5 research outputs found
Beneficial effects of multisensory and cognitive stimulation on age-related cognitive decline in long-term-care institutions
M and P retinal ganglion cells of diurnal and nocturnal new-world monkeys
M and P retinal ganglion cell morphology revealed by bio- cytin retrograde labelling was compared in two closely related New-World monkeys, Cebus and Aotus, to investigate whether nocturnal and diurnal species of primates have similar cell classes. Monkey and cat ganglion cells from regions of matching cell class densities were also compared. Cat a, cat /3, Aotus M, and Cebus M cells were similar in many aspects, but Cebus M cells had higher branching density. Cebus and Aotus P cells formed a distinct group and represent a primate specialization com-mon to diurnal and nocturnal simians.</p
Diffuse axonal damage, myelin impairment, astrocytosis and inflammatory response following microinjections of NMDA into the rat striatum
White matter damage and inflammatory response are important secondary outcomes after acute neural disorders. Nevertheless, a few studies addressed the temporal outcomes of these pathological events using non-traumatic models of acute brain injury. In the present study, we describe acute inflammatory response and white matter neuropathology between 1 and 7 days after acute excitotoxic striatal damage. Twenty micrometer sections were stained by hematoxylin and eosin technique for gross histopathological analysis and immunolabed for neutrophils (anti-mbs-1), activated macrophages/microglia (anti-ed1), astrocytes (anti-gfap), damaged axons (anti-beta app) and myelin basic protein (MBP). Recruitment peak of neutrophils and macrophages occurred at 1 and 7 days post-nmda injection, respectively. Diffuse damaged axons (beta-app + end-bulbs) were apparent at 7 days, concomitant with progressive myelin impairment and astrocytosis. Further studies using electron microscopy and blockers of inflammatory response and glutamatergic receptors should be performed to confirm and address the mechanisms of white matter damage following an excitotoxic lesion