HIPPOCAMPAL P75 NERVE GROWTH-FACTOR RECEPTOR IMMUNOREACTIVITY IN DEVELOPMENT, NORMAL AGING AND SENESCENCE

Citation
Jm. Kerwin et al., HIPPOCAMPAL P75 NERVE GROWTH-FACTOR RECEPTOR IMMUNOREACTIVITY IN DEVELOPMENT, NORMAL AGING AND SENESCENCE, Acta anatomica, 147(4), 1993, pp. 216-222
Citations number
29
Categorie Soggetti
Anatomy & Morphology
Journal title
ISSN journal
00015180
Volume
147
Issue
4
Year of publication
1993
Pages
216 - 222
Database
ISI
SICI code
0001-5180(1993)147:4<216:HPNGRI>2.0.ZU;2-P
Abstract
Using the monoclonal antibody ME 20.4, p75 nerve growth factor (NGF) r eceptor immunoreactivity has been studied in the hippocampus and adjac ent cortex in a series of 57 cases ranging in age from 24 weeks gestat ion to 95 years of age. The activity of the neurotransmitter-synthesiz ing enzyme choline acetyltransferase (ChAT), the activity of which is regulated by NGF, has also been determined in parallel experiments. p7 5 NGF receptor immunoreactivity was detected in the fetal neocortex as nerve terminal staining, potentially derived from basal forebrain neu rons which were positive for NGF receptor, and was also localized in n erve cells of the cerebral cortex. Cortical reactivity for NGF recepto r increased with age up to the 4th decade thereafter remaining constan t. NGF receptor reactivity localized to neocortical neuronal cell bodi es was not present in the postnatal or adult brain.- Hippocampal react ivity for the NGF receptor was not present before birth appearing firs t in the postnatal period and thereafter showing an identical developm ent pattern to the neocortex. ChAT activity in the entorhinal cortex a nd hippocampus partially paralleled NGF receptor development being pre sent in the neocortex in the fetus but not in the fetal hippocampal fo rmation and increasing postnatally to reach maximum levels in the 4th decade. Whilst entorhinal cortex ChAT values remain relatively constan t with ageing, hippocampal ChAT declined with age after the 4th decade . The results may have implications for the aetiology of age-related c holinergic deficits in the hippocampus