Plasticity of aged perivascular axons following exogenous NGF: analysis of catecholamines.
The present study investigated the atrophy of aged perivascular sympathetic axons and the response of these cerebrovascular neurons to the neurotrophin nerve growth factor (NGF). Using high performance liquid chromatography coupled with electrochemical detection (HPLC-ECD) to quantify catecholamines and immunohistochemical methods to quantify the density of TH immunoreactive fibers, we found a significant decrease in norepinephrine (NE) and TH in aged sympathetic axons. However, following in vivo administration of exogenous neurotrophin, aged neurons exhibited a robust response to NGF that was similar to the young adult, suggesting little decline in the capability of aged neurons to utilize exogenous neurotrophin. These results suggest that the age-related atrophy of aged sympathetic axons may result primarily from reduced availability of target-derived neurotrophin rather than from intrinsic alterations of neuronal function.
Dickason
A K
AK
Center for Neuroscience, Department of Zoology, Miami University, Oxford, OH 45056, USA.
Isaacson
L G
LG
D000375:Aging / Q000502:physiology*; D000818:Animals; D001369:Axons / Q000187:drug effects / Q000502:physiology*; D001808:Blood Vessels / Q000294:innervation*; D002395:Catecholamines / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid; D004563:Electrochemistry; D005260:Female; D007150:Immunohistochemistry; D007260:Infusion Pumps; D009414:Nerve Growth Factors / Q000008:administration & dosage / Q000494:pharmacology*; D009473:Neuronal Plasticity / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013564:Sympathetic Nervous System / Q000166:cytology / Q000502:physiology; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D002395:Catecholamines; D009414:Nerve Growth Factors; D014446:Tyrosine 3-Monooxygenase