Battaglia Fortunato, Ghilardi Maria Felice, Quartarone Angelo, Bagnato Sergio, Girlanda Paolo, Hallett Mark
Department of Physiology and Pharmacology, CUNY School of Medicine, New York, New York 10031, USA.
Mov Disord. 2006 Dec;21(12):2230-3. doi: 10.1002/mds.21138.
We investigated the hypothesis that Parkinsons's disease (PD) is associated with abnormal plasticity of the neuronal circuits mediating blink reflex. We induced long-term potentiation (LTP)-like plasticity in trigeminal wide dynamic range neurons of the blink reflex circuit by pairing an high-frequency train of electrical stimuli over the right supraorbital nerve (SO) coincident with the R2 response elicited by a preceding SO stimulus. The facilitation of the R2 response after the induction protocol was markedly decreased in patients relative to controls. Treatment with dopaminergic drugs normalized the LTP-like plasticity of the R2 response. We conclude that nigrostriatal denervation disrupts LTP-like plasticity in the trigeminal reflex circuit.
我们研究了帕金森病（PD）与介导眨眼反射的神经回路异常可塑性相关的假说。我们通过将右侧眶上神经（SO）上的高频电刺激序列与先前SO刺激引发的R2反应同时配对，在眨眼反射回路的三叉神经宽动态范围神经元中诱导出类似长时程增强（LTP）的可塑性。与对照组相比，诱导方案后患者的R2反应的易化明显降低。多巴胺能药物治疗使R2反应的LTP样可塑性恢复正常。我们得出结论，黑质纹状体去神经支配会破坏三叉神经反射回路中的LTP样可塑性。
