Voloshin M Ia, Lukhanina E P, Kolomiets B P, Burchinskaia L F, Nosenko N D
Neirofiziologiia. 1989;21(5):620-9.
Peculiarities of excitation and inhibition evoked in motor thalamic nuclei (VA-VL) neurons by electrical stimulation of red nucleus were studied on intact cats and after injection of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 5 mg/kg i.m., p.d. during five days). Two days after the last injection as much as 48% of nigral neurons were destroyed and the content of dopamine in the caudate nucleus fell to 30% as compared to intact animals. Before acute experiments all cats were anaesthetized with ketalar and immobilized with myorelaxine. It was found that MPTP injections caused a decrease of the inhibition duration and effectiveness in relay and nonrelay VA-VL neurons. The inhibition deficiency was accompanied by shortening of latencies of orthodromic responses evoked by red nucleus stimulation and facilitation of antidromic spikes invasion into somata of relay neurons after motor cortex stimulation. It was suggested that the reduction of GABAergic nigro-thalamic influences modulated by dopamine underlay the developing deficiency of inhibition.
在完整的猫以及注射N-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP;5mg/kg,肌肉注射,连续五天)后,研究了电刺激红核在运动丘脑核(VA-VL)神经元中诱发的兴奋和抑制特性。最后一次注射两天后,与完整动物相比,黑质神经元多达48%被破坏,尾状核中的多巴胺含量降至30%。在急性实验前,所有猫均用氯胺酮麻醉并用肌松剂固定。发现注射MPTP导致中继和非中继VA-VL神经元的抑制持续时间和有效性降低。抑制不足伴随着红核刺激诱发的顺行反应潜伏期缩短以及运动皮层刺激后逆向动作电位侵入中继神经元胞体的促进。有人认为,多巴胺调节的GABA能黑质-丘脑影响的减少是抑制不足发展的基础。