Selective vulnerability in ageing rat sympathetic neurons
K.P. Gatzinsky1, C. Thrasivoulou2, M. Campioni-Noack2, C. Underwood2, T.Cowen2
1Dept. of Anatomy and Cell Biology, University of Goteborg, Sweden;
2Dept. of Anatomy and Developmental Biology, University College London, Royal Free Campus, London NW3 2PF
We have examined the hypothesis that differences in NGF uptake and
transport determine vulnerability to age-related neurodegeneration.
Neurons projecting to cerebral blood vessels (CV) have been found to be
more vulnerable to this kind of degeneration than those projecting to
the iris. Uptake of NGF was therefore examined in sympathetic neurons
projecting from the superior cervical ganglion (SCG) to CV and iris in
young and old rats by treating the peripheral processes of these
neurons with different doses of I125-NGF. Total uptake of
I125-NGF (cpm per ganglion) was reduced in old rats
following treatment of CV, but not iris, neurons. Numbers of labelled
neurons were counted in autoradiographic preparations of sectioned
ganglia. Data showed age-related reductions in numbers of labelled
sympathetic and sensory neurons projecting to CV, but no change in
numbers of neurons projecting to iris. Calculation of uptake of
I125-NGF per neuron showed no major age-related differences.
However, uptake per neuron was considerably lower for CV-projecting,
compared to iris-projecting, SCG neurons. Counts of SCG neurons using a
physical disector following retrograde tracing with fluorogold
confirmed the selective vulnerability of CV-projecting neurons by
showing a loss of these neurons in the period between 15 and 24m,
contrasting with no change in numbers of iris-projecting neurons. We
conclude that vulnerability to age-related neurodegeneration leading to
neuronal cell death is associated with life-long low levels of NGF
uptake while, conversely, life-long high levels of NGF uptake are
associated with protection from age-related neurodegeneration.
Key words:
neurodegeneration, SCG, iris, cerebral blood vessels, NGF
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