Farkas-Szallasi T, Bennett G J, Blumberg P M, Hökfelt T, Lundberg J M, Szallasi A
Department of Pharmacology, Karolinska Institute, Stockholm, Sweden.
Brain Res. 1996 May 6;719(1-2):213-8. doi: 10.1016/0006-8993(96)00065-0.
Resiniferatoxin (RTX) depletes vanilloid (capsaicin) receptors from lumbar dorsal root ganglia (DRG) of the rat. In addition, RTX causes changes in neuropeptide and nitric oxide synthase expression in lumbar DRG neurons, similar to those described following axotomy; this latter phenomenon is referred to as messenger plasticity. These findings suggested that vanilloid receptor loss may be part of the plasticity that follows RTX treatment. Here we show that vanilloid receptor expression, as detected by [3H]RTX autoradiography, is not changed in lumbar DRGs of axotomized rats, nor is it altered in a rat model (chronic constriction injury) of neuropathic pain. Thus, the in vivo expression of vanilloid receptors detected by specific [3H]RTX binding does not require the presence of intraaxonally transported trophic factors such as nerve growth factor. We conclude that messenger plasticity and vanilloid receptor loss are mediated by distinct mechanisms.
树脂毒素（RTX）可使大鼠腰段背根神经节（DRG）中的香草酸（辣椒素）受体减少。此外，RTX会导致腰段DRG神经元中神经肽和一氧化氮合酶表达发生变化，这与轴突切断后所描述的情况相似；后一种现象被称为信使可塑性。这些发现表明，香草酸受体的丧失可能是RTX治疗后可塑性的一部分。在此我们表明，通过[3H]RTX放射自显影检测到的香草酸受体表达在轴突切断的大鼠腰段DRG中并未改变，在神经性疼痛的大鼠模型（慢性压迫损伤）中也未改变。因此，通过特异性[3H]RTX结合检测到的香草酸受体的体内表达并不需要轴突内运输的营养因子如神经生长因子的存在。我们得出结论，信使可塑性和香草酸受体丧失是由不同机制介导的。
