Malcangio Marzia, Lessmann Volkmar
Sensory Function, Centre for Neuroscience, King's College London, London SE1 1UL, UK.
Trends Pharmacol Sci. 2003 Mar;24(3):116-21. doi: 10.1016/S0165-6147(03)00025-7.
Recent evidence indicates that trophic factors can exert fast effects on neurones and so alter synaptic plasticity. Here, we focus on brain-derived neurotrophic factor (BDNF), which exerts a modulatory action at hippocampal synapses that are involved in learning and memory, and at the first pain synapse between primary sensory neurones and dorsal horn neurones. Hippocampal and sensory neurones share some properties for the release of endogenous BDNF. In the Schaffer collateral pathway of the hippocampus, binding of BDNF to high-affinity trkB receptors is essential for the induction of long-term potentiation, a specific type of synaptic plasticity. However, the consequences of BDNF binding to trkB receptors in the dorsal horn in relation to pain mechanisms are less well established and are considered in detail.
最近的证据表明，营养因子可对神经元产生快速影响，从而改变突触可塑性。在此，我们聚焦于脑源性神经营养因子（BDNF），它在参与学习和记忆的海马突触以及初级感觉神经元与背角神经元之间的第一痛觉突触处发挥调节作用。海马神经元和感觉神经元在释放内源性BDNF方面具有一些共同特性。在海马的沙氏侧支通路中，BDNF与高亲和力trkB受体的结合对于诱导长时程增强（一种特定类型的突触可塑性）至关重要。然而，BDNF与背角trkB受体结合在疼痛机制方面的后果尚未完全明确，本文将对此进行详细探讨。
