Journal
NEUROBIOLOGY OF AGING
Volume 29, Issue 11, Pages 1666-1679Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2007.04.001
Keywords
aging cholinergic axons; cholinergic neurons; septohippocampal pathways; medial septal nucleus; hippocampus; stereology; spherical probe; optical fractionator probe; synaptophysin; nerve growth factor; brain-derived neurotrophic factor; tropomyosin related kinase receptor A; tropomyosin related kinase receptor B; p75 neurotrophin receptor; choline acetyltransferase
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Funding
- MBF Bioscience
- Canadian Institutes of Health Research
- Canadian Neurotrauma Research Program
- Alzheimer Society of Canada
- Canada Foundation for Innovation
- Ontario Innovation Trust
- University of Toronto Open Fellowship
- Ontario Graduate Scholarship
- Fundacao para a Ciencia e a Tecnologia-postdoctoral fellowship [SFRH/BPD/14581/2003]
- Ontario Mental Health Foundation Studentship
- Fundação para a Ciência e a Tecnologia [SFRH/BPD/14581/2003] Funding Source: FCT
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Cholinergic deficits occur in the aged hippocampus and they are significant in Alzheimer's disease. Using stereological and biochemical approaches, we characterized the cholinergic septohippocampal pathway in old (24 months) and young adult (3 months) rats. The total length of choline acetyltransferase (ChAT)-positive fibers in the dorsal hippocampus was significantly decreased by 32% with aging (F-(1.9) = 20.94, p = 0.0014), along with the levels of synaptophysin, a presynaptic marker. No significant changes were detected in ChAT activity or in the amounts of ChAT protein, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), tropomyosin related kinase receptor (Trk) A, TrkB, or p75 neurotrophin receptor (p75(NTR)) in the aged dorsal hippocampus. The number and size of ChAT-positive neurons and the levels of ChAT activity, NGF and BDNF were not statistically different in the septum of aged and young adult rats. This study suggests that substantial synaptic loss and cholinergic axonal degeneration occurs during aging and reinforces the importance of therapies that can protect axons and promote their growth in order to restore cholinergic neurotransmission. (C) 2007 Elsevier Inc. All rights reserved.
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