Baumbauer Kyle M, Young Erin E, Hoy Kevin C, Joynes Robin L
Department of Psychology, Texas A&M University, College Station, TX 77843, USA.
Behav Neurosci. 2007 Oct;121(5):1082-94. doi: 10.1037/0735-7044.121.5.1082.
Previous research has demonstrated that spinally transected rats can acquire a prolonged flexion response to prevent the delivery of shock. However, rats that receive shock irrespective of leg position cannot learn to maintain the same response. The present experiments examined the role of neurokinin receptors in this learning deficit. Results demonstrated that neurokinin (NK1 and NK2) antagonists blocked the induction of the learning deficit, whereas NK agonists induced a learning deficit. The study found that NK agonist administration did not substitute for uncontrollable shock exposure. Finally, administration of an NK1 agonist prior to uncontrollable shock prevented the induction of the deficit. These results provide additional evidence that engaging nociceptive plasticity undermines the capability of spinal neurons to support adaptive changes.
先前的研究表明，脊髓横断的大鼠能够获得一种延长的屈曲反应以避免电击。然而，无论腿部位置如何都会受到电击的大鼠无法学会保持相同的反应。本实验研究了神经激肽受体在这种学习缺陷中的作用。结果表明，神经激肽（NK1和NK2）拮抗剂可阻断学习缺陷的诱导，而NK激动剂则会诱导学习缺陷。该研究发现，给予NK激动剂并不能替代不可控的电击暴露。最后，在不可控电击前给予NK1激动剂可防止缺陷的诱导。这些结果提供了额外的证据，表明参与伤害性可塑性会破坏脊髓神经元支持适应性变化的能力。
