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Journal of Neuroscience, Vol 15, 7929-7939, Copyright © 1995 by Society for Neuroscience
Brain-derived neurotrophic factor promotes the survival and sprouting of serotonergic axons in rat brain
LA Mamounas, ME Blue, JA Siuciak and CA Altar
Laboratory of Cellular and Molecular Biology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA.
A pathology of brain serotonergic (5-HT) systems has been found in
psychiatric disturbances, normal aging and in neurodegenerative disorders
including Alzheimer's and Parkinson's disease. Despite the clinical
importance of 5-HT, little is known about the endogenous factors that have
neurotrophic influences upon 5-HT neurons. The present study examined
whether chronic pain parenchymal administration of the neurotrophins
brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) or NGF
could prevent the severe degenerative loss of serotonergic axons normally
caused by the selective 5-HT neurotoxin p-chloroamphetamine (PCA). The
neurotrophins (5-12 micrograms/d) or the control substances (cytochrome c
or PBS vehicle) were continuously infused into the rat frontoparietal
cortex using an osmotic minipump. One week later, rats were subcutaneously
administered PCA (10 mg/kg) or vehicle, and the 5-HT innervation was
evaluated after two more weeks of neurotrophin infusion. As revealed with
5-HT immunocytochemistry, BDNF infusions into the neocortex of intact
(non-PCA-lesioned) rats caused a substantial increase in 5-HT axon density
in a 3 mm diameter region surrounding the cannula tip. In PCA-lesioned
rats, intracortical infusions of BDNF completely prevented the severe
neurotoxin-induced loss of 5-HT axons near the infusion cannula. In
contrast, cortical infusions of vehicle or the control protein cytochrome c
did not alter the density of serotonergic axons in intact animals, nor did
control infusions prevent the loss of 5-HT axons in PCA-treated rats. NT-3
caused only a modest sparing of the 5-HT innervation in PCA-treated rats,
and NGF failed to prevent the loss of 5-HT axon density. The
immunocytochemical data were supported by neurochemical evaluations which
showed that BDNF attenuated the PCA-induced loss of 5-HT and 5- HIAA
contents and 3H-5-HT uptake near the infusion cannula. Thus, BDNF can
promote the sprouting of mature, uninjured serotonergic axons and
dramatically enhance the survival or sprouting of 5-HT axons normally
damaged by the serotonergic neurotoxin PCA.
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