Département Nociception et Douleur, Institut des Neurosciences Cellulaires et Intégratives, UPR 3212 Centre National de la Recherche Scientifique, Université de Strasbourg, 21 rue René Descartes, F-67084 Strasbourg, France.
Eur J Neurosci. 2012 Dec;36(11):3500-8. doi: 10.1111/j.1460-9568.2012.08273.x. Epub 2012 Sep 12.
In acute rat spinal cord slices, the application of capsaicin (5 μm, 90 s), an agonist of transient receptor potential vanilloid 1 receptors expressed by a subset of nociceptors that project to laminae I-II of the spinal cord dorsal horn, induced an increase in the frequency of spontaneous excitatory and spontaneous inhibitory postsynaptic currents in about half of the neurons in laminae II, III-IV and V. In the presence of tetrodotoxin, which blocks action potential generation and polysynaptic transmission, capsaicin increased the frequency of miniature excitatory postsynaptic currents in only 30% of lamina II neurons and had no effect on the frequency of miniature excitatory postsynaptic currents in laminae III-V or on the frequency of miniature inhibitory postsynaptic currents in laminae II-V. When the communication between lamina V and more superficial laminae was interrupted by performing a mechanical section between laminae IV and V, capsaicin induced an increase in spontaneous excitatory postsynaptic current frequency in laminae II-IV and an increase in spontaneous inhibitory postsynaptic current frequency in lamina II that were similar to those observed in intact slices. However, in laminae III-IV of transected slices, the increase in spontaneous inhibitory postsynaptic current frequency was virtually abolished. Our results indicate that nociceptive information conveyed by transient receptor potential vanilloid 1-expressing nociceptors is transmitted from lamina II to deeper laminae essentially by an excitatory pathway and that deep laminae exert a 'feedback' control over neurons in laminae III-IV by increasing inhibitory synaptic transmission in these laminae. Moreover, we provide evidence that laminae III-IV might play an important role in the processing of nociceptive information in the dorsal horn.
在急性大鼠脊髓切片中，应用辣椒素（5μm，90s），一种表达于痛觉感受器的瞬时受体电位香草酸 1 型受体（TRPV1）的激动剂，该受体投射到脊髓背角的 I-II 层，可增加 II、III-IV 和 V 层中约一半神经元的自发性兴奋性和自发性抑制性突触后电流频率。在河豚毒素（TTX）存在下，TTX 阻断动作电位产生和多突触传递，辣椒素仅增加 30%的 II 层神经元的微小兴奋性突触后电流频率，对 III-V 层的微小兴奋性突触后电流频率或 II-V 层的微小抑制性突触后电流频率均无影响。当在 IV 和 V 层之间进行机械性横切以中断 V 层与更浅层之间的通讯时，辣椒素可增加 II-IV 层的自发性兴奋性突触后电流频率，并增加 II 层的自发性抑制性突触后电流频率，与完整切片中观察到的相似。然而，在横切切片的 III-IV 层中，自发性抑制性突触后电流频率的增加几乎被消除。我们的结果表明，表达 TRPV1 的伤害感受器传递的伤害性信息主要通过兴奋性途径从 II 层传递到更深的层，并且深层层通过增加这些层中的抑制性突触传递来对 III-IV 层中的神经元施加“反馈”控制。此外，我们提供的证据表明，III-IV 层可能在背角中伤害性信息的处理中发挥重要作用。
