house sparrow. Chickadees and house sparrows were captured in the wild in fall and spring and received multiple injections of the cell birth marker bromodeoxyuridine (BrdU). Birds were held in captivity and the level of hippocampal neuron recruitment was assessed after 6 weeks. Chickadees showed significantly more hippocampal neuronal recruitment than house sparrows. We found no seasonal differences in hippocampal neuronal recruitment in either species. In chickadees and in house sparrows, one-third of new cells labeled for BrdU also expressed the mature neuronal protein, NeuN. In a region adjacent to the hippocampus, the hyperpallium apicale, we observed no significant differences in neuronal recruitment between species or between seasons. Hippocampal volume and total neuron number both were greater in spring than in fall in chickadees, but no seasonal differences were observed in house sparrows. Enhanced neuronal recruitment in the hippocampus of food-storing chickadees suggests a degree of neurogenic specialization that may be associated with the spatial memory requirements of food-storing behavior. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007. [source] Hippocampal neuron and glial cell numbers in Parkinson's disease,A stereological study,HIPPOCAMPUS, Issue 10 2006F.C. Joelving Abstract Hippocampal atrophy and neuron loss are early and reproducible findings in Alzheimer's disease, and recent magnetic resonance imaging studies indicate that hippocampal atrophy may also be present in Parkinson's disease (PD). To determine whether or not cell loss occurs in PD, we estimated the total neuron and glial cell numbers as well as the total volume unilaterally in the hippocampi of eight demented PD patients and eight control subjects. Cell numbers were estimated in the neuron-containing layers of CA1, CA2-(3), CA4, the dentate gyrus, and subiculum using the optical-fractionator technique. The Cavalieri method was used to estimate the volume of the total hippocampus and its subregions. We did not find significant differences in cell numbers or volumes in PD brains when compared with control subjects. Our results thus indicate that hippocampal atrophy and cell loss are not necessarily involved in the memory impairment and dementia observed in PD. © 2006 Wiley-Liss, Inc. [source] Differential long-term neurotoxicity of HIV-1 proteins in the rat hippocampal formation: A design-based stereological studyHIPPOCAMPUS, Issue 2 2008Sylvia Fitting Abstract The human immunodeficiency virus type 1 (HIV-1) proteins, gp120 and Tat, are believed to play a role in mediating central nervous system (CNS) pathology in HIV-1 infected patients. Using design-based stereology, we examined the role of neonatal intrahippocampal injections of gp120 and Tat on the adult hippocampus (,7½ month). Postnatal day (P)1-treated Sprague-Dawley rats were bilaterally injected with vehicle (VEH, 0.5 ,l sterile buffer), gp120 (100 ng), Tat (25 ,g) or combined gp120 + Tat (100 ng + 25 ,g). Using Nissl-stained tissue sections, we quantified total neurons in five subregions of the rat hippocampus [granual layer (GL), hilus of the dentate gyrus (DGH), cornu ammonis fields (CA)2/3, CA1, and subiculum (SUB)], and total glial cells (astrocytes and oligodendrocytes) in two subregions (DGH and SUB). Estimates of cell area and cell volume were taken in the DGH. There was a significant reduction of neuron number in the CA2/3 subfield by Tat and gp120, and a significant reduction in the DGH by Tat only. For glial cells, numbers of astrocytes in the DGH and SUB were increased by the Tat protein, whereas no effects were noted for gp120. Finally, for oligodendrocytes Tat increased cell number in the DGH but not in any other region; gp120 had no detectable effect in any brain region. Estimates of cell area and cell volume of the three different cell types revealed no significant differences between treatments. Collectively, these results suggest differential effects of gp120 and Tat on the estimated total number of neurons, as well as on the number of glial cells. © 2007 Wiley-Liss, Inc. [source] Preferential neurotrophic activity of fibroblast growth factor-20 for dopaminergic neurons through fibroblast growth factor receptor-1cJOURNAL OF NEUROSCIENCE RESEARCH, Issue 4 2003Shigeki Ohmachi Abstract Degeneration of dopaminergic neurons of the substantia nigra causes Parkinson's disease. Therefore, neurotrophic factors for dopaminergic neurons are of substantial clinical interest. Fibroblast growth factor (FGF)-20 preferentially expressed in the substantia nigra pars compacta (SNPC) of the rat brain significantly enhanced the survival of midbrain dopaminergic neurons. Here we examined the mechanism of action of FGF-20 on dopaminergic neurons. FGF-20 slightly enhanced the survival of total neurons of the midbrain, indicating that it preferentially enhanced the survival of dopaminergic neurons. FGF receptor (FGFR)-1c was found to be expressed abundantly in dopaminergic neurons in the SNPC but at much lower levels in neurons of other midbrain regions by in situ hybridization. FGF-20 was also found to bind FGFR-1c with high affinity with the BIAcore system. Furthermore, FGF-20 activated the mitogen-activated protein kinase (MAPK) pathway, which is the major intracellular signaling pathway of FGFs. Both the FGFR-1 inhibitor SU5402 and the MAPK pathway inhibitor PD98059 also significantly inhibited the activation of the MAPK pathway by FGF-20 and the neurotrophic activity of FGF-20. The present findings indicate that the activation of the MAPK pathway by FGF-20 signaling through FGFR-1c plays important roles in the survival of dopaminergic neurons in the SNPC. © 2003 Wiley-Liss, Inc. [source] Distribution and Cytoarchitecture of Sympathetic Neurons Innervating the Pineal Gland in Chick: A CTB-HRP StudyANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 1 2009L. Jia Summary The neurons in bilateral superior cervical ganglia (SCG) innervating the chick pineal gland were labelled by using the technique of retrograde axonal labelling with cholera toxin B subunit linked to horseradish peroxidase (CTB-HRP). To our results, perikarya of these sympathetic neurons distributed from rostral to caudal in the SCG, and mainly localized in the opposite side of the paravertebral trunk. The fibres of these neurons were collected by the cephalic carotid nerve. According to the sizes of somal area and dendritic field, these sympathetic neurons projecting to the pineal gland were classified into four major groups: group I cells (52.4%) with a small somal area (303.5 ,m2 on average) and narrow dendritic field (3767.8 ,m2 on average), group II cells (39.0%) with a middle-sized somal area (473.3 ,m2) and middle-sized dendritic field (7522.2 ,m2), group III cells (6.4%) with a middle-sized somal area (473.4 ,m2) and wide dendritic field (13 104.4 ,m2), and group IV cells (2.2%) with a large somal area (940.7 ,m2) and wide dendritic field (14 553.2 ,m2). Of these pineal projecting neurons, most took on a lesser dendritic field. The neurons with small or middle-sized dendritic field from group I and II were about 91.4% of the total neurons labelled with CTB-HRP, and the neurons with wide dendritic field from group III and IV were less with 8.6%. [source] | ||||||||||