engleski

Large pyramidal neurons in the associative prefrontal cortex preserve dendritic morphology during normal aging

In the present study, we have analyzed changes in dendritic morphology and spine density on large layer IIIc and layer V pyramidal neurons of human prefrontal cortex (Brodmann area 9). Postmortal tissue of adult (38-64 years, n=8) and aged subjects (72-91 years, n=7) was processed by rapid Golgi method. None of the subjects had clinical record of psychiatric and neurological disorders, nor were any neuropathological deviations detected in their brains postmortem. From each layer, 10-15 well impregnated pyramidal neurons per subject were three-dimensionally reconstructed using Neurolucida system. Soma size, total dendritic length, total segment number, individual segment length and spine density were quantitatively analyzed, separately for basal dendritic tree and apical side branches. In aged group the mean values of spine density were 20-25% lower in both apical side branches and basal dendrites in layer IIIc pyramidal neurons. This difference was nearly at the statistically significant level. However, from 7 aged subjects only 2 cases with highest values had the spine density around mean level of adult group and in the remaining aged subjects the dendritic spine density values were lower than in all mature adult subjects. At the other hand, for both layers, all dendritic morphology parameters were comparable in both, the adult and aged group, so no significant difference was statistically obtained. For the layer V the spine density was also around the same in individuals of both groups. Our data show that there is a large population of cortical neurons that preserve their dendritic structure during normal aging. However, majority of aged individuals show a trend for decrease in spine density of layer IIIc pyramids. Therefore, we conclude that synaptic elements of processing higher cognitive functions might be less resistant to aging process and this might depend on level of cognitive stimulation during aging.

cognition ; schizophrenia ; cortical circuitry

nije evidentirano