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The neurotoxin 2'-NH2-MPTP degenerates serotonin axons and evokes increases in hippocampal BDNF.

Abstract：

:1-Methyl-4-(2'-aminophenyl)-1,2,3,6-tetrahydropyridine (2'-NH2-MPTP) causes long-term depletions in cortical and hippocampal serotonin (5-HT) and norepinephrine (NE) that are accompanied by acute elevations in glial fibrillary acidic protein (GFAP) and argyrophilia. To further investigate the hypothesis that these changes are reflective of serotonergic and noradrenergic axonal degeneration, 2'-NH2-MPTP was administered to mice and innervation densities were determined immunocytochemically. Regional responses of the neurotrophin, brain-derived neurotrophic factor (BDNF), to putative damage were also assessed. Three days after 2'-NH2-MPTP, 5-HT axons exhibited a beaded, tortuous appearance indicative of ongoing degeneration. At 21 days, numbers of serotonin axons were significantly decreased, with the greatest axonal losses occurring in cortex and hippocampus. Serotonin axons in the amygdala were contrastingly spared long-term damage, as were 5-HT and NE cell bodies in the brain stem. BDNF protein levels were selectively increased in the hippocampus 3 days post-dose and returned to normal 21 days later. These results, in conjunction with previous findings, demonstrate that 2'-NH2-MPTP causes degeneration of serotonergic axons innervating the cortex and hippocampus on par with depletions in neurotransmitter levels. Moreover, damage to the hippocampus, a brain region important for learning and memory, and the modulation of anxiety and stress responsiveness, results in a transitory increase in BDNF.

journal_name

Neuropharmacology

journal_title

Neuropharmacology

authors

Luellen BA,Szapacs ME,Materese CK,Andrews AM

doi

10.1016/j.neuropharm.2005.09.006

subject

Has Abstract

pub_date

2006-03-01 00:00:00

pages

297-308

issue

3

eissn

0028-3908

issn

1873-7064

pii

S0028-3908(05)00331-X

journal_volume

50

pub_type

杂志文章

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