Grau James W, Crown Eric D, Ferguson Adam R, Washburn Stephanie N, Hook Michelle A, Miranda Rajesh C
Department of Psychology, Texas A&M University, College Station, TX 77843-4235, USA.
Behav Cogn Neurosci Rev. 2006 Dec;5(4):191-239. doi: 10.1177/1534582306289738.
Using spinally transected rats, research has shown that neurons within the L4-S2 spinal cord are sensitive to response-outcome (instrumental) relations. This learning depends on a form of N-methyl-D-aspartate (NMDA)-mediated plasticity. Instrumental training enables subsequent learning, and this effect has been linked to the expression of brain-derived neurotrophic factor. Rats given uncontrollable stimulation later exhibit impaired instrumental learning, and this deficit lasts up to 48 hr. The induction of the deficit can be blocked by prior training with controllable shock, the concurrent presentation of a tonic stimulus that induces antinociception, or pretreatment with an NMDA or gamma-aminobutyric acid-A antagonist. The expression of the deficit depends on a kappa opioid. Uncontrollable stimulation enhances mechanical reactivity (allodynia), and treatments that induce allodynia (e.g., inflammation) inhibit learning. In intact animals, descending serotonergic neurons exert a protective effect that blocks the adverse consequences of uncontrollable stimulation. Uncontrollable, but not controllable, stimulation impairs the recovery of function after a contusion injury.
利用脊髓横断的大鼠进行的研究表明，L4 - S2脊髓内的神经元对反应 - 结果（工具性）关系敏感。这种学习依赖于一种N - 甲基 - D - 天冬氨酸（NMDA）介导的可塑性。工具性训练能够促进后续学习，且这种效应与脑源性神经营养因子的表达有关。随后给予不可控刺激的大鼠表现出工具性学习受损，且这种缺陷可持续长达48小时。该缺陷的诱导可通过先前的可控电击训练、同时呈现诱导抗伤害感受的强直刺激或用NMDA或γ - 氨基丁酸 - A拮抗剂进行预处理来阻断。该缺陷的表达依赖于κ阿片样物质。不可控刺激会增强机械反应性（异常性疼痛），而诱导异常性疼痛的处理（如炎症）会抑制学习。在完整动物中，下行的5 - 羟色胺能神经元发挥保护作用，可阻断不可控刺激的不良后果。不可控而非可控刺激会损害挫伤性损伤后的功能恢复。
