The growth factors BDNF and GDNF are gaining more and more attention as modulators of synaptic transmission in the mature central nervous system (CNS). The two molecules undergo a regulated secretion in neurons and may be anterogradely transported to terminals where they can positively or negatively modulate fast synaptic transmission. There is today a wide consensus on the role of BDNF as a pro-nociceptive modulator, as the neurotrophin has an important part in the initiation and maintenance of inflammatory, chronic, and/or neuropathic pain at the peripheral and central level. At the spinal level, BDNF intervenes in the regulation of chloride equilibrium potential, decreases the excitatory synaptic drive to inhibitory neurons, with complex changes in GABAergic/glycinergic synaptic transmission, and increases excitatory transmission in the superficial dorsal horn. Differently from BDNF, the role of GDNF still remains to be unraveled in full. This review resumes the current literature on the interplay between BDNF and GDNF in the regulation of nociceptive neurotransmission in the superficial dorsal horn of the spinal cord. We will first discuss the circuitries involved in such a regulation, as well as the reciprocal interactions between the two factors in nociceptive pathways. The development of small molecules specifically targeting BDNF, GDNF and/or downstream effectors is opening new perspectives for investigating these neurotrophic factors as modulators of nociceptive transmission and chronic pain. Therefore, we will finally consider the molecules of (potential) pharmacological relevance for tackling normal and pathological pain.

生长因子 BDNF 和 GDNF 作为成熟中枢神经系统 (CNS) 突触传递的调节剂越来越受到关注。这两种分子在神经元中进行受调节的分泌，并可能顺行转运至末端，在那里它们可以正向或负向调节快速突触传递。如今，对于 BDNF 作为促伤害性调节剂的作用已达成广泛共识，因为神经营养素在外周和中枢水平的炎症、慢性和/或神经性疼痛的引发和维持中发挥着重要作用。在脊髓水平，BDNF 干预氯平衡电位的调节，减少对抑制性神经元的兴奋性突触驱动，伴随 GABA 能/甘氨酸能突触传递的复杂变化，并增加浅表背角的兴奋性传递。与 BDNF 不同，GDNF 的作用仍有待完全阐明。本综述回顾了有关 BDNF 和 GDNF 在脊髓浅背角伤害性神经传递调节中相互作用的最新文献。我们将首先讨论参与这种调节的电路，以及伤害感受通路中两个因素之间的相互作用。专门针对 BDNF、GDNF 和/或下游效应器的小分子的开发为研究这些神经营养因子作为伤害性传播和慢性疼痛的调节剂开辟了新的视角。因此，我们最终将考虑与解决正常和病理性疼痛具有（潜在）药理学相关性的分子。