Spinal cord injury-specific depression of monosynaptic spinal reflex transmission by L-5-hydroxytryptophan results from loss of the 5-HT uptake system and not 5-HT receptor supersensitivity

被引：4

作者：

Honda, Motoko ^{[1
]}

Tanabe, Mitsuo ^{[1
]}

Ono, Hideki ^{[1
]}

机构：

[1] Nagoya City Univ, Lab CNS Pharmacol, Grad Sch Pharmaceut Sci, Mizuho Ku, Nagoya, Aichi 4678603, Japan

来源：

EXPERIMENTAL NEUROLOGY | 2006年 / 202卷 / 01期

关键词：

spinal cord injury; spinal reflexes; 5-HT; 5-HT reuptake;

D O I：

10.1016/j.expneurol.2006.05.022

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

We studied changes in the spinal segmental reflex and serotonergic (5-HT) responses in rats after spinal cord injury (SCI) produced by the weight-dropping method at the T8 level. The spinal monosynaptic reflex amplitude (MSR) was recorded from the L5 ventral root following stimulation of the ipsilateral L5 dorsal root. The 5-HT precursor L-5-hydroxytryptophan (L-5-HTP) depressed NISR in the spinal cord injured rats but not in normal rats. We investigated whether the SCI-specific depression of NISR by L-5-HTP was attributable to postsynaptic supersensitivity of 5-HT receptors or presynaptic loss of the 5-HT uptake system. Sumatriptan, a selective 5-HT1B/1D receptor agonist that is not taken up by 5-HT transporters, depressed the MSR similarly in both SCI and normal rats, suggesting that SCI resulted in the loss of 5-HT terminals and not postsynaptic supersensitivity of 5-HT receptors. (c) 2006 Elsevier Inc. All rights reserved.

引用

页码：258 / 261

页数：4