Effects of red nucleus inactivation on burst discharge in turtle cerebellum in vitro: evidence for positive feedback.

Effects of red nucleus inactivation on burst discharge in turtle cerebellum in vitro: evidence for positive feedback.
复制标题

红核失活对体外龟小脑爆发放电的影响:正反馈的证据。

DOI:
10.1152/jn.1996.76.4.2200
复制
发表时间:
1996
影响因子:
2.5
通讯作者:
Keifer,J
Keifer,J
中科院分区:
医学3区
文献类型:
--
作者:
Keifer,J

文献摘要

被引文献

相似文献

1.在有行为的动物中,红核在肢体运动期间产生持续的动作电位放电。这些爆发被认为是对运动参数进行编码,从而代表运动指令。在海龟的离体脑干-小脑中也可以记录到类似的爆发。在该制剂中,红核神经元的持续放电被假定为通过N-甲基-D-天冬氨酸介导的细胞机制与复发性小脑红核网络中的正反馈相结合而产生。本研究旨在验证这一正反馈假说。在记录小脑深核和皮层的持续放电过程中,红核被显微注射可逆失活。如果小脑的活动因红核失活而减弱,则正反馈假说将得到支持。如果小脑活动不受影响,就必须假定一种非复发性的兴奋源。2.细胞外单单位记录来自小脑深核、小脑皮质和前庭核中的神经元。短时间电刺激脊髓,激活感觉结构,诱发爆发性放电。在失活的红核,感觉投射到小脑,可能引起爆发性放电不受影响。用钴、利多卡因、γ-氨基丁酸(GABA)或6-氰基-7-硝基喹喔啉-2,3-二酮(CNQX)的压力显微注射可逆地使红核染色。还测试了盐水注射。3.持续放电记录在小脑外侧核的所有神经元大大衰减或完全阻断注射到红核的药物。这些影响是可逆的。在小脑皮层的记录中,63%的记录被阻断。测试的所有四种化合物都是爆发的有效阻断剂,尽管GABA的效果不如其他化合物。向红核中注射生理盐水没有效果。在小脑内侧核或前庭复合体中记录的单个单位的爆发性放电,其不接收来自红核的输入,没有显示红核失活的影响。4.结果表明,尽管可能触发爆发的感觉输入是完整的,但小脑的持续放电被红核的失活显著减弱。这些数据支持这一假设,持续放电的小脑红回路产生的分布式神经网络,使用正反馈。这些结果对正常脑功能和一些运动障碍的潜在机制有影响。
1. In behaving animals the red nucleus produces sustained action potential discharge during movements of the limbs. These bursts are thought to encode parameters of movement and thereby represent motor commands. Similar bursts can be recorded in the in vitro brain stem-cerebellum from the turtle. In this preparation, sustained discharge of red nucleus neurons was postulated to be generated by N-methyl-D-aspartate-mediated cellular mechanisms acting in combination with positive feedback in a recurrent cerebellorubral network. The present study was designed to test this positive feedback hypothesis. During recording of sustained discharge in the deep cerebellar nuclei and cortex, the red nucleus was reversibly inactivated by microinjection. The positive feedback hypothesis would be supported if activity in the cerebellum was attenuated by inactivation of the red nucleus. A nonrecurrent source of excitation would have to be postulated if cerebellar activity was unaffected. 2. Extracellular single-unit recordings were made from neurons in the deep cerebellar nuclei, cerebellar cortex, and vestibular nuclei. Burst discharges were evoked by brief electrical stimuli applied to the spinal cord that activated sensory structures. During inactivation of the red nucleus, sensory projections to the cerebellum that may evoke burst discharge were unaffected. Pressure microinjections of cobalt, lidocaine, gamma-aminobutyric acid (GABA), or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) were used to reversibly inactivate the red nucleus. Saline injections were also tested. 3. Sustained discharge of all neurons recorded in the lateral cerebellar nucleus was greatly attenuated or blocked completely by injection of the pharmacological agents into the red nucleus. These effects were reversible. Of the recordings in the cerebellar cortex, 63% of these were blocked. All four compounds tested were effective blockers of the bursts, although the effects of GABA were less potent than the others. Saline injections into the red nucleus showed no effect. Burst discharges of single units recorded in either the medial cerebellar nucleus or the vestibular complex, which do not receive input from the red nucleus, showed no effect of red nucleus inactivation. 4. The results showed that sustained discharge in the cerebellum was significantly attenuated by inactivation of the red nucleus even though sensory input that may trigger the bursts was intact. These data support the hypothesis that sustained discharge in the cerebellorubral circuit is generated by a distributed neuronal network that uses positive feedback. The results have implications for mechanisms underlying normal brain function and some motor disorders.