Abstract
Modulation of neural cell adhesion molecule polysialylation (NCAM PSA) state has been proposed to underlie morphofunctional change associated with consolidation of memory in the rodent, and its age-dependent decline to be related to impaired cognitive function. To establish whether this may be a human correlate of cognitive decline, we determined the age-dependent expression of PSA in the human hippocampal dentate gyrus using postmortem tissue derived from individuals who exhibited no obvious neuropathology. As in the rodent, PSA immunoreactivity in the 5-month human infant was associated mainly with a population of granule-like cells and their mossy fibre axons. Cell numbers were maximal during the first 3 years of life but declined by an order of magnitude between the second and third decades and remained relatively constant thereafter and was restricted to the granule cell layer/hilar border. In contrast to the rodent, diffuse immunostaining was observed in the inner molecular layer; however, as development advanced, this became relocated to the outer molecular layer from 2 years of age onwards. In addition, numerous polysialylated hilar neurons became evident at 2-3 years of age and remained constant until the eighth decade of life. These findings suggest NCAM polysialylation to play a crucial developmental role within a period concluding with adolescence, and that an attenuated NCAM PSA- mediated neuroplasticity continues throughout the human lifespan. The importance of the developmental phase of NCAM PSA expression in the emergence of schizophrenia is discussed.
Original language | English (US) |
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Pages (from-to) | 99-106 |
Number of pages | 8 |
Journal | Journal of Neuroscience Research |
Volume | 55 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1 1999 |
Keywords
- Granule cells
- Hilar neurons
- NCAM PSA
- Neuroplasticity
- Schizophrenia
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience